Author: "Cash, D" / Publication Year Range: Last 50 years - Searchworks@Jio Institute Digital Library Search Results

Your search keyword '"Cash, D"' showing total 356 results

Start Over Author "Cash, D" Publication Year Range Last 50 years

356 results on '"Cash, D"'

1. Longitudinal cerebral perfusion in presymptomatic genetic frontotemporal dementia: GENFI results

Author: Pasternak, M., Mirza, S., Luciw, N., Mutsaerts, H., (0000-0002-3201-6002) Petr, J., Thomas, D., Cash, D., Bocchetta, M., Tartaglia, C., Mitchell, S., Black, S., Freedman, M., Tang-Wai, D., Rogaeva, E., Russell, L., Bouzigues, A., Swieten, J., Jiskoot, L., Seelaar, H., Laforce Jr., R., Tiraboschi, P., Borroni, B., Galimberti, D., Rowe, J., Graff, C., Finger, E., Sandro, S., Mendonça, A., Butler, C., Gerhard, A., Sánchez-Valle, R., Moreno, F., Synofzik, M., Vandenberghe, R., Ducharme, S., Levin, J., Otto, M., Santana, I., Strafella, A., Macintosh, B., Rohrer, J., Masellis, M., Pasternak, M., Mirza, S., Luciw, N., Mutsaerts, H., (0000-0002-3201-6002) Petr, J., Thomas, D., Cash, D., Bocchetta, M., Tartaglia, C., Mitchell, S., Black, S., Freedman, M., Tang-Wai, D., Rogaeva, E., Russell, L., Bouzigues, A., Swieten, J., Jiskoot, L., Seelaar, H., Laforce Jr., R., Tiraboschi, P., Borroni, B., Galimberti, D., Rowe, J., Graff, C., Finger, E., Sandro, S., Mendonça, A., Butler, C., Gerhard, A., Sánchez-Valle, R., Moreno, F., Synofzik, M., Vandenberghe, R., Ducharme, S., Levin, J., Otto, M., Santana, I., Strafella, A., Macintosh, B., Rohrer, J., and Masellis, M.
Abstract: Genetic frontotemporal dementia is most commonly attributable to mutations in the C9orf72, GRN, or MAPT genes. The disease has near-complete penetrance, making presymptomatic carriers an ideal population for ascertaining the earliest changes in disease progression and the identification of suitable biomarkers for designing therapeutic trials when minimal neuronal loss has occurred. Cerebral perfusion, as measured by arterial spin labelling (ASL) MRI, has shown promise in being one such biomarker. However, longitudinal profiles of change in perfusion over time in presymptomatic carriers across all three genetic subgroups are lacking. Using data from the multicenter GENetic Frontotemporal dementia Initiative, we investigated longitudinal profiles of cerebral perfusion using ASL-MRI in C9orf72 (n = 42), GRN (n = 70), and MAPT (n = 31) presymptomatic mutation carriers and non-carrier controls (n = 158). ASL and T1w scans were processed with the ExploreASL pipeline to produce partial volume corrected perfusion images, which were parcellated to extract mean perfusion values from whole brain grey matter and regions defined by the second version of the automated anatomical atlas (AAL2). Linear mixed effects models were used to assess longitudinal perfusion change. Mutation carrier groups and non-carriers were statistically indistinguishable by baseline demographic and clinical measures. Decline in whole brain grey matter perfusion over time was more pronounced in all three carrier subgroups relative to controls, with changes most pronounced in GRN, followed by C9orf72 and MAPT variants. Additionally, GRN and MAPT groups featured global grey matter hypoperfusion relative to non-carrier controls as early as one year after baseline measurement, with C9orf72 featuring significant hypoperfusion after two years. Region of interest analysis demonstrated that each genetic subgroup had its own regional profile in terms of longitudinal perfusion decline. Perfusion decline in C9orf72
Published: 2024

2. Striatal Dopaminergic Deficit and Sleep in Idiopathic Rapid Eye Movement Behaviour Disorder: An Explorative Study

Author: Wasserman D, Bindman D, Nesbitt AD, Cash D, Milosevic M, Francis PT, Chaudhuri KR, Leschziner GD, Ferini-Strambi L, Ballard C, Eccles A, and Rosenzweig I
Subjects: isolated rapid eye movement behaviour disorder, polysomnography, sleep architecture, striatum, striatal dopamine transporter uptake tracer signalling imaging, datscan., Psychiatry, RC435-571, Neurophysiology and neuropsychology, QP351-495
Abstract: Danielle Wasserman,1,2,* Dorothea Bindman,1,* Alexander D Nesbitt,1– 3 Diana Cash,4 Milan Milosevic,5 Paul T Francis,6 K Ray Chaudhuri,7 Guy D Leschziner,1,2 Luigi Ferini-Strambi,8 Clive Ballard,9 Amy Eccles,10 Ivana Rosenzweig1,2 1Sleep and Brain Plasticity Centre, Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King’s College London, London, UK; 2Sleep Disorders Centre, Guy’s and St Thomas’ NHS Foundation Trust, London, UK; 3Headache Group, Department of Clinical Neurosciences, King’s College Hospital NHS Foundation Trust, London, UK; 4BRAIN, Department of Neuroimaging, King’s College London, London, UK; 5School of Public Health “Andrija Stampar“, University of Zagreb School of Medicine, Zagreb, Croatia; 6Wolfson Centre for Age-Related Diseases, King’s College London, London, UK; 7Movement Disorders Unit, King’s College Hospital, Department of Clinical and Basic Neurosciences, Institute of Psychiatry, Psychology & Neuroscience, Parkinson Foundation Centre of Excellence, King’s College London, London, UK; 8Sleep Disorders Center, Department of Clinical Neurosciences, Università Vita-Salute San Raffaele, Milan, Italy; 9Medical School, University of Exeter, Exeter, UK; 10Department of Nuclear Medicine, Guy’s and St. Thomas’ NHS Foundation Trust, London, UK*These authors contributed equally to this workCorrespondence: Ivana RosenzweigSleep and Brain Plasticity Centre, Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King’s College London, Box 089, De Crespigny Park, London SE5 8AF, UKEmail ivana.1.rosenzweig@kcl.ac.ukIntroduction: Idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) is increasingly recognised as an important precursor disease state of alpha-synucleinopathies. This parasomnia is characterized by a history of recurrent nocturnal dream enactment behaviour, loss of skeletal muscle atonia, and increased phasic muscle activity during REM sleep. Neuroimaging studies of striatal dopamine transporter uptake tracer signaling suggest increasing dopaminergic deficit across the continuum of the alpha-synucleinopathies, with early sleep dysfunction suggestive of early caudate dysfunction. Henceforth, we set out to investigate the relationship between early sleep changes and the striatal dopaminergic availability in iRBD.Methods: Twelve patients with iRBD, who had undergone a video polysomnography and a neuroimaging assessment of striatal dopamine transporter (DaT) uptake tracer signaling, and 22 matched controls who had similarly undergone a video polysomnography were retrospectively identified. Data were statistically analyzed to identify altered sleep parameters and correlate them with striatal dopamine transporter uptake tracer signaling.Results: The iRBD patients exhibited an increased number of periodic limb movements during sleep (P=0.001), compared to 22 age-matched healthy subjects. In addition, several significant links were found between regional DaT-uptakes and sleep architecture. Correlational analyses suggested a strong positive association between sleep fragmentation and dopamine deficiency in left caudate (r=− 0.630, P=0.028), whilst an increased uptake in the whole striatum was strongly linked to the sleep efficiency, and to a lesser degree to the length of sleep duration.Discussion: To the best of our knowledge, this is the first demonstration of a close relationship between dopaminergic availability in striatum and the quality of sleep in iRBD. Taken together, our exploratory findings suggest that subtle but functionally significant striatal changes in early stages of iRBD may contribute to the further shaping of sleep architecture.Keywords: isolated rapid eye movement behaviour disorder, polysomnography, sleep architecture, striatum, striatal dopamine transporter uptake tracer signalling imaging, DaTSCAN
Published: 2021

3. Intraperitoneal delivery of acetate-encapsulated liposomal nanoparticles for neuroprotection of the penumbra in a rat model of ischemic stroke

Author: So PW, Ekonomou A, Galley K, Brody L, Sahuri-Arisoylu M, Rattray I, Cash D, and Bell JD
Subjects: ischemic stroke, acetate, liposomes, neuroinflammation, microglia, mid-cerebral artery occlusion, Medicine (General), R5-920
Abstract: Po-Wah So,1 Antigoni Ekonomou,1 Kim Galley,1 Leigh Brody,2 Meliz Sahuri-Arisoylu,2 Ivan Rattray,3 Diana Cash,1 Jimmy D Bell2 1King’s College London, Institute of Psychiatry, Psychology and Neuroscience, Department of Neuroimaging, London, UK; 2University of Westminster, Research Centre for Optimal Health, London, UK; 3King’s College London, Institute of Psychiatry, Psychology and Neuroscience, Department of Basic and Clinical Neuroscience, London, UK Background: Ischemic stroke is a devastating condition, with metabolic derangement and persistent inflammation enhancing the initial insult of ischaemia. Recombinant tissue plasminogen remains the only effective treatment but limited as therapy must commence soon after the onset of symptoms.Purpose: We investigated whether acetate, which modulates many pathways including inflammation, may attenuate brain injury in stroke. As acetate has a short blood half-life and high amounts irritate the gastrointestinal tract, acetate was administered encapsulated in a liposomal nanoparticle (liposomal-encapsulated acetate, LITA).Methods: Transient ischemia was induced by 90 mins middle-cerebral artery occlusion (MCAO) in Sprague-Dawley rats, and LITA or control liposomes given intraperitoneally at occlusion and daily for up to two weeks post-MCAO. Magnetic resonance imaging (MRI) was used to estimate lesion volume at 24 h, 1 and 2 weeks post-MCAO and anterior lateral ventricular volume (ALVv) at 2 weeks post-MCAO. Locomotive behaviour was tested prior to the final MRI scan. After the final scan, brains were collected, and immunohistochemistry was performed. Results: Lesion volumes were decreased by ~80% from 24 h to one-week post-MCAO, in both control and LITA groups (P
Published: 2019

4. Cerebellar and subcortical atrophy contribute to psychiatric symptoms in frontotemporal dementia

Author: Bussy, A., Levy, J., Best, T., Patel, R., Cupo, L., Van Langenhove, T., Nielsen, J., Pijnenburg, Y., Waldö, M., Remes, A., Schroeter, M., Santana, I., Pasquier, F., Otto, M., Danek, A., Levin, J., Le Ber, I., Vandenberghe, R., Synofzik, M., Moreno, F., de Mendonça, A., Sanchez‐Valle, R., Laforce, R., Langheinrich, T., Gerhard, A., Graff, C., Butler, C., Sorbi, S., Jiskoot, L., Seelaar, H., van Swieten, J., Finger, E., Tartaglia, M., Masellis, M., Tiraboschi, P., Galimberti, D., Borroni, B., Rowe, J., Bocchetta, M., Rohrer, J., Devenyi, G., Chakravarty, M., Ducharme, S., Esteve, A., Nelson, A., Bouzigues, A., Heller, C., Greaves, C., Cash, D., Thomas, D., Todd, E., Benotmane, H., Zetterberg, H., Swift, I., Nicholas, J., Samra, K., Russell, L., Shafei, R., Convery, R., Timberlake, C., Cope, T., Rittman, T., Benussi, A., Premi, E., Gasparotti, R., Archetti, S., Gazzina, S., Cantoni, V., Arighi, A., Fenoglio, C., Scarpini, E., Fumagalli, G., Borracci, V., Rossi, G., Giaccone, G., Di Fede, G., Caroppo, P., Prioni, S., Redaelli, V., Tang‐Wai, D., Rogaeva, E., Castelo‐Branco, M., Freedman, M., Keren, R., Black, S., Mitchell, S., Shoesmith, C., Bartha, R., Rademakers, R., Poos, J., Papma, J., Giannini, L., van Minkelen, R., Nacmias, B., Ferrari, C., Polito, C., Lombardi, G., Bessi, V., Veldsman, M., Andersson, C., Thonberg, H., Öijerstedt, L., Jelic, V., Thompson, P., Lladó, A., Antonell, A., Olives, J., Balasa, M., Bargalló, N., Borrego‐Ecija, S., Verdelho, A., Maruta, C., Ferreira, C., Miltenberger, G., do Couto, F., Gabilondo, A., Gorostidi, A., Villanua, J., Cañada, M., Tainta, M., Zulaica, M., Barandiaran, M., Alves, P., Bender, B., Wilke, C., Graf, L., Vogels, A., Vandenbulcke, M., Van Damme, P., Bruffaerts, R., Poesen, K., Rosa‐Neto, P., Gauthier, S., Camuzat, A., Brice, A., Bertrand, A., Funkiewiez, A., Rinaldi, D., Saracino, D., Colliot, O., Sayah, S., Prix, C., Wlasich, E., Wagemann, O., Loosli, S., Schönecker, S., Hoegen, T., Lombardi, J., Anderl‐Straub, S., Rollin, A., Kuchcinski, G., Bertoux, M., Lebouvier, T., Deramecourt, V., Santiago, B., Duro, D., Leitão, M., Almeida, M., Tábuas‐Pereira, M., Afonso, S., Engel, A., Polyakova, M., Erasmus MC other, Neurology, Radiology & Nuclear Medicine, Clinical Genetics, GENetic Frontotemporal dementia Initiative (GENFI), Lombardi, Gemma, Bessi, Valentina, Veldsman, Michele, Andersson, Christin, Thonberg, Hakan, Öijerstedt, Linn, Jelic, Vesna, Thompson, Paul, Langheinrich, Tobias, Lladó, Albert, Antonell, Anna, Olives, Jaume, Balasa, Mircea, Bargalló, Nuria, Borrego-Ecija, Sergi, Verdelho, Ana, Maruta, Carolina, Ferreira, Catarina B, Miltenberger, Gabriel, do Couto, Frederico Simões, Gabilondo, Alazne, Gorostidi, Ana, Villanua, Jorge, Cañada, Marta, Tainta, Mikel, Zulaica, Miren, Barandiaran, Myriam, Alves, Patricia, Bender, Benjamin, Wilke, Carlo, Graf, Lisa, Vogels, Annick, Vandenbulcke, Mathieu, Van Damme, Philip, Bruffaerts, Rose, Poesen, Koen, Rosa-Neto, Pedro, Gauthier, Serge, Camuzat, Agnès, Brice, Alexis, Bertrand, Anne, Funkiewiez, Aurélie, Rinaldi, Daisy, Saracino, Dario, Colliot, Olivier, Sayah, Sabrina, Prix, Catharina, Wlasich, Elisabeth, Wagemann, Olivia, Loosli, Sandra, Schönecker, Sonja, Hoegen, Tobias, Lombardi, Jolina, Anderl-Straub, Sarah, Rollin, Adeline, Kuchcinski, Gregory, Bertoux, Maxime, Lebouvier, Thibaud, Deramecourt, Vincent, Santiago, Beatriz, Duro, Diana, Leitão, Maria João, Almeida, Maria Rosario, Tábuas-Pereira, Miguel, Afonso, Sónia, Engel, Annerose, Polyakova, Maryna, Esteve, Aitana Sogorb, Nelson, Annabel, Bouzigues, Arabella, Heller, Carolin, Greaves, Caroline V, Cash, David, Thomas, David L, Todd, Emily, Benotmane, Hanya, Zetterberg, Henrik, Swift, Imogen J, Nicholas, Jennifer, Samra, Kiran, Russell, Lucy L, Bocchetta, Martina, Shafei, Rachelle, Convery, Rhian S, Timberlake, Carolyn, Cope, Thomas, Rittman, Timothy, Benussi, Alberto, Premi, Enrico, Gasparotti, Roberto, Archetti, Silvana, Gazzina, Stefano, Cantoni, Valentina, Arighi, Andrea, Fenoglio, Chiara, Scarpini, Elio, Fumagalli, Giorgio, Borracci, Vittoria, Rossi, Giacomina, Giaccone, Giorgio, Di Fede, Giuseppe, Caroppo, Paola, Tiraboschi, Pietro, Prioni, Sara, Redaelli, Veronica, Tang-Wai, David, Rogaeva, Ekaterina, Castelo-Branco, Miguel, Freedman, Morris, Keren, Ron, Black, Sandra, Mitchell, Sara, Shoesmith, Christen, Bartha, Robart, Rademakers, Rosa, Poos, Jackie, Papma, Janne M, Giannini, Lucia, van Minkelen, Rick, Pijnenburg, Yolande, Nacmias, Benedetta, Ferrari, Camilla, Polito, Cristina, Bussy, Aurélie [0000-0001-6695-9941], Nielsen, Jørgen E [0000-0003-0453-5582], Borroni, Barbara [0000-0001-9340-9814], Bocchetta, Martina [0000-0003-1814-5024], Devenyi, Gabriel A [0000-0002-7766-1187], Apollo - University of Cambridge Repository, and Amsterdam Neuroscience - Neurodegeneration
Subjects: C9orf72 Protein, Radiological and Ultrasound Technology, Medizin, frontotemporal dementia, Neurology, Frontotemporal Dementia, Cerebellum, Humans, magnetic resonance imaging, genetics, neuropsychiatry, Radiology, Nuclear Medicine and imaging, Human medicine, ddc:610, Neurology (clinical), Atrophy, Anatomy, genetics [Frontotemporal Dementia], genetics [C9orf72 Protein]
Abstract: Funder: Alzheimer Society of Canada; Id: http://dx.doi.org/10.13039/501100000143, Funder: Weston Brain Institute; Id: http://dx.doi.org/10.13039/100012479, Funder: Fonds de Recherche du Québec ‐ Santé, Funder: Canadian Institutes of Health Research; Id: http://dx.doi.org/10.13039/501100000024, Funder: NIHR Rare Diseases Translational Research Collaboration, Funder: Deutsche Forschungsgemeinschaft; Id: http://dx.doi.org/10.13039/501100001659, Recent studies have reported early cerebellar and subcortical impact in the disease progression of genetic frontotemporal dementia (FTD) due to microtubule-associated protein tau (MAPT), progranulin (GRN) and chromosome 9 open reading frame 72 (C9orf72). However, the cerebello-subcortical circuitry in FTD has been understudied despite its essential role in cognition and behaviors related to FTD symptomatology. The present study aims to investigate the association between cerebellar and subcortical atrophy, and neuropsychiatric symptoms across genetic mutations. Our study included 983 participants from the Genetic Frontotemporal dementia Initiative including mutation carriers and noncarrier first-degree relatives of known symptomatic carriers. Voxel-wise analysis of the thalamus, striatum, globus pallidus, amygdala, and the cerebellum was performed, and partial least squares analyses (PLS) were used to link morphometry and behavior. In presymptomatic C9orf72 expansion carriers, thalamic atrophy was found compared to noncarriers, suggesting the importance of this structure in FTD prodromes. PLS analyses demonstrated that the cerebello-subcortical circuitry is related to neuropsychiatric symptoms, with significant overlap in brain/behavior patterns, but also specificity for each genetic mutation group. The largest differences were in the cerebellar atrophy (larger extent in C9orf72 expansion group) and more prominent amygdalar volume reduction in the MAPT group. Brain scores in the C9orf72 expansion carriers and MAPT carriers demonstrated covariation patterns concordant with atrophy patterns detectable up to 20 years before expected symptom onset. Overall, these results demonstrated the important role of the subcortical structures in genetic FTD symptom expression, particularly the cerebellum in C9orf72 and the amygdala in MAPT carriers.
Published: 2023

5. Obstructive sleep apnoea and Alzheimer’s disease: In search of shared pathomechanisms

Author: Polsek, D., Gildeh, N., Cash, D., Winsky-Sommerer, R., Williams, S.C.R., Turkheimer, F., Leschziner, G.D., Morrell, M.J., and Rosenzweig, I.
Published: 2018
Full Text: View/download PDF

6. Motor symptoms in genetic frontotemporal dementia: developing a new module for clinical rating scales

Author: Samra, K, MacDougall, AM, Peakman, G, Bouzigues, A, Bocchetta, M, Cash, DM, Greaves, CV, Convery, RS, van Swieten, JC, Jiskoot, L, Seelaar, H, Butler, CR, Fenoglio, C, Rohrer, JD, Gerhard, A, Ducharme, S, Le Ber, I, Tiraboschi, P, Santana, I, Pasquier, F, Levin, J, Shoesmith, C, Otto, M, Russell, LL, Nelson, A, Cash, D, Thomas, DL, Todd, E, Ferrari, C, Benotmane, H, Timberlake, C, Gabilondo, A, Cope, T, Rittman, T, Benussi, A, Premi, E, Gasparotti, R, Thompson, P, Archetti, S, Fumagalli, G, do Couto, FS, Borracci, V, Polito, C, Rossi, G, Giaccone, G, Di Fede, G, Caroppo, P, Ferreira, CB, Prioni, S, Langheinrich, T, Redaelli, V, Lladó, A, Bartha, R, Tang-Wai, D, Rogaeva, E, Castelo-Branco, M, Freedman, M, Keren, R, Black, S, Mitchell, S, Miltenberger, G, Rademakers, R, Poos, J, Papma, JM, Giannini, L, van Minkelen, R, Pijnenburg, Y, Gauthier, S, Nacmias, B, Lombardi, G, Bessi, V, Veldsman, M, Andersson, C, Thonberg, H, Öijerstedt, L, Prix, C, Jelic, V, Antonell, A, Graff, C, Olives, J, Balasa, M, Bargalló, N, Borrego-Ecija, S, Verdelho, A, Kuchcinski, G, Maruta, C, Gorostidi, A, Laforce, R, Villanua, J, Wlasich, E, Cañada, M, Tainta, M, Zulaica, M, Barandiaran, M, Moreno, F, Alves, P, Bender, B, Bertoux, M, Wilke, C, Lebouvier, T, Camuzat, A, Graf, L, Vogels, A, Vandenbulcke, M, Van Damme, P, Bruffaerts, R, Poesen, K, Rosa-Neto, P, Sanchez-Valle, R, Brice, A, Bertrand, A, Funkiewiez, A, Rinaldi, D, Saracino, D, Colliot, O, Sorbi, S, Sayah, S, Wagemann, O, Loosli, S, Schönecker, S, Hoegen, T, Lombardi, J, Anderl-Straub, S, Nicholas, J, Rollin, A, Deramecourt, V, Arighi, A, Santiago, B, Duro, D, Leitão, MJ, Almeida, MR, Tábuas-Pereira, M, Gazzina, S, Afonso, S, Masellis, M, Tartaglia, C, Shafei, R, Rowe, JB, Borroni, B, Finger, E, Synofzik, M, Galimberti, D, Vandenberghe, R, de Mendonça, A, Cantoni, V, Genetic FTD Initiative (GENFI), Samra, Kiran [0000-0002-3105-7099], Apollo - University of Cambridge Repository, Maruta, Carolina, Ferreira, Catarina B, Miltenberger, Gabriel, do Couto, Frederico Simões, Gabilondo, Alazne, Gorostidi, Ana, Villanua, Jorge, Cañada, Marta, Tainta, Mikel, Zulaica, Miren, Barandiaran, Myriam, Alves, Patricia, Bender, Benjamin, Wilke, Carlo, Graf, Lisa, Vogels, Annick, Vandenbulcke, Mathieu, Van Damme, Philip, Bruffaerts, Rose, Poesen, Koen, Rosa-Neto, Pedro, Gauthier, Serge, Camuzat, Agnès, Brice, Alexis, Bertrand, Anne, Funkiewiez, Aurélie, Rinaldi, Daisy, Saracino, Dario, Colliot, Olivier, Sayah, Sabrina, Prix, Catharina, Wlasich, Elisabeth, Wagemann, Olivia, Loosli, Sandra, Schönecker, Sonja, Hoegen, Tobias, Lombardi, Jolina, Anderl-Straub, Sarah, Rollin, Adeline, Kuchcinski, Gregory, Bertoux, Maxime, Lebouvier, Thibaud, Deramecourt, Vincent, Santiago, Beatriz, Duro, Diana, Leitão, Maria João, Almeida, Maria Rosario, Tábuas-Pereira, Miguel, Afonso, Sónia, Nelson, Annabel, Bocchetta, Martina, Cash, David, Thomas, David L, Todd, Emily, Benotmane, Hanya, Nicholas, Jennifer, Samra, Kiran, Shafei, Rachelle, Timberlake, Carolyn, Cope, Thomas, Rittman, Timothy, Benussi, Alberto, Premi, Enrico, Gasparotti, Roberto, Archetti, Silvana, Gazzina, Stefano, Cantoni, Valentina, Arighi, Andrea, Fenoglio, Chiara, Fumagalli, Giorgio, Borracci, Vittoria, Rossi, Giacomina, Giaccone, Giorgio, Di Fede, Giuseppe, Caroppo, Paola, Tiraboschi, Pietro, Prioni, Sara, Redaelli, Veronica, Tang-Wai, David, Rogaeva, Ekaterina, Castelo-Branco, Miguel, Freedman, Morris, Keren, Ron, Black, Sandra, Mitchell, Sara, Shoesmith, Christen, Bartha, Robart, Rademakers, Rosa, Poos, Jackie, Papma, Janne M, Giannini, Lucia, van Minkelen, Rick, Pijnenburg, Yolande, Nacmias, Benedetta, Ferrari, Camilla, Polito, Cristina, Lombardi, Gemma, Bessi, Valentina, Veldsman, Michele, Andersson, Christin, Thonberg, Hakan, Öijerstedt, Linn, Jelic, Vesna, Thompson, Paul, Langheinrich, Tobias, Lladó, Albert, Antonell, Anna, Olives, Jaume, Balasa, Mircea, Bargalló, Nuria, Borrego-Ecija, Sergi, and Verdelho, Ana
Subjects: Progranulin, Clinical Neurology, C9ORF72, tau Proteins, AMYOTROPHIC-LATERAL-SCLEROSIS, diagnosis [Frontotemporal Dementia], C9orf72, Tremor, Genetics, Humans, ddc:610, genetics [Frontotemporal Dementia], genetics [C9orf72 Protein], MUTATION, Science & Technology, C9orf72 Protein, HERITABILITY, Amyotrophic Lateral Sclerosis, PROGRESSIVE SUPRANUCLEAR PALSY, COGNITIVE IMPAIRMENT, REPEAT EXPANSION, genetics [tau Proteins], Motor, PATHOLOGICAL FEATURES, Neurology, FOS: Biological sciences, Frontotemporal Dementia, Mutation, Human medicine, Neurosciences & Neurology, Neurology (clinical), Tau, TAU, Life Sciences & Biomedicine, Frontotemporal dementia, PARKINSONISM
Abstract: Funder: CIBERNED, Funder: Canadian Institutes of Health Research; doi: http://dx.doi.org/10.13039/501100000024, Funder: Lemaire Family Foundation, Funder: Swedish Frontotemporal Dementia Initiative, Funder: Italian Ministry of Health, Funder: Weston Brain Institute; doi: http://dx.doi.org/10.13039/100012479, Funder: Mady Browaaeys Fund, Funder: Miriam Marks Brain Research UK, Funder: Bluefield Project, OBJECTIVE: To investigate the optimal method of adding motor features to a clinical rating scale for frontotemporal dementia (FTD). METHODS: Eight hundred and thirty-two participants from the international multicentre Genetic FTD Initiative (GENFI) study were recruited: 522 mutation carriers (with C9orf72, GRN and MAPT mutations) and 310 mutation-negative controls. A standardised clinical questionnaire was used to assess eight motor symptoms (dysarthria, dysphagia, tremor, slowness, weakness, gait disorder, falls and functional difficulties using hands). Frequency and severity of each motor symptom was assessed, and a principal component analysis (PCA) was performed to identify how the different motor symptoms loaded together. Finally, addition of a motor component to the CDR® plus NACC FTLD was investigated (CDR® plus NACC FTLD-M). RESULTS: 24.3% of mutation carriers had motor symptoms (31.7% C9orf72, 18.8% GRN, 19.3% MAPT) compared to 6.8% of controls. Slowness and gait disorder were the commonest in all genetic groups while tremor and falls were the least frequent. Symptom severity scores were similar to equivalent physical motor examination scores. PCA revealed that all motor symptoms loaded together so a single additional motor component was added to the CDR® plus NACC FTLD to form the CDR® plus NACC FTLD-M. Individual global scores were more severe with the CDR® plus NACC FTLD-M, and no patients with a clinically diagnosed motor disorder (ALS/FTD-ALS or parkinsonism) were classified anymore as asymptomatic (unlike the CDR® plus NACC FTLD alone). CONCLUSIONS: Motor features are present in mutation carriers at all disease stages across all three genetic groups. Inclusion of motor symptoms in a rating scale that can be used in future clinical trials will not only ensure a more accurate severity measure is recorded but that a wider spectrum of FTD phenotypes can be included in the same trial.
Published: 2022

7. A consensus protocol for functional connectivity analysis in the rat brain

Author: Grandjean, J., Desrosiers-Gregoire, G., Anckaerts, C., Angeles-Valdez, D., Ayad, F., Barrière, D., Blockx, I., Bortel, A., Broadwater, M., Cardoso, B., Célestine, M., Chavez-Negrete, J., Choi, S., Christiaen, E., Clavijo, P., Colon-Perez, L., Cramer, S., Daniele, T., Dempsey, E., Diao, Y., Doelemeyer, A., Dopfel, D., Dvořáková, L., Falfán-Melgoza, C., Fernandes, F., Fowler, C., Fuentes-Ibañez, A., Garin, C., Gelderman, E., Golden, C., Guo, C., Henckens, M., Hennessy, L., Herman , P., Hofwijks, N., Horien, C., Ionescu, T., Jones, J., Kaesser, J., Kim, E., Lambers, H., Lazari, A., Lee, S., Lillywhite, A., Liu, Y., López-Castro, A., López-Gil , X., Ma, Z., MacNicol, E., Madularu, D., Mandino, F., Marciano, S., McAuslan, M., McCunn, P., McIntosh, A., Meng, X., Meyer-Baese, L., Missault, S., Moro, F., Naessens, D., Nava-Gomez, L., Nonaka, H., Ortiz, J., Paasonen, J., Pais-Roldán, P., Peeters, L., Pereira, M., Perez, P., Pompilus, M., Prior, M., Rakhmatullin, R., Reimann, H., Reinwald, J., Triana Del Rio, R., Rivera-Olvera, A., Ruiz-Pérez, D., Russo, G., Rutten, T., Ryoke, R., Sack, M., Salvan, P., Sanganahalli, B., Schroeter, A., Seewoo , B., Selingue, E., Seuwen, A., Shi, B., Sirmpilatze, N., Smith, J., Smith, C., Sobczak, F., Stenroos, P., Straathof, M., Strobelt, S., Sumiyoshi, A., Takahashi, K., Torres-García, M., Tudela, R., van den Berg, M., van der Marel, K., van Hout, A., Vertullo, R., Vidal, B., Vrooman, R., Wang, X., Wank, I., Watson, D., Yin, T., Zhang, Y., Zurbruegg, S., Achard, S., Alcauter, S., Auer, D., Barbier, E., Baudewig, J., Beckmann, C., Beckmann, N., Becq, G., Blezer, E., Bolbos, R., Boretius, S., Bouvard, S., Budinger, E., Buxbaum, J., Cash, D., Chapman, V., Chuang, K., Ciobanu, L., Coolen, B., Dalley, J., Dhenain, M., Dijkhuizen, R., Esteban, O., Faber, C., Febo, M., Feindel, K., Forloni, G., Fouquet, J., Garza-Villarreal, E., Gass, N., Glennon, J., Gozzi, A., Gröhn, O., Harkin, A., Heerschap, A., Helluy, X., Herfert , K., Heuser, A., Homberg, J., Houwing, D., Hyder, F., Ielacqua, G., Jelescu, I., Johansen-Berg, H., Kaneko, G., Kawashima, R., Keilholz, S., Keliris, G., Kelly, C., Kerskens, C., Khokhar, J., Kind, P., Langlois, J., Lerch, J., López-Hidalgo, M., Manahan-Vaughan, D., Marchand, F., Mars, R., Marsella, G., Micotti , E., Muñoz-Moreno , E., Near, J., Niendorf, T., Otte, W., Pan , W., Prado-Alcalá, R., Quirarte, G., Rodger , J., Rosenow, T., Sampaio-Baptista, C., Sartorius, A., Sawiak, S., Scheenen, T., Shemesh, Shih, Y., Shmuel, A., Soria, G., Stoop, R., Thompson, G., Till, S., Todd, N., Van Der Linden, A., van der Toorn, A., van Tilborg, G., Vanhove, C., Veltien, A., Verhoye, M., Wachsmuth, L., Weber-Fahr, W., Wenk , P., Yu, X., Zerbi , V., Zhang , N., Zhang, B., Zimmer, L., Devenyi, G., Chakravarty, M., and Hess, A.
Subjects: Action, intention, and motor control, General Neuroscience, fmri, Medizin, Stress-related disorders Donders Center for Medical Neuroscience [Radboudumc 13], Human medicine
Abstract: Task-free functional connectivity in animal models provides an experimental framework to examine connectivity phenomena under controlled conditions and allows for comparisons with data modalities collected under invasive or terminal procedures. Currently, animal acquisitions are performed with varying protocols and analyses that hamper result comparison and integration. Here we introduce StandardRat, a consensus rat functional magnetic resonance imaging acquisition protocol tested across 20 centers. To develop this protocol with optimized acquisition and processing parameters, we initially aggregated 65 functional imaging datasets acquired from rats across 46 centers. We developed a reproducible pipeline for analyzing rat data acquired with diverse protocols and determined experimental and processing parameters associated with the robust detection of functional connectivity across centers. We show that the standardized protocol enhances biologically plausible functional connectivity patterns relative to previous acquisitions. The protocol and processing pipeline described here is openly shared with the neuroimaging community to promote interoperability and cooperation toward tackling the most important challenges in neuroscience. The authors pooled resources to identify best practices and develop a new standardized protocol for estimating functional connectivity in rats with magnetic resonance imaging.
Published: 2023

8. Associations between ASL-derived cerebrovascular health and cognitive performance: results from the Insight 46 study

Author: Dijsselhof, M. B., Lu, K., Lorenzini, L., Collij, L. E., James, S.-N., Thomas, D. L., Scott, C. J., Manning, E. N., Cash, D. M., Hughes, A. D., Richard, M., Barkhof, F., Schott, J. M., (0000-0002-3201-6002) Petr, J., Mutsaerts, H. J. M. M., Dijsselhof, M. B., Lu, K., Lorenzini, L., Collij, L. E., James, S.-N., Thomas, D. L., Scott, C. J., Manning, E. N., Cash, D. M., Hughes, A. D., Richard, M., Barkhof, F., Schott, J. M., (0000-0002-3201-6002) Petr, J., and Mutsaerts, H. J. M. M.
Abstract: Cardiovascular and cerebrovascular pathology may accelerate brain aging and cognitive decline. Structural cerebrovascular imaging biomarkers, such as white matter hyperintensities, reflect mostly irreversible accumulated damage. In contrast, cerebral blood flow (CBF), measured with arterial spin labelling (ASL) perfusion MRI, is a potential early haemodynamic biomarker of cognitive impairment. However, our understanding of physiological CBF variability and its relation with cognition is limited.
Published: 2023

9. Cardiovascular and cerebrovascular health in 70-year-olds: a population-based ASL study

Author: Dijsselhof, M. B. J., James, S.-N., Lorenzini, L., Collij, L., Thomas, D. L., Scott, C., Manning, E., Józsa, T. I., Cash, D., Study, I., Sudre, C., Hughes, A. D., Richards, M., Barkhof, F., Schott, J., (0000-0002-3201-6002) Petr, J., Mutsaerts, H. J. M. M., Dijsselhof, M. B. J., James, S.-N., Lorenzini, L., Collij, L., Thomas, D. L., Scott, C., Manning, E., Józsa, T. I., Cash, D., Study, I., Sudre, C., Hughes, A. D., Richards, M., Barkhof, F., Schott, J., (0000-0002-3201-6002) Petr, J., and Mutsaerts, H. J. M. M.
Abstract: While mid-life cardiovascular pathology may lead to late-life cognitive decline, our understanding of the role of cerebrovascular health as an intermediate biomarker is limited. We explored the association between cardiovascular health biomarkers and cross-sectional and longitudinal cerebrovascular health assessed by ASL MRI in Insight46, a well-characterised cognitively normal population-based sample. We found several cross-sectional and longitudinal associations between blood pressure and CBF. These findings suggest that the effects of BP on cerebrovascular health can be imaged with ASL perfusion MRI, possibly offering opportunities to prevent or intervene before cognitive decline sets in.
Published: 2023

10. Author Correction: A consensus protocol for functional connectivity analysis in the rat brain

Author: Grandjean, J., Desrosiers-Gregoire, G., Anckaerts, C., Angeles-Valdez, D., Ayad, F., Barrière, D., Blockx, I., Bortel, A., Broadwater, M., Cardoso, B., Célestine, M., Chavez-Negrete, J., Choi, S., https://orcid.org/0000-0001-7327-1344, Christiaen, E., Clavijo, P., Colon-Perez, L., Cramer, S., Daniele, T., Dempsey, E., Diao, Y., Doelemeyer, A., Dopfel, D., Dvořáková, L., Falfán-Melgoza, C., Fernandes, F., Fowler, C., Fuentes-Ibañez, A., Garin, C., Gelderman, E., Golden, C., Guo, C., Henckens, M., Hennessy, L., Herman , P., Hofwijks, N., Horien, C., Ionescu, T., Jones, J., Kaesser, J., Kim, E., Lambers, H., Lazari, A., Lee, S., Lillywhite, A., Liu, Y., López-Castro, A., López-Gil , X., Ma, Z., MacNicol, E., Madularu, D., Mandino, F., Marciano, S., McAuslan, M., McCunn, P., McIntosh, A., Meng, X., Meyer-Baese, L., Missault, S., Moro, F., Naessens, D., Nava-Gomez, L., Nonaka, H., Ortiz, J., Paasonen, J., Pais-Roldán, P., https://orcid.org/0000-0002-9381-3048, Peeters, L., Pereira, M., Perez, P., Pompilus, M., Prior, M., Rakhmatullin, R., Reimann, H., Reinwald, J., Triana Del Rio, R., Rivera-Olvera, A., Ruiz-Pérez, D., Russo, G., Rutten, T., Ryoke, R., Sack, M., Salvan, P., Sanganahalli, B., Schroeter, A., Seewoo , B., Selingue, E., Seuwen, A., Shi, B., Sirmpilatze, N., Smith, J., Smith, C., Sobczak, F., Stenroos, P., Straathof, M., Strobelt, S., Sumiyoshi, A., Takahashi, K., Torres-García, M., Tudela, R., van den Berg, M., van der Marel, K., van Hout, A., Vertullo, R., Vidal, B., Vrooman, R., Wang, X., Wank, I., Watson, D., Yin, T., Zhang, Y., Zurbruegg, S., Achard, S., Alcauter, S., Auer, D., Barbier, E., Baudewig, J., Beckmann, C., Beckmann, N., Becq, G., Blezer, E., Bolbos, R., Boretius, S., Bouvard, S., Budinger, E., Buxbaum, J., Cash, D., Chapman, V., Chuang, K., Ciobanu, L., Coolen, B., Dalley, J., Dhenain, M., Dijkhuizen, R., Esteban, O., Faber, C., Febo, M., Feindel, K., Forloni, G., Fouquet, J., Garza-Villarreal, E., Gass, N., Glennon, J., Gozzi, A., Gröhn, O., Harkin, A., Heerschap, A., Helluy, X., Herfert , K., Heuser, A., Homberg, J., Houwing, D., Hyder, F., Ielacqua, G., Jelescu, I., Johansen-Berg, H., Kaneko, G., Kawashima, R., Keilholz, S., Keliris, G., Kelly, C., Kerskens, C., Khokhar, J., Kind, P., Langlois, J., Lerch, J., López-Hidalgo, M., Manahan-Vaughan, D., Marchand, F., Mars, R., Marsella, G., Micotti , E., Muñoz-Moreno , E., Near, J., Niendorf, T., Otte, W., Pan , W., Prado-Alcalá, R., Quirarte, G., Rodger , J., Rosenow, T., Sampaio-Baptista, C., Sartorius, A., Sawiak, S., Scheenen, T., Shemesh, Shih, Y., Shmuel, A., https://orcid.org/0000-0003-3028-6639, Soria, G., Stoop, R., https://orcid.org/0000-0002-3532-1512, Thompson, G., Till, S., Todd, N., Van Der Linden, A., van der Toorn, A., van Tilborg, G., Vanhove, C., Veltien, A., Verhoye, M., Wachsmuth, L., Weber-Fahr, W., Wenk , P., Yu, X., Zerbi , V., Zhang , N., Zhang, B., Zimmer, L., Devenyi, G., Chakravarty, M., and Hess, A.
Subjects: General Neuroscience, Medizin
Abstract: Weitere Nicht-UDE Autoren sind nicht mit aufgeführt. in press
Published: 2023

11. Blunted glucocorticoid responsiveness to stress causes behavioural and biological alterations that lead to PTSD vulnerability in rats

Author: Monari, S., primary, Guillot de Suduiraut, I., additional, Grosse, J., additional, Zanoletti, O., additional, Walker, E.S., additional, Mesquita, M., additional, Wood, T., additional, Cash, D., additional, Astori, S., additional, and Sandi, C., additional
Published: 2023
Full Text: View/download PDF

12. Cognitive dysfunction in ‘pure’ OSA patients without any other comorbidities

Author: Gnoni, V., primary, Wasserman, D., additional, Duncan, I., additional, Tsai, C.-C., additional, Cash, D., additional, Higgins, S., additional, Drakatos, P., additional, Nesbitt, A., additional, Leschziner, G., additional, O'Regan, D., additional, and Rosenzweig, I., additional
Published: 2022
Full Text: View/download PDF

13. Modelling the cascade of biomarker changes in GRN-related frontotemporal dementia

Author: Panman, J. L., Venkatraghavan, V., Van Der Ende, E. L., Steketee, R. M. E., Jiskoot, L. C., Poos, J. M., Dopper, E. G. P., Meeter, L. H. H., Kaat, L. D., Rombouts, S. A. R. B., Vernooij, M. W., Kievit, A. J. A., Premi, E., Cosseddu, M., Bonomi, E., Olives, J., Rohrer, J. D., Sanchez-Valle, R., Borroni, B., Bron, E. E., Van Swieten, J. C., Papma, J. M., Klein, S., Afonso, S., Almeida, M. R., Anderl-Straub, S., Andersson, C., Antonell, A., Archetti, S., Arighi, A., Balasa, M., Barandiaran, M., Bargallo, N., Bartha, R., Bender, B., Black, S., Butler, C., Bocchetta, M., Borrego-Ecija, S., Bras, J., Bruffaerts, R., Caroppo, P., Cash, D., Castelo-Branco, M., Convery, R., Cope, T., Danek, A., De Arriba, M., De Mendonca, A., Di Fede, G., Diaz, Z., Ducharme, S., Duro, D., Fenoglio, C., Ferreira, C. B., Finger, E., Flanagan, T., Fox, N., Freedman, M., Fumagalli, G., Gabilondo, A., Galimberti, D., Gasparotti, R., Gauthier, S., Gazzina, S., Gerhard, A., Giaccone, G., Gorostidi, A., Graff, C., Greaves, C., Guerreiro, R., Heller, C., Hoegen, T., Indakoetxea, B., Jelic, V., Karnath, H. -O., Keren, R., Laforce, R., Leitao, M. J., Levin, J., Llado, A., Loosli, S., Maruta, C., Masellis, M., Mead, S., Miltenberger, G., Van Minkelenm Sara Mitchell, R., Moore, K., Moreno, F., Nicholas, J., Oijerstedt, L., Otto, M., Ourselin, S., Padovani, A., Peakman, G., Pijnenburg, Y., Polito, C., Prioni, S., Prix, C., Rademakers, R., Redaelli, V., Rittman, T., Rogaeva, E., Rosa-Neto, P., Rossi, G., Rosser, M., Rowe, J., Santana, I., Santiago, B., Scarpini, E., Schonecker, S., Shafei, E. S. R., Shoesmith, C., Synofzik, M., Tabuas-Pereira, M., Tagliavini, F., Tartaglia, C., Tainta, M., Taipa, R., Tang-Wai, D., Thomas, D. L., Thonberg, H., Timberlake, C., Tiraboschi, P., Todd, E., Vandamme, P., Vandenberghe, R., Vandenbulcke, M., Veldsman, M., Verdelho, A., Villanua, J., Warren, J., Wilkeione, C., Elisabeth, W., Henrik, W., Zulaica, Z. M., Neurology, Physics and medical technology, Radiology & Nuclear Medicine, Clinical Genetics, and Medical Research Council
Subjects: Male, Oncology, Disease, Neuropsychological Tests, GENFI consortium investigators, Primary progressive aphasia, Cognition, Progranulins, 0302 clinical medicine, Neurofilament Proteins, BEHAVIORAL VARIANT, HETEROGENEITY, Gray Matter, 11 Medical and Health Sciences, Language, Psychiatry, 0303 health sciences, Brain, Middle Aged, Magnetic Resonance Imaging, White Matter, 17 Psychology and Cognitive Sciences, ALZHEIMERS-DISEASE, Psychiatry and Mental health, Phenotype, medicine.anatomical_structure, Frontotemporal Dementia, Disease Progression, Biomarker (medicine), Female, Life Sciences & Biomedicine, Frontotemporal dementia, medicine.medical_specialty, Clinical Neurology, EVENT-BASED MODEL, Grey matter, Lateralization of brain function, White matter, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Internal medicine, NEUROFILAMENT LIGHT-CHAIN, medicine, Humans, LOBAR DEGENERATION, PROGRANULIN, Aged, 030304 developmental biology, Science & Technology, Neurology & Neurosurgery, business.industry, DISEASE PROGRESSION, medicine.disease, Mutation, WHITE-MATTER INTEGRITY, Surgery, Neurosciences & Neurology, Neurology (clinical), business, GENFI, Biomarkers, 030217 neurology & neurosurgery, Progressive disease
Abstract: ObjectiveProgranulin-related frontotemporal dementia (FTD-GRN) is a fast progressive disease. Modelling the cascade of multimodal biomarker changes aids in understanding the aetiology of this disease and enables monitoring of individual mutation carriers. In this cross-sectional study, we estimated the temporal cascade of biomarker changes for FTD-GRN, in a data-driven way.MethodsWe included 56 presymptomatic and 35 symptomatic GRN mutation carriers, and 35 healthy non-carriers. Selected biomarkers were neurofilament light chain (NfL), grey matter volume, white matter microstructure and cognitive domains. We used discriminative event-based modelling to infer the cascade of biomarker changes in FTD-GRN and estimated individual disease severity through cross-validation. We derived the biomarker cascades in non-fluent variant primary progressive aphasia (nfvPPA) and behavioural variant FTD (bvFTD) to understand the differences between these phenotypes.ResultsLanguage functioning and NfL were the earliest abnormal biomarkers in FTD-GRN. White matter tracts were affected before grey matter volume, and the left hemisphere degenerated before the right. Based on individual disease severities, presymptomatic carriers could be delineated from symptomatic carriers with a sensitivity of 100% and specificity of 96.1%. The estimated disease severity strongly correlated with functional severity in nfvPPA, but not in bvFTD. In addition, the biomarker cascade in bvFTD showed more uncertainty than nfvPPA.ConclusionDegeneration of axons and language deficits are indicated to be the earliest biomarkers in FTD-GRN, with bvFTD being more heterogeneous in disease progression than nfvPPA. Our data-driven model could help identify presymptomatic GRN mutation carriers at risk of conversion to the clinical stage.
Published: 2021

14. SHORT REPORT: Molecular analysis of imipenem-resistant Acinetobacter baumannii isolated from US service members wounded in Iraq, 2003—2008

Author: HUANG, X.-Z., CHAHINE, M. A., FRYE, J. G., CASH, D. M., LESHO, E. P., CRAFT, D. W., LINDLER, L. E., and NIKOLICH, M. P.
Published: 2012
Full Text: View/download PDF

15. Multimodal MRI-derived phenotypes in preclinical Alzheimer’s Disease: results from the EPAD cohort

Author: Lorenzini, L., Ingala, S., Wink, A. M., Kuijer, J. P. A., Wottschel, V., Sudre, C. H., Haller, S., Molinuevo, J. L., Gispert, J. D., Cash, D. M., Thomas, D. L., Vos, S. B., Ferran, P., (0000-0002-3201-6002) Petr, J., Wolz, R., Palombit, A., Schwarz, A. J., Chételat, G., Payoux, P., Di Perri, C., Pernet, C., Frisoni, G., Fox, N. C., Ritchie, C., Wardlaw, J., Waldman, A., Barkhof, F., Mutsaerts, H. J. M. M., Lorenzini, L., Ingala, S., Wink, A. M., Kuijer, J. P. A., Wottschel, V., Sudre, C. H., Haller, S., Molinuevo, J. L., Gispert, J. D., Cash, D. M., Thomas, D. L., Vos, S. B., Ferran, P., (0000-0002-3201-6002) Petr, J., Wolz, R., Palombit, A., Schwarz, A. J., Chételat, G., Payoux, P., Di Perri, C., Pernet, C., Frisoni, G., Fox, N. C., Ritchie, C., Wardlaw, J., Waldman, A., Barkhof, F., and Mutsaerts, H. J. M. M.
Abstract: Image-derived phenotypes (IDPs) from multimodal MRI sequences constitute an important resource that allows the characterization of brain alterations in the early stages of Alzheimer diseases and other neurodegenerative conditions. Here, we showed the computation of multimodal IDPs from the European Prevention of Alzheimer Dementia (EPAD) cohort and assessed their relationship with non-imaging markers of neurodegeneration. We demonstrated the clinical relevance of IDPs to uncover early brain alteration in AD by showing expected association with non-imaging data.
Published: 2022

16. The Open-Access European Prevention of Alzheimer’s Dementia (EPAD) MRI dataset and processing workflow

Author: Lorenzini, L., Ingala, S., Wink, A. M., Kuijer, J. P. A., Wottschel, V., Dijsselhof, M., Sudre, C. H., Haller, S., Molinuevo, J. L., Gispert, J. D., Cash, D. M., Thomas, D. L., Vos, S. B., Prados, F., (0000-0002-3201-6002) Petr, J., Wolz, R., Palombit, A., Schwarz, A. J., Chételat, G., Payoux, P., Di Perri, C., Wardlaw, J. M., Frisoni, G. B., Foley, C., Fox, N. C., Ritchie, C., Pernet, C., Waldman, A., Barkhof, F., Mutsaerts, H. J. M. M., Lorenzini, L., Ingala, S., Wink, A. M., Kuijer, J. P. A., Wottschel, V., Dijsselhof, M., Sudre, C. H., Haller, S., Molinuevo, J. L., Gispert, J. D., Cash, D. M., Thomas, D. L., Vos, S. B., Prados, F., (0000-0002-3201-6002) Petr, J., Wolz, R., Palombit, A., Schwarz, A. J., Chételat, G., Payoux, P., Di Perri, C., Wardlaw, J. M., Frisoni, G. B., Foley, C., Fox, N. C., Ritchie, C., Pernet, C., Waldman, A., Barkhof, F., and Mutsaerts, H. J. M. M.
Abstract: The European Prevention of Alzheimer Dementia (EPAD) is a multi-center study that aims to characterize the preclinical and prodromal stages of Alzheimer’s Disease. The EPAD imaging dataset includes core (3D T1w, 3D FLAIR) and advanced (ASL, diffusion MRI, and resting-state fMRI) MRI sequences. Here, we give an overview of the semi-automatic multimodal and multisite pipeline that we developed to curate, preprocess, quality control (QC), and compute image-derived phenotypes (IDPs) from the EPAD MRI dataset. This pipeline harmonizes DICOM data structure across sites and performs standardized MRI pre- processing steps. A semi-automated MRI QC procedure was implemented to visualize and flag MRI images next to site-specific distributions of QC features — i.e. metrics that represent image quality. The value of each of these QC features was evaluated through comparison with visual assessment and step-wise parameter selection based on logistic regression. IDPs were computed from 5 different MRI modalities and their sanity and potential clinical relevance were ascertained by assessing their relationship with biological markers of aging and dementia. The EPAD v1500.0 data release encompassed core structural scans from 1356 participants 842 fMRI, 831 dMRI, and 858 ASL scans. From 1356 3D T1w images, we identified 17 images with poor quality and 61 with moderate quality. Five QC features — Signal to Noise Ratio (SNR), Contrast to Noise Ratio (CNR), Coefficient of Joint Variation (CJV), Foreground-Background energy Ratio (FBER), and Image Quality Rate (IQR) — were selected as the most informative on image quality by comparison with visual assessment. The multimodal IDPs showed greater impairment in associations with age and dementia biomarkers, demonstrating the potential of the dataset for future clinical analyses.
Published: 2022

17. A Multi-component similarity measure for improved robustness of non-rigid registration of combined FDG PET-CT head and neck images

Author: Papastavrou, Y., Cash, D., Hawkes, D., Hutton, B., Magjarevic, R., editor, Nagel, J. H., editor, Vander Sloten, Jos, editor, Verdonck, Pascal, editor, Nyssen, Marc, editor, and Haueisen, Jens, editor
Published: 2009
Full Text: View/download PDF

18. Erbb4 deletion from fast-spiking interneurons causes psychosis-relevant neuroimaging phenotypes

Author: Kiemes, A., primary, Serrano Navacerrada, M. E., additional, Kim, E., additional, Randall, K., additional, Simmons, C., additional, Rojo Gonzalez, L., additional, Petrinovic, M.M., additional, Lythgoe, D.J., additional, Rotaru, D., additional, Di Censo, D., additional, Hirshler, L., additional, Barbier, E. L., additional, Vernon, A. C., additional, Stone, J. M., additional, Davies, C., additional, Cash, D., additional, and Modinos, G., additional
Published: 2022
Full Text: View/download PDF

19. SHORT REPORT: Methicillin-resistant Staphylococcus aureus infection in combat support hospitals in three regions of Iraq

Author: HUANG, X.-Z., CASH, D. M., CHAHINE, M. A., VAN HORN, G. T., ERWIN, D. P., McKAY, J. T., HAMILTON, L. R., JERKE, K. H., CO, E.-M. A., ALDOUS, W. K., LESHO, E. P., LINDLER, L. E., BOWDEN, R. A., and NIKOLICH, M. P.
Published: 2011
Full Text: View/download PDF

20. Neuroimaging-based markers of parvalbumin interneuron disruption

Author: Kiemes, A., Navacerrada, M.E. Serrano, Kim, E., Randall, K., Simmons, C., Gonzalez, L. Rojo, Petrinovic, M.M., Lythgoe, D.J., Rotaru, D., Di Censo, D., Hirschler, L., Barbier, E.L., Vernon, A., Stone, J.M., Davies, C., Cash, D., and Modinos, G.
Published: 2022
Full Text: View/download PDF

21. Scrutiny of the Bounty or Teaching Critical Thinking in

Author: Cash, D. Michele
Abstract: This paper, presented at the Indiana Library Association Meeting, discusses critical thinking in general terms and then briefly discusses why it is important to include critical thinking skills in bibliographic instruction sessions at the higher education level. A discussion of the instructional design of bibliographic instruction in relation to teaching critical thinking is followed by specific examples of how one educator has incorporated critical thinking skills into library instruction sessions. A 19-item bibliography divided into sections on Critical Thinking in General and Critical Thinking in Library Instruction is included. (THC)
Published: 1985

22. Neuroimaging Pre-Processing and Quality Control for The European Prevention of Alzheimer's Dementia (EPAD) Cohort Study

Author: Lorenzini, L., Ingala, S., Wink, A. M., Kuijer, J., Wottschel, V., Sudre, C., Haller, S., Molinuevo, J. L., Gispert, J. D., Cash, D., Thomas, D., Vos, S., Prados Carrasco, F., Petr, J., Wolz, R., Palombit, A., Schwarz, A., Chételat, G., Payoux, P., Di Perri, C., Pernet, C., Giovanni, F., Fox, N., Ritchie, C., Wardlaw, J., Waldman, A., Barkhof, F., and Mutsaerts, H.
Abstract: The neuroimaging community strives to obtain large data cohorts, usually through association within consortia spanning different sites and countries. This results in increased variability of acquisition parameters and scan quality, which can affect image processing and statistical analyses. We propose a semi-automatic data management pipeline to process raw data, assess quality and compute image-derived phenotypes from multi-modal MRI scans, as developed for the multi-centre European Prevention of Alzheimer Dementia longitudinal cohort study (EPAD LCS).
Published: 2021

23. Periodic limb movements during sleep:A narrative review

Author: Drakatos, P, Olaithe, M, Verma, D, Ilic, K, Cash, D, Fatima, Y, Higgins, S, Young, A H, Chaudhuri, K R, Steier, J, Skinner, Timothy, Bucks, R, Rosenzweig, I, Drakatos, P, Olaithe, M, Verma, D, Ilic, K, Cash, D, Fatima, Y, Higgins, S, Young, A H, Chaudhuri, K R, Steier, J, Skinner, Timothy, Bucks, R, and Rosenzweig, I
Abstract: Objective: Using narrative review techniques, this paper evaluates the evidence for separable underlying patho-mechanisms of periodic limb movements (PLMs) to separable PLM motor patterns and phenotypes, in order to elucidate potential new treatment modalities. Background: Periodic limb movement disorder (PLMD) is estimated to occur in 5–8% of the paediatric population and 4–11% of the general adult population. Due to significant sleep fragmentation, PLMD can lead to functional impairment, including hyperactivity and delayed language development in children, and poor concentration and work performance in adults. Longitudinal data demonstrate that those with PLMD are at greater risk of depression and anxiety, and a 4-fold greater risk of developing dementia. PLMD has been extensively studied over the past two decades, and several key insights into the genetic, pathophysiological, and neural correlates have been proposed. Amongst these proposals is the concept of separable PLM phenotypes, proposed on the basis of nocturnal features such as the ratio of limb movements and distribution throughout the night. PLM phenotype and presentation, however, varies significantly depending on the scoring utilized and the nocturnal features examined, across age, and co-morbid clinical conditions. Furthermore, associations between these phenotypes with major neurologic and psychiatric disorders remain controversial. Methods: In order to elucidate potential divergent biological pathways that may help clarify important new treatment modalities, this paper utilizes narrative review and evaluates the evidence linking PLM motor patterns and phenotypes with hypothesised underlying patho-mechanisms. Distinctive, underlying patho-mechanisms include: a pure motor mechanism originating in the spinal cord, iron deficiency, dopamine system dysfunction, thalamic glutamatergic hyperactivity, and a more cortical-subcortical interplay. In support of the latter hypothesis, PLM rhyth
Published: 2021

24. Margaret Joan Cash

Author: Cash, D. M.
Published: 1997

25. A data-driven model of brain volume changes in progressive supranuclear palsy.

Author: Scotton, W. J., Bocchetta, M., Todd, E., Cash, D. M., Oxtoby, N., VandeVrede, L., Heuer, H., Alexander, D. C., Rowe, J. B., Morris, H. R., Boxer, A., Rohrer, J. D., and Wijeratne, P. A.
Published: 2022
Full Text: View/download PDF

26. Atlas-Based Brain Extraction Is Robust Across RAT MRI Studies

Author: MacNicol, E., primary, Ciric, R., additional, Kim, E., additional, Censo, D. Di, additional, Cash, D., additional, Poldrack, R. A., additional, and Esteban, O., additional
Published: 2021
Full Text: View/download PDF

27. P.107 Hippocampal GABA-A α5 receptor subunits are down-regulated in the methylazoxymethanol model of schizophrenia

Author: Kiemes, A., primary, Gomes, F., additional, Cash, D., additional, Singh, N., additional, Turkheimer, F., additional, Grace, A.A., additional, and Modinos, G., additional
Published: 2021
Full Text: View/download PDF

28. Analysis of brain atrophy and local gene expression in genetic frontotemporal dementia

Author: Altmann, A., Cash, D. M., Bocchetta, M., Heller, C., Reynolds, R., Moore, K., Convery, R. S., Thomas, D. L., Van Swieten, J. C., Moreno, F., Sanchez-Valle, R., Borroni, B., Laforce, R., Masellis, M., Tartaglia, M. C., Graff, C., Galimberti, D., Rowe, J. B., Finger, E., Synofzik, M., Vandenberghe, R., De Mendonca, A., Tagliavini, F., Santana, I., Ducharme, S., Butler, C. R., Gerhard, A., Levin, J., Danek, A., Frisoni, G., Ghidoni, R., Sorbi, S., Otto, M., Ryten, M., Rohrer, J. D., Greaves, C., Peakman, G., Shafei, R., Todd, E., Rossor, M. N., Warren, J. D., Fox, N. C., Zetterberg, H., Guerreiro, R., Bras, J., Nicholas, J., Mead, S., Jiskoot, L., Meeter, L., Panman, J., Papma, J. M., Van Minkelen, R., Pijnenburg, Y., Barandiaran, M., Indakoetxea, B., Gabilondo, A., Tainta, M., De Arriba, M., Gorostidi, A., Zulaica, M., Villanua, J., Diaz, Z., Borrego-Ecija, S., Olives, J., Llado, A., Balasa, M., Antonell, A., Bargallo, N., Premi, E., Cosseddu, M., Gazzina, S., Padovani, A., Gasparotti, R., Archetti, S., Black, S., Mitchell, S., Rogaeva, E., Freedman, M., Keren, R., Tang-Wai, D., Oijerstedt, L., Andersson, C., Jelic, V., Thonberg, H., Arighi, A., Fenoglio, C., Scarpini, E., Fumagalli, G., Cope, T., Timberlake, C., Rittman, T., Shoesmith, C., Bartha, R., Rademakers, R., Wilke, C., Karnarth, H. -O., Bender, B., Bruffaerts, R., Van Damme, P., Vandenbulcke, M., Ferreira, C. B., Miltenberger, G., Maruta, C., Verdelho, A., Afonso, S., Taipa, R., Caroppo, P., Di Fede, G., Giaccone, G., Prioni, S., Redaelli, V., Rossi, G., Tiraboschi, P., Duro, D., Almeida, M. R., Castelo-Branco, M., Leitao, M. J., Tabuas-Pereira, M., Santiago, B., Gauthier, S., Rosa-Neto, P., Veldsman, M., Thompson, P., Langheinrich, T., Prix, C., Hoegen, T., Wlasich, E., Loosli, S., Schonecker, S., Semler, E., Anderl-Straub, S., Benussi, L., Binetti, G., Pievani, M., Lombardi, G., Nacmias, B., Ferrari, C., Bessi, V., Polito, C., Rowe, James [0000-0001-7216-8679], Apollo - University of Cambridge Repository, Medical Research Council, and Genetic FTD Initiative, GENFI
Subjects: 0301 basic medicine, Cell type, Imaging genetics, Clinical Neurology, Medizin, Biology, Article, DISEASE, 03 medical and health sciences, 0302 clinical medicine, Atrophy, atrophy, C9orf72, Gene expression, medicine, Astrocytes, Frontotemporal dementia, ddc:610, 10. No inequality, Gene, 030304 developmental biology, Genetics, 0303 health sciences, Science & Technology, TREM2, AcademicSubjects/SCI01870, Neurodegeneration, General Engineering, C9orf72 Gene, Neurosciences, astrocytes, Genetic FTD Initiative, GENFI, medicine.disease, C9orf72 Protein, 030104 developmental biology, gene expression, imaging genetics, Original Article, AcademicSubjects/MED00310, Human medicine, Neurosciences & Neurology, Life Sciences & Biomedicine, 030217 neurology & neurosurgery
Abstract: Frontotemporal dementia is a heterogeneous neurodegenerative disorder characterized by neuronal loss in the frontal and temporal lobes. Despite progress in understanding which genes are associated with the aetiology of frontotemporal dementia, the biological basis of how mutations in these genes lead to cell loss in specific cortical regions remains unclear. In this work, we combined gene expression data for 16 772 genes from the Allen Institute for Brain Science atlas with brain maps of grey matter atrophy in symptomatic C9orf72, GRN and MAPT mutation carriers obtained from the Genetic Frontotemporal dementia Initiative study. No significant association was seen between C9orf72, GRN and MAPT expression and the atrophy patterns in the respective genetic groups. After adjusting for spatial autocorrelation, between 1000 and 5000 genes showed a negative or positive association with the atrophy pattern within each individual genetic group, with the most significantly associated genes being TREM2, SSBP3 and GPR158 (negative association in C9Orf72, GRN and MAPT respectively) and RELN, MXRA8 and LPA (positive association in C9Orf72, GRN and MAPT respectively). An overrepresentation analysis identified a negative association with genes involved in mitochondrial function, and a positive association with genes involved in vascular and glial cell function in each of the genetic groups. A set of 423 and 700 genes showed significant positive and negative association, respectively, with atrophy patterns in all three maps. The gene set with increased expression in spared cortical regions was enriched for neuronal and microglial genes, while the gene set with increased expression in atrophied regions was enriched for astrocyte and endothelial cell genes. Our analysis suggests that these cell types may play a more active role in the onset of neurodegeneration in frontotemporal dementia than previously assumed, and in the case of the positively associated cell marker genes, potentially through emergence of neurotoxic astrocytes and alteration in the blood–brain barrier, respectively., Altmann et al. investigated the concordance between spatial cortical gene expression in healthy subjects and atrophy patterns in genetic frontotemporal dementia. They found that elevated gene expression of endothelial cell and astrocyte-related genes in regions with atrophy, suggesting a role of these cell types in the aetiology of frontotemporal dementia., Graphical Abstract Graphical Abstract
Published: 2020

29. ExploreQC: A toolbox for MRI quality control in the EPAD multicentre study

Author: Lorenzini, L., Ingala, S., Wottschel, V., Wink, A. M., Kuijer, J., Sudre, C. H., Haller, S., Molinuevo, J. L., Gispert, J. D., Cash, D. M., Thomas, D. L., Vos, S., Petr, J., Wolz, R., Pernet, C., Waldman, A., Barkhof, F., Mutsaerts, H. J. M. M., and Epad, C.
Abstract: Magnetic Resonance Imaging (MRI) of the brain is prone to artefacts that may worsen image quality and subsequent analyses. Despite the growing number of large-scale multi-institutional imaging studies, standardized approaches for defining inclusion and exclusion criteria on the basis of image data quality are still lacking and quality assessment is often based on visual inspection. We introduce ExploreQC, a MATLAB-based toolbox which implements a semi-automatic pipeline to assess QC metrics, select the most relevant parameters, and to derive informed inclusion thresholds.
Published: 2020

30. Neuronal pentraxin 2: a synapse-derived CSF biomarker in genetic frontotemporal dementia

Author: van der Ende, Emma, Xiao, MF, Xu, DS, Poos, Jackie, Panman, Jessica, Jiskoot, Lize, Meeter, Lieke, Dopper, Elise, Papma, Janne, Heller, C, Convery, H, Moore, K, Bocchetta, M, Neason, M, Peakman, G, Cash, D, Teunissen, CE, Graff, C, Synofzik, M, Moreno, F, Finger, E, Sanchez-Valle, R, Vandenberghe, R, Laforce, R, Jr, Masellis, M, Carmela Tartaglia, M, Rowe, JB, Butler, CR, Ducharme, S, Gerhard, A, Danek, A, Levin, J, Pijnenburg, YAL, Otto, M, Borroni, B, Tagliavini, F, De Mendonca, A, Santana, I, Galimberti, D, Seelaar, Harro, Rohrer, JD, Worley, PF, van Swieten, J.C., van der Ende, Emma, Xiao, MF, Xu, DS, Poos, Jackie, Panman, Jessica, Jiskoot, Lize, Meeter, Lieke, Dopper, Elise, Papma, Janne, Heller, C, Convery, H, Moore, K, Bocchetta, M, Neason, M, Peakman, G, Cash, D, Teunissen, CE, Graff, C, Synofzik, M, Moreno, F, Finger, E, Sanchez-Valle, R, Vandenberghe, R, Laforce, R, Jr, Masellis, M, Carmela Tartaglia, M, Rowe, JB, Butler, CR, Ducharme, S, Gerhard, A, Danek, A, Levin, J, Pijnenburg, YAL, Otto, M, Borroni, B, Tagliavini, F, De Mendonca, A, Santana, I, Galimberti, D, Seelaar, Harro, Rohrer, JD, Worley, PF, and van Swieten, J.C.
Published: 2020

31. Peripheral Oxidative Stress Markers Are Related To Vascular Risk Factors And Subcortical Small Vessel Disease

Author: Warrick, N., Seitz, D., Prorok, J., Shawcross, D., Mahootchi, T., Esensoy, A., Yu, D., Danieli, E., Pushpakumar, D., Tony, J., Jacob, K., Dong, J., Javed, F., D’Souza, A., Mollayeva, T., Colantonio, A., Schulz, M., Burhan, A., Naidu, A. Srinivasan, Sarquis-Adamson, Y., Montero-Odasso, M., Cooper, N., Sekhon, H., Launay, C., Allali, G., Chabot, J., Beauchet, O., Watson, B., Lin, T., Korczak, A., Bartha, C., Best, S., Truemner, J., Borrie, M., Cammer, A., Whiting, S., Morgan, D., Newman, K., Duong, J. A., Mok, A., Wang, A. H., Lavoie, M., Bier, N., Macoir, J., Adlimoghaddam, A., Turner, R. S., Cadonic, C., Albensi, B. C., Davis, J., Lewis, V.-L., Pacione, J., Skanes, C., Feltz, N., Loncar, A., Naglie, G., Sanford, S., Stasiulis, E., Rapoport, M., Vrkljan, B., Tuokko, H., Porter, M., Polgar, J., Moorhouse, P., Mazer, B., Marshall, S., Gelinas, I, Crizzle, A, Belchior, P., Bedard, M, Kokorelias, K., Cameron, J., Gignac, M., Bechard, L., Beaton, D., McGilton, K.A., Tartaglia, M. C., Black, S., Mirza, S., Mutsaerts, H.-J., Cash, D., Bocchetta, M., Thomas, D., Dick, K., van Swieten, J., Borroni, B., Galimberti, D., Rowe, J., Bethell, J., Pringle, D., Commisso, E., Chambers, L., Cohen, C., Cowan, K., Fehr, P., Szeto, P., McGilton, K., Shaw, C., Okamura, H., Otani, M., Shimoyama, N., Fujii, T., Lusk, J., Punzalan, M., Dove, E., Cotnam, K., Astell, A., Chow, A. Froehlich, Bayly, M., Kosteniuk, J., Elliot, V., O’Connell, M. E., Kirk, A., Stewart, N., Holroyd-Leduc, J., Daku, J., Kennett-Russill, D., Hack, T., Dilara, A., Astell, A. J., Hernandez, A., Divine, A., Hunter, S., Jacova, C., Alexander, C., Joseph, J. T., Alvarez, A., Smith, E., Woo, S. M. S., Chan, P., Wilkins-Ho, M., Blackburn, P., Fernando, N., Mehra, A., Vasser, E., Musacchio, M., Waxman, R., Fischler, I., Ghaffar, O., DeBay, D. R., Macdonald, I. R., Reid, G. A., Pottie, I. R., Maxwell, S. P., Cash, M. K., Martin, E., Bowen, C. V., Darvesh, S., MacPhee, J., Jorgensen, M., Fogarty, J., Phillips, N., Diprospero, C., Parent, A., Whitehead, V., Campbell, T., Mohades, Z., Chertkow, H., Wong, S., Wilchesky, M., McCusker, J., Champoux, N., Vu, T.T. M., Ciampi, A., Monette, J., Lungu, O., Ballard, S. A., Belzile, E., Carmichael, P.-H., Voyer, P., Cetin-Sahin, D., Gore, B., Peretti, M., Gore, G., Landry, V., Yetman, L., MacDonald, E., McGibbon, C., MacNeil, D., Jarrett, P., Iaboni, A., Andrews, J., Hafezi, S., Marshall, C., Tsokas, M., Martin, L. Schindel, Van Ooteghem, K., Mansfield, A., Marcil, M., Gold, D., Musselman, K., Flint, A., Finger, E., Feldman, H., Cummings, J., Coleman, K., Boxer, A., Berry, S., Hsiung, R., Curtis, A., Zhang, K., Davidson, H. R., Boccone, G., Camicioli, R., Masellis, M., Tierney, M., Dolatabadi, E., Taati, B., Jonas-Simpson, C., Donovan, L., Cross, N., Keren, R., Shan, R., Holley, J., Waisman, Z., Katchaluba, J., Wimhurst, C., Steele, M., Loganathan, P., Gural, P., Shearer, T., Reardon, J., Pilgrim, J., Pitawanakwat, K., Jones, L., Piriano, E., Blind, M., Otowadjiwan, J., Makela, R., Spicer, B., Bretzlaff, M., Jacklin, K., McKay, Kristy, Graham, N., Tang-Wai, D., Leonard, C., Mitchell, S., Laird, L., Rochon, E., Maclagan, L., Maxwell, C., Guan, J., Campitelli, M., Herrmann, N., Lapane, K., Hogan, D., Amuah, J., Gill, S., Bronskill, S., Ebert, P., Kwok, J., Watt, A., Garrett, S., Hoefling, L., Ellery, C., Leggieri, M., Fornazzari, L., Thaut, M., Munoz, D., Barfett, J., Fischer, C., Schweizer, T., Yogaparan, T., Dallaire-Théroux, C., Potvin, O., Dieumegarde, L., Duchesne, Simon, Amini, A.E. Ebrahim, Amini, A.Z. Ebrahim, Dao, E., Barha, C. K., Best, J. R., Hsiung, G.-Y. R., Tam, R., Liu-Ambrose, T., Sztramko, R., Wurster, A., Papaiouannou, A., Cowan, D., St. Onge, J., Allaby, C., Harrison, L., Cimino, C., Marr, S., Patterson, C., Woo, T., Levinson, A., Fisher, S., Mojaverian, N., Hsu, A., Taljaard, M., Manuel, D., Tanuseputro, P., Park, E., Liu, L., VanderPloeg, K., Black, A., Bartha, R., Rabin, J., Yang, H.-S., Schultz, A., Hanseeuw, B., Marshall, G., Hedden, T., Rentz, D., Johnson, K., Sperling, R., Chhatwal, J., Desmarais, P., Miville, C., Keith, J., Lanctôt, K., Thomas, N., Mattek, N., Riley, T., Witter, P., Reynolds, C., Austin, J., Sharma, N., Kaye, J., Bechard, L. E., Mitchell, C. M., Regan, K., Bergelt, M. D., Middleton, L.E., Hewston, P., Kennedy, C., Merom, D., Trainor, L., Grenier, A., Ioannidis, G., Lee, J., Papaioannou, A., Qian, W., Churchill, N., Kumar, S., Rajji, T., Ojeda-López, C., Milán-Tomás, Á., Lam, B., Gao, F. Q., Cumberbatch, S., Gies, S., Tomas, A. Milan, Ojeda-Lopez, C., Lim, A. S., Black, S. E., Sharma, M. J., Ramirez, J., Holmes, M. F., Gao, F., Varatharajah, B., Yhap, V., Appel, L., Bogler, O., Appel, E., Wiseman, M., Cohen, L., Hill, D., Abrams, H., Campos, J., Sapkota, S., Adamo, S., Stuss, D. T., Martinez, M., Multani, N., Anor, C. J., Fox, S., Lang, A. E., Marras, C., Compagnone, J., Li, J., Freedman, M., Kleiner-Fisman, G., Kennedy, J., Chen, R., Lang, A., Sévigny-Dupont, P., Bocti, C., Joannette, M., Lavallée, M. M., Joubert, S., Knoefel, F., Goubran, R., Baker, A., Fraser, S., Allard, B., Wallace, B., Stroulia, E., Guana, V., Masson, P., Alli, S., Kolla, N., De Luca, V., Bouvier, L., Monetta, L., Vitali, P., Laforce, R., Martel-Sauvageau, V., Talebzadeh, A., Ashourinia, K., Moy, S., Lake, A., Cockburn, A., Krisman, D., Sadasivan, B., Sit, W., Stoops, S., McCurbin, S., Cullen, S., Carroll, S., Tasmim, S., Kapoor, E., Callahan, B., Sharma, M., Bierstone, D., Stuss, D., Kapadia, M., Mian, F., Ma, D., Rosa, E., Michalski, B., Zovkic, I., Forsythe, P., Sakic, B., Fahnestock, M., Baxter, J., Peloso, S., Tung, J., Cox, L., Benjamin, S., An, H., Ho, J., Turcotte, V., Parent, C., Gauthier-Beaupré, A., Biss, R., Sultana, A., Chu, C. H., Sun, W., Bartfay, E., Smye, V., Newton, D., Pepin, M., Biswas, S., Madahey, H., Crawford, S. J., Gutmanis, I., Blake, C., Duchesne, S., Hudon, C., Mah, L., Ali, A., Shorey, C., Szabuniewicz, C. M., Anderson, N. D., Verhoeff, N. P. L. G., Cheers, S., Penko, M., Gevaert, V., Yang, Y., Law, J., Modarresi, S., Grahn, J., Overend, T., Amini, D., Thiruparanathan, T., Cheung, T., Iskandar, S., Arone, Y., Young, C., Berezuk, C., and Zakzanis, K.
Subjects: Abstracts
Published: 2018

32. Gamma shielding materials for MR-compatible PET

Author: Strul, D., Cash, D., Keevil, S.F., Halsted, P., Williams, S.C.R., and Marsden, P.K.
Subjects: Nuclear research -- Analysis, Gamma rays -- Usage, Magnetic resonance imaging -- Equipment and supplies, PET imaging -- Methods, Nonferrous metals, Metallic oxides, Business, Electronics, Electronics and electrical industries
Abstract: As for standard positron emission tomography (PET) scanners, MR-compatible PET scanners will require gamma shielding to suppress the influence of activity outside the PET field of view (FOV). Suitable materials must have very specific properties, including magnetic properties close to those of water, high density, high atomic number, and ideally a low conductivity. In order to identify potential suitable materials, we have selected several heavy-metal-based candidates based on the available data for magnetic and shielding properties. These materials include several nonferromagnetic metals and metal oxides, two scintillating crystals (bismuth germanate and lead tungstate) and two metal/epoxy compounds. The magnetic resonance imaging (MRI) compatibility of these materials was assessed under various conditions, both on a human and a small-animal MRI scanner. In parallel, we assessed the shielding efficiency at 661 kev of the most promising candidates. These experiments showed that there is a range of possibilities for the design of MR-compatible gamma shields. Lead has acceptable magnetic compatibility but can induce significant conductivity-related artefacts. Heavy-metal-based minerals are fully insulating and hot-pressed lead monoxide showed good MR compatibility combined with good shielding properties. Other possibilities include the use of lead based powders and heavy-metal oxide composites. Index Terms--Magnetic resonance imaging (MRI), positron emission tomography (PET), shielding.
Published: 2003

33. Molecular analysis of imipenem-resistant Acinetobacter baumannii isolated from US service members wounded in Iraq, 2003–2008

Author: HUANG, X.-Z., CHAHINE, M. A., FRYE, J. G., CASH, D. M., LESHO, E. P., CRAFT, D. W., LINDLER, L. E., and NIKOLICH, M. P.
Published: 2012

34. Sensitivity to Urea Fertilization in Three Amphibian Species

Author: Marco, A., Cash, D., Belden, L. K., and Blaustein, A. R.
Published: 2001
Full Text: View/download PDF

35. Methicillin-resistant Staphylococcus aureus infection in combat support hospitals in three regions of Iraq

Author: HUANG, X.-Z., CASH, D. M., CHAHINE, M. A., VAN HORN, G. T., ERWIN, D. P., MCKAY, J. T., HAMILTON, L. R., JERKE, K. H., CO, E.-M. A., ALDOUS, W. K., LESHO, E. P., LINDLER, L. E., BOWDEN, R. A., and NIKOLICH, M. P.
Published: 2011

36. The role of tenodesis in surgery of the upper limb

Author: Cash, D. J. W. and Jones, J. W. M.
Published: 2011
Full Text: View/download PDF

37. P.457 Does ebselen decrease synaptic glutamate availability?

Author: Singh, N., primary, Moses, N., additional, Taddei, C., additional, Mota, F., additional, Sementa, T., additional, Bordoloi, J., additional, Cash, D., additional, Hader, S., additional, Eykyn, T., additional, Veronese, M., additional, and Turkheimer, F., additional
Published: 2019
Full Text: View/download PDF

38. Cerebral perfusion changes in presymptomatic genetic frontotemporal dementia: a GENFI study

Author: Mutsaerts, H. J. M. M., Mirza, S. S., Petr, J., Thomas, D. L., Cash, D. M., Bocchetta, M., De Vita, E., Metcalfe, A. W. S., Shirzadi, Z., Robertson, A. D., Tartaglia, M. C., Mitchell, S. B., Black, S. E., Freedman, M., Tang-Wai, D., Keren, R., Rogaeva, E., Van Swieten, J., Laforce, R., Tagliavini, F., Borroni, B., Galimberti, D., Rowe, J. B., Graff, C., Frisoni, G. B., Finger, E., Sorbi, S., De Mendonca, A., Rohrer, J. D., Macintosh, B. J., Masellis, M., Andersson, C., Archetti, S., Arighi, A., Benussi, L., Binetti, G., Cosseddu, M., Dick, K. M., Fallstrom, M., Ferreira, C., Fenoglio, C., Fox, N. C., Fumagalli, G., Gazzina, S., Ghidoni, R., Grisoli, M., Jelic, V., Jiskoot, L., Lombardi, G., Maruta, C., Mead, S., Meeter, L., Van Minkelen, R., Nacmias, B., Oijerstedt, L., Ourselin, S., Padovani, A., Panman, J., Pievani, M., Polito, C., Premi, E., Prioni, S., Rademakers, R., Redaelli, V., Rossi, G., Rossor, M. N., Scarpini, E., Thonberg, H., Tiraboschi, P., Verdelho, A., Warren, J. D., Rowe, James [0000-0001-7216-8679], Apollo - University of Cambridge Repository, Neurology, Amsterdam Neuroscience - Neurodegeneration, and Radiology and Nuclear Medicine
Subjects: 0301 basic medicine, Male, Pathology, Tau Proteins/genetics, cerebral blood flow, Gene mutation, Neuropsychological Tests, Arterial spin labelling, Frontotemporal Dementia/genetics, 0302 clinical medicine, Progranulins, C9orf72, Brain, Middle Aged, Corrigenda, Magnetic Resonance Imaging, Cerebral blood flow, Cerebrovascular Circulation, Frontotemporal Dementia, Female, arterial spin labelling, Frontotemporal dementia, Adult, medicine.medical_specialty, Heterozygote, genetic frontotemporal dementia, presymptomatic biomarker, C9orf72 Protein/genetics, tau Proteins, Progranulins/genetics, 03 medical and health sciences, Neuroimaging, mental disorders, medicine, Brain/metabolism, Dementia, Humans, Cerebral perfusion pressure, Aged, C9orf72 Protein, business.industry, Original Articles, Voxel-based morphometry, medicine.disease, arterial spin labeling, ddc:616.8, Genetic frontotemporal dementia, Presymptomatic biomarker, 030104 developmental biology, Cross-Sectional Studies, Mutation, Neurology (clinical), business, 030217 neurology & neurosurgery, Cerebrovascular Circulation/genetics
Abstract: Imaging biomarkers are needed to detect early brain changes in presymptomatic carriers harbouring FTD mutations. Using arterial spin labelling-MRI, Mutsaerts, Mirza et al. identify an inverse association between cerebral perfusion in frontotemporoparietal regions and expected age of onset. Cerebral perfusion may be a promising imaging biomarker for presymptomatic genetic FTD., Genetic forms of frontotemporal dementia are most commonly due to mutations in three genes, C9orf72, GRN or MAPT, with presymptomatic carriers from families representing those at risk. While cerebral blood flow shows differences between frontotemporal dementia and other forms of dementia, there is limited evidence of its utility in presymptomatic stages of frontotemporal dementia. This study aimed to delineate the cerebral blood flow signature of presymptomatic, genetic frontotemporal dementia using a voxel-based approach. In the multicentre GENetic Frontotemporal dementia Initiative (GENFI) study, we investigated cross-sectional differences in arterial spin labelling MRI-based cerebral blood flow between presymptomatic C9orf72, GRN or MAPT mutation carriers (n = 107) and non-carriers (n = 113), using general linear mixed-effects models and voxel-based analyses. Cerebral blood flow within regions of interest derived from this model was then explored to identify differences between individual gene carrier groups and to estimate a timeframe for the expression of these differences. The voxel-based analysis revealed a significant inverse association between cerebral blood flow and the expected age of symptom onset in carriers, but not non-carriers. Regions included the bilateral insulae/orbitofrontal cortices, anterior cingulate/paracingulate gyri, and inferior parietal cortices, as well as the left middle temporal gyrus. For all bilateral regions, associations were greater on the right side. After correction for partial volume effects in a region of interest analysis, the results were found to be largely driven by the C9orf72 genetic subgroup. These cerebral blood flow differences first appeared approximately 12.5 years before the expected symptom onset determined on an individual basis. Cerebral blood flow was lower in presymptomatic mutation carriers closer to and beyond their expected age of symptom onset in key frontotemporal dementia signature regions. These results suggest that arterial spin labelling MRI may be a promising non-invasive imaging biomarker for the presymptomatic stages of genetic frontotemporal dementia.
Published: 2019

39. Inflammatory biomarkers in Alzheimer's disease plasma

Author: Leckey, C, Nevado-Holgado, AJ, Barkhof, F, Bertram, L, Blin, O, Bos, I, Dobricic, V, Engelborghs, S, Frisoni, G, Frolich, L, Gabel, S, Johannsen, P, Kettunen, P, Koszewska, I, Legido-Quigley, C, Lleo, A, Martinez-Lage, P, Mecocci, P, Meersmans, K, Molinuevo, JL, Peyratout, G, Popp, J, Richardson, J, Sala, I, Scheltens, P, Streffer, J, Soininen, H, Tainta-Cuezva, M, Teunissen, C, Tsolaki, M, Vandenberghe, R, Visser, PJ, Vos, S, Wahlund, LO, Wallin, A, Westwood, S, Zetterberg, H, Bullmore, ET, Bhatti, J, Chamberlain, SJ, Correia, MM, Crofts, AL, Dickinson, A, Foster, AC, Kitzbichler, MG, Knight, C, Lynall, ME, Maurice, C, O'Donnell, C, Pointon, LJ, Hyslop, PS, Turner, L, Vertes, P, Widmer, B, Williams, GB, Morgan, BP, Morgan, AR, O'Hagan, C, Touchard, S, Cavanagh, J, Deith, C, Farmer, S, McClean, J, McColl, A, McPherson, A, Scouller, P, Sutherland, M, Boddeke, HWGM, Richardson, JC, Khan, S, Murphy, P, Parker, CA, Patel, J, Jones, D, Boer, P, Kemp, J, Drevets, WC, Nye, JS, Wittenberg, G, Isaac, J, Bhattacharya, A, Carruthers, N, Kolb, H, Pariante, CM, Turkheimer, F, Barker, GJ, Byrom, H, Cash, D, Cattaneo, A, Gee, A, Hastings, C, Mariani, N, McLaughlin, A, Mondelli, V, Nettis, M, Nikkheslat, N, Randall, K, Sheridan, H, Simmons, C, Singh, N, Van Loo, V, Vicente-Rodriguez, M, Wood, TC, Worrell, C, Zajkowska, Z, Plath, N, Egebjerg, J, Eriksson, H, Gastambide, F, Adams, KH, Jeggo, R, Thomsen, C, Pederson, JT, Campbell, B, Moller, T, Nelson, B, Zorn, S, O'Connor, J, Attenburrow, MJ, Baird, A, Benjamin, J, Clare, S, Cowen, P, Huang, IS, Hurley, S, Jones, H, Lovestone, S, Mada, F, Nevado-Holgado, A, Oladejo, A, Ribe, E, Smith, K, Vyas, A, Hughes, Z, Balice-Gordon, R, Duerr, J, Piro, JR, Sporn, J, Perry, VH, Cleal, M, Fryatt, G, Gomez-Nicola, D, Mancuso, R, Reynolds, R, Harrison, NA, Cercignani, M, Clarke, CL, Hoskins, E, Kohn, C, Murray, R, Wilcock, L, Wlazly, D, NIMA Consortium, and NIMA-Wellcome Trust Consortium
Subjects: Inflammation, Plasma, Complement, Biomarker, Alzheimer's disease
Abstract: Introduction: Plasma biomarkers for Alzheimer's disease (AD) diagnosis/stratification are a "Holy Grail" of AD research and intensively sought; however, there are no well-established plasma markers. Methods: A hypothesis-led plasma biomarker search was conducted in the context of international multicenter studies. The discovery phase measured 53 inflammatory proteins in elderly control (CTL; 259), mild cognitive impairment (MCI; 199), and AD (262) subjects from AddNeuroMed. Results: Ten analytes showed significant intergroup differences. Logistic regression identified five (FB, FH, sCR1, MCP-1, eotaxin-1) that, age/APOe4 adjusted, optimally differentiated AD and CTL (AUC: 0.79), and three (sCR1, MCP-1, eotaxin-1) that optimally differentiated AD and MCI (AUC: 0.74). These models replicated in an independent cohort (EMIF; AUC 0.81 and 0.67). Two analytes (FB, FH) plus age predicted MCI progression to AD (AUC: 0.71). Discussion: Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. Further replication is needed before clinical translation. (C) 2019 The Authors. Published by Elsevier Inc. on behalf of the Alzheimer's Association. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Published: 2019

40. Use of 82Br− radiotracer to study transmembrane halide flux: The effect of a tranquilizing drug, chlordiazepoxide on channel opening of a GABAA receptor

Author: Cash, D. J., Serfözö, P., and Zinn, K.
Published: 1995
Full Text: View/download PDF

41. Anorectal Abscess and Fistula Caused by an Ingested Chicken Bone

Author: Cash, D. J. W., Sadat, M. M., and Abu-Own, A. S.
Published: 2004

42. Comparison of arterial spin labeling registration strategies in the multi-center GENetic frontotemporal dementia initiative (GENFI)

Author: Mutsaerts, H. J. M. M., Petr, J., Thomas, D. L., De Vita, E., Cash, D. M., van Osch, M. J. P., Golay, X., Groot, P. F. C., Ourselin, S., van Swieten, J., Laforce, R., Tagliavini, F., Borroni, B., Galimberti, D., Rowe, J. B., Graff, C., Pizzini, F. B., Finger, E., Sorbi, S., Castelo Branco, M., Rohrer, J. D., Masellis, M., Macintosh, B. J., Rossor, M., Fox, N., Warren, J., Bocchetta, M., Dick, K., Pievani, M., Ghidoni, R., Benussi, L., Padovani, A., Cosseddu, M., Mendonca, A., Frisoni, G., Premi, E., Archetti, S., Scarpini, E., Fumagalli, G., Arighi, A., Fenoglio, C., Prioni, S., Redaelii, V., Grisoli, M., Tiraboschi, P., Black, S., Rogaeva, E., Freedman, M., Tartaglia, M. C., Tang-Wai, D., Keren, R., Panman, J., Meeter, L., Jiskoot, L., van Minkelen, R., Lombardi, G., Polito, C., Nacmias, B., Jelic, V., Andersson, C., Oijerstedt, L., Fallstrom, M., Thonberg, H., Verdelho, A., Maruta, C., Neurology, Mutsaerts, Henri JMM [0000-0003-0894-0307], Apollo - University of Cambridge Repository, and Other departments
Subjects: Adult, Male, cerebral blood flow, Brain, Reproducibility of Results, Arteries, Middle Aged, arterial spin labeling, Magnetic Resonance Imaging, Article, Perfusion, image registration, Young Adult, Imaging, Three-Dimensional, Cerebrovascular Circulation, Frontotemporal Dementia, Image Processing, Computer-Assisted, Humans, Female, Spin Labels, Gray Matter
Abstract: PURPOSE: To compare registration strategies to align arterial spin labeling (ASL) with 3D T1-weighted (T1w) images, with the goal of reducing the between-subject variability of cerebral blood flow (CBF) images. MATERIALS AND METHODS: Multi-center 3T ASL data were collected at eight sites with four different sequences in the multi-center GENetic Frontotemporal dementia Initiative (GENFI) study. In a total of 48 healthy controls, we compared the following image registration options: (I) which images to use for registration (perfusion-weighted images [PWI] to the segmented gray matter (GM) probability map (pGM) (CBF-pGM) or M0 to T1w (M0-T1w); (II) which transformation to use (rigid-body or non-rigid); and (III) whether to mask or not (no masking, M0-based FMRIB software library Brain Extraction Tool [BET] masking). In addition to visual comparison, we quantified image similarity using the Pearson correlation coefficient (CC), and used the Mann-Whitney U rank sum test. RESULTS: CBF-pGM outperformed M0-T1w (CC improvement 47.2% ± 22.0%; P < 0.001), and the non-rigid transformation outperformed rigid-body (20.6% ± 5.3%; P < 0.001). Masking only improved the M0-T1w rigid-body registration (14.5% ± 15.5%; P = 0.007). CONCLUSION: The choice of image registration strategy impacts ASL group analyses. The non-rigid transformation is promising but requires validation. CBF-pGM rigid-body registration without masking can be used as a default strategy. In patients with expansive perfusion deficits, M0-T1w may outperform CBF-pGM in sequences with high effective spatial resolution. BET-masking only improves M0-T1w registration when the M0 image has sufficient contrast. LEVEL OF EVIDENCE: 1 Technical Efficacy: Stage 1 J. Magn. Reson. Imaging 2018;47:131-140.
Published: 2018
Full Text: View/download PDF

43. Uncovering the heterogeneity and temporal complexity of neurodegenerative diseases with Subtype and Stage Inference

Author: Young, A. L., Marinescu, R. V., Oxtoby, N. P., Bocchetta, M., Yong, K., Firth, N. C., Cash, D. M., Thomas, D. L., Dick, K. M., Cardoso, J., van Swieten, J., Borroni, B., Galimberti, D., Masellis, M., Tartaglia, M. C., Rowe, J. B., Graff, C., Tagliavini, F., Frisoni, G. B., Laforce, R., Finger, E., de Mendonca, A., Sorbi, S., Warren, J. D., Crutch, S., Fox, N. C., Ourselin, S., Schott, J. M., Rohrer, J. D., Alexander, D. C., Andersson, C., Archetti, S., Arighi, A., Benussi, L., Binetti, G., Black, S., Cosseddu, M., Fallstrom, M., Ferreira, C., Fenoglio, C., Freedman, M., Fumagalli, G. G., Gazzina, S., Ghidoni, R., Grisoli, M., Jelic, V., Jiskoot, L., Keren, R., Lombardi, G., Maruta, C., Meeter, L., Mead, S., van Minkelen, R., Nacmias, B., Oijerstedt, L., Padovani, A., Panman, J., Pievani, M., Polito, C., Premi, E., Prioni, S., Rademakers, R., Redaelli, V., Rogaeva, E., Rossi, G., Rossor, M., Scarpini, E., Tang-Wai, D., Thonberg, H., Tiraboschi, P., Verdelho, A., Weiner, M. W., Aisen, P., Petersen, R., Jack, C. R., Jagust, W., Trojanowki, J. Q., Toga, A. W., Beckett, L., Green, R. C., Saykin, A. J., Morris, J., Shaw, L. M., Khachaturian, Z., Sorensen, G., Kuller, L., Raichle, M., Paul, S., Davies, P., Fillit, H., Hefti, F., Holtzman, D., Mesulam, M. M., Potter, W., Snyder, P., Schwartz, A., Montine, T., Thomas, R. G., Donohue, M., Walter, S., Gessert, D., Sather, T., Jiminez, G., Harvey, D., Bernstein, M., Thompson, P., Schuff, N., Borowski, B., Gunter, J., Senjem, M., Vemuri, P., Jones, D., Kantarci, K., Ward, C., Koeppe, R. A., Foster, N., Reiman, E. M., Chen, K., Mathis, C., Landau, S., Cairns, N. J., Householder, E., Taylor-Reinwald, L., Lee, V., Korecka, M., Figurski, M., Crawford, K., Neu, S., Foroud, T. M., Potkin, S., Shen, L., Faber, K., Kim, S., Nho, K., Thal, L., Buckholtz, N., Albert, M., Frank, R., Hsiao, J., Kaye, J., Quinn, J., Lind, B., Carter, R., Dolen, S., Schneider, L. S., Pawluczyk, S., Beccera, M., Teodoro, L., Spann, B. M., Brewer, J., Vanderswag, H., Fleisher, A., Heidebrink, J. L., Lord, J. L., Mason, S. S., Albers, C. S., Knopman, D., Johnson, K., Doody, R. S., Villanueva-Meyer, J., Chowdhury, M., Rountree, S., Dang, M., Stern, Y., Honig, L. S., Bell, K. L., Ances, B., Carroll, M., Leon, S., Mintun, M. A., Schneider, S., Oliver, A., Marson, D., Griffith, R., Clark, D., Geldmacher, D., Brockington, J., Roberson, E., Grossman, H., Mitsis, E., de Toledo-Morrell, L., Shah, R. C., Duara, R., Varon, D., Greig, M. T., Roberts, P., Onyike, C., D'Agostino, D., Kielb, S., Galvin, J. E., Cerbone, B., Michel, C. A., Rusinek, H., de Leon, M. J., Glodzik, L., De Santi, S., Doraiswamy, P. M., Petrella, J. R., Wong, T. Z., Arnold, S. E., Karlawish, J. H., Wolk, D., Smith, C. D., Jicha, G., Hardy, P., Sinha, P., Oates, E., Conrad, G., Lopez, O. L., Oakley, M. A., Simpson, D. M., Porsteinsson, A. P., Goldstein, B. S., Martin, K., Makino, K. M., Ismail, M. S., Brand, C., Mulnard, R. A., Thai, G., Mc-Adams-Ortiz, C., Womack, K., Mathews, D., Quiceno, M., Diaz-Arrastia, R., King, R., Weiner, M., Martin-Cook, K., Devous, M., Levey, A. I., Lah, J. J., Cellar, J. S., Burns, J. M., Anderson, H. S., Swerdlow, R. H., Apostolova, L., Tingus, K., Woo, E., Silverman, D. H., P. H., Lu, Bartzokis, G., Graff-Radford, N. R., Parfitt, F., Kendall, T., Johnson, H., Farlow, M. R., Hake, A. M., Matthews, B. R., Herring, S., Hunt, C., van Dyck, C. H., Carson, R. E., Macavoy, M. G., Chertkow, H., Bergman, H., Hosein, C., Stefanovic, B., Caldwell, C., Hsiung, G. -Y. R., Feldman, H., Mudge, B., Assaly, M., Kertesz, A., Rogers, J., Bernick, C., Munic, D., Kerwin, D., Mesulam, M. -M., Lipowski, K., C. -K., Wu, Johnson, N., Sadowsky, C., Martinez, W., Villena, T., Turner, R. S., Reynolds, B., Sperling, R. A., Johnson, K. A., Marshall, G., Frey, M., Lane, B., Rosen, A., Tinklenberg, J., Sabbagh, M. N., Belden, C. M., Jacobson, S. A., Sirrel, S. A., Kowall, N., Killiany, R., Budson, A. E., Norbash, A., Johnson, P. L., Allard, J., Lerner, A., Ogrocki, P., Hudson, L., Fletcher, E., Carmichael, O., Olichney, J., Decarli, C., Kittur, S., Borrie, M., Lee, T. -Y., Bartha, R., Johnson, S., Asthana, S., Carlsson, C. M., Potkin, S. G., Preda, A., Nguyen, D., Tariot, P., Reeder, S., Bates, V., Capote, H., Rainka, M., Scharre, D. W., Kataki, M., Adeli, A., Zimmerman, E. A., Celmins, D., Brown, A. D., Pearlson, G. D., Blank, K., Anderson, K., Santulli, R. B., Kitzmiller, T. J., Schwartz, E. S., Sink, K. M., Williamson, J. D., Garg, P., Watkins, F., Ott, B. R., Querfurth, H., Tremont, G., Salloway, S., Malloy, P., Correia, S., Rosen, H. J., Miller, B. L., Mintzer, J., Spicer, K., Bachman, D., Pasternak, S., Rachinsky, I., Drost, D., Pomara, N., Hernando, R., Sarrael, A., Schultz, S. K., Ponto, L. L. B., Shim, H., Smith, K. E., Relkin, N., Chaing, G., Raudin, L., Smith, A., Fargher, K., Raj, B. A., Neylan, T., Grafman, J., Davis, M., Morrison, R., Hayes, J., Finley, S., Friedl, K., Fleischman, D., Arfanakis, K., James, O., Massoglia, D., Fruehling, J. J., Harding, S., Peskind, E. R., Petrie, E. C., Li, G., Yesavage, J. A., Taylor, J. L., and Furst, A. J.
Published: 2018

44. P.1.25 Effects of antipsychotic treatment on GABA-A receptor function

Author: Peris, A., primary, Kiemes, A., additional, Cash, D., additional, Vernon, A., additional, and Modinos, G., additional
Published: 2019
Full Text: View/download PDF

45. Obstructive Sleep Apnoea and Alzheimer’s Disease: in Search of Shared Pathomechanisms

Author: Polsek, D., Gildeh, N., Cash, D., Winsky-Sommerer, R., Williams, S.C.R., Turkheimer, F., Leschziner, G.D., Morrell, M.J., and Rosenzweig, I.
Subjects: Inflammation, Sleep Wake Disorders, Sleep Apnea, Obstructive, Neuroinflammation, Alzheimer Disease, Astrocytes, Humans, Obstructive sleep apnea, Alzheimer’s disease, Models, Biological, Article, respiratory tract diseases
Abstract: Highlights • Alzheimer’s disease (AD) is a significant public health concern. • The processes involved in the pathogenesis of AD are shown to overlap with those found in cognitive decline in Obstructive Sleep Apnoea (OSA). • An excessive and prolonged neuronal activity might contribute to genesis and acceleration of both AD and OSA. • External factors, such are systemic inflammation and obesity, can interfere with immunological processes of the brain, and promote disease progression., Alzheimer’s disease (AD) is a significant public health concern. The incidence continues to rise, and it is set to be over one million in the UK by 2025. The processes involved in the pathogenesis of AD have been shown to overlap with those found in cognitive decline in patients with Obstructive Sleep Apnoea (OSA). Currently, the standard treatment for OSA is Continuous Positive Airway Pressure. Adherence to treatment can, however, be an issue, especially in patients with dementia. Also, not all patients respond adequately, necessitating the use of additional treatments. Based on the body of data, we here suggest that excessive and prolonged neuronal activity might contribute to genesis and acceleration of both AD and OSA in the absence of appropriately structured sleep. Further, we argue that external factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain, and further promote disease progression. If this hypothesis is proven in future studies, it could have far-reaching clinical translational implications, as well as implications for future treatment strategies in OSA.
Published: 2017

46. Obstructive sleep apnoea and Alzheimer's disease: in search of shared pathomechanisms

Author: Polsek, D, Gildeh, N, Cash, D, Winsky-Sommerer, R, Williams, SCR, Turkheimer, F, Leschziner, GD, Morrell, MJ, and Rosenzweig, I
Subjects: MILD COGNITIVE IMPAIRMENT, INTERMITTENT HYPOXIA, DECLINE, ARCHITECTURE, Science & Technology, Neuroinflanunation, MEMORY, Neurosciences, BRAIN STRUCTURE, 11 Medical And Health Sciences, Alzheimer's disease, Behavioral Science & Comparative Psychology, Obstructive sleep apnea, RECEPTORS, 17 Psychology And Cognitive Sciences, Neuroinflammation, Astrocytes, EXTRACELLULAR-SPACE, CO-MORBIDITIES, Neurosciences & Neurology, Life Sciences & Biomedicine, Behavioral Sciences, NEURONS, Alzheimer’s disease
Abstract: Alzheimer’s disease (AD) is a significant public health concern. The incidence continues to rise, and it is set to be over one million in the UK by 2025. The processes involved in the pathogenesis of AD have been shown to overlap with those found in cognitive decline in patients with Obstructive Sleep Apnoea (OSA). Currently, the standard treatment for OSA is Continuous Positive Airway Pressure. Adherence to treatment can, however, be an issue, especially in patients with dementia. Also, not all patients respond adequately, necessitating the use of additional treatments. Based on the body of data, we here suggest that excessive and prolonged neuronal activity might contribute to genesis and acceleration of both AD and OSA in the absence of appropriately structured sleep. Further, we argue that external factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain, and further promote disease progression. If this hypothesis is proven in future studies, it could have far-reaching clinical translational implications, as well as implications for future treatment strategies in OSA.
Published: 2017

47. INHIBITION OF GABAA RECEPTOR AND GABA UPTAKE BY BICUCULLINE AND NORBICUCULLINE ENANTIOMERS.

Author: Kardos, J., Kovács, I., Blandl, T., and Cash, D. J.
Published: 1997

48. GABAA receptor availability is not altered in adults with autism spectrum disorder or in mouse models

Author: Horder, J., Andersson, M., Mendez, M., Singh, N., Tangen, A., Lundberg, J., Gee, A., Halldin, C., Veronese, M., Bolte, Sven, Farde, L., Sementa, T., Cash, D., Higgins, K., Spain, D., Turkheimer, F., Mick, I., Selvaraj, S., Nutt, D., Lingford-Hughes, A., Howes, O., Murphy, D., Borg, J., Horder, J., Andersson, M., Mendez, M., Singh, N., Tangen, A., Lundberg, J., Gee, A., Halldin, C., Veronese, M., Bolte, Sven, Farde, L., Sementa, T., Cash, D., Higgins, K., Spain, D., Turkheimer, F., Mick, I., Selvaraj, S., Nutt, D., Lingford-Hughes, A., Howes, O., Murphy, D., and Borg, J.
Abstract: Copyright © 2018 The Authors, some rights reserved. Preliminary studies have suggested that -aminobutyric acid type A (GABAA) receptors, and potentially the GABAA 5 subtype, are deficient in autism spectrum disorder (ASD). However, prior studies have been confounded by the effects of medications, and these studies did not compare findings across different species. We measured both total GABAA and GABAA 5 receptor availability in two positron emission tomography imaging studies. We used the tracer [11C]flumazenil in 15 adults with ASD and in 15 control individuals without ASD and the tracer [11C]Ro15-4513 in 12 adults with ASD and in 16 control individuals without ASD. All participants were free of medications. We also performed autoradiography, using the same tracers, in three mouse models of ASD: the Cntnap2 knockout mouse, the Shank3 knockout mouse, and mice carrying a 16p11.2 deletion. We found no differences in GABAA receptor or GABAA 5 subunit availability in any brain region of adults with ASD compared to those without ASD. There were no differences in GABAA receptor or GABAA 5 subunit availability in any of the three mouse models. However, adults with ASD did display altered performance on a GABA-sensitive perceptual task. Our data suggest that GABAA receptor availability may be normal in adults with ASD, although GABA signaling may be functionally impaired.
Published: 2018

49. Downregulation of exosomal miR-204-5p and miR-632 as a biomarker for FTD: a GENFI study

Author: Schneider, R., Mckeever, P., Kim, T., Graff, C., Van Swieten, J. C., Karydas, A., Boxer, A., Rosen, H., Miller, B. L., Laforce, R., Galimberti, D., Masellis, M., Borroni, B., Zhang, Z., Zinman, L., Rohrer, J. D., Tartaglia, M. C., Robertson, J., Andersson, C., Archetti, S., Arighi, A., Benussi, L., Binetti, G., Black, S., Bocchetta, M., Cash, D., Cosseddu, M., Dick, K., Fallström, M., Ferreira, C., Fenoglio, C., Fox, N., Freedman, M., Frisoni, G., Fumagalli, G., Gazzina, S., Ghidoni, R., Grisoli, M., Jelic, V., Jiskoot, L., Keren, R., Lombardi, G., Maruta, C., Meeter, L., van Minkelen, M., Nacmias, B., Öijerstedt, L., Ourselin, S., Padovani, A., Panman, J., Pievani, M., Polito, C., Premi, E., Prioni, S., Rademakers, R. Redaelli V., Rogaeva, E., Rossi, G., Rossor, M., Row, J., Scarpini, E., Tagliavini, F., Sorbi, S., Tang-Wai, D., Thomas, D., Thonberg, H., Tiraboschi, P., Verdelho, A., Warren, J., Neurology, Schneider, Raphael [0000-0003-1776-2418], and Apollo - University of Cambridge Repository
Subjects: 0301 basic medicine, Oncology, Male, Aging, Neurodegenerative, Alzheimer's Disease, medicine.disease_cause, Exosomes, Medical and Health Sciences, 0302 clinical medicine, Mutation Carrier, Alzheimer's Disease Related Dementias (ADRD), screening and diagnosis, Mutation, biology, Cognitive Neurology, 3. Good health, Detection, Psychiatry and Mental health, Real-time polymerase chain reaction, Frontotemporal Dementia, Neurological, Cohort, Biomarker (medicine), Female, Biotechnology, Frontotemporal dementia, medicine.medical_specialty, Tau protein, Down-Regulation, Chromosome 9, tau Proteins, 03 medical and health sciences, Rare Diseases, Internal medicine, mental disorders, Acquired Cognitive Impairment, Genetics, medicine, Humans, Neurology & Neurosurgery, business.industry, Prevention, Psychology and Cognitive Sciences, Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Genetic FTD Initiative, medicine.disease, Brain Disorders, 4.1 Discovery and preclinical testing of markers and technologies, MicroRNAs, 030104 developmental biology, biology.protein, Dementia, Surgery, Neurology (clinical), business, 030217 neurology & neurosurgery, Biomarkers
Abstract: ObjectiveTo determine whether exosomal microRNAs (miRNAs) in cerebrospinal fluid (CSF) of patients with frontotemporal dementia (FTD) can serve as diagnostic biomarkers, we assessed miRNA expression in the Genetic Frontotemporal Dementia Initiative (GENFI) cohort and in sporadic FTD.MethodsGENFI participants were either carriers of a pathogenic mutation in progranulin, chromosome 9 open reading frame 72 or microtubule-associated protein tau or were at risk of carrying a mutation because a first-degree relative was a known symptomatic mutation carrier. Exosomes were isolated from CSF of 23 presymptomatic and 15 symptomatic mutation carriers and 11 healthy non-mutation carriers. Expression of 752 miRNAs was measured using quantitative PCR (qPCR) arrays and validated by qPCR using individual primers. MiRNAs found differentially expressed in symptomatic compared with presymptomatic mutation carriers were further evaluated in a cohort of 17 patients with sporadic FTD, 13 patients with sporadic Alzheimer’s disease (AD) and 10 healthy controls (HCs) of similar age.ResultsIn the GENFI cohort, miR-204-5p and miR-632 were significantly decreased in symptomatic compared with presymptomatic mutation carriers. Decrease of miR-204-5p and miR-632 revealed receiver operator characteristics with an area of 0.89 (90% CI 0.79 to 0.98) and 0.81 (90% CI 0.68 to 0.93), respectively, and when combined an area of 0.93 (90% CI 0.87 to 0.99). In sporadic FTD, only miR-632 was significantly decreased compared with AD and HCs. Decrease of miR-632 revealed an area of 0.90 (90% CI 0.81 to 0.98).ConclusionsExosomal miR-204-5p and miR-632 have potential as diagnostic biomarkers for genetic FTD and miR-632 also for sporadic FTD.
Published: 2017

50. Factors Affecting Mortality and Length of Stay Following Clostridium Difficile Associated Diarrhoea: Validating A Consistent Scoring System

Author: Wynell Mayow W, Cash D, Muniz Tererra G, Gkrania Klotsas E, and Khanduja V
Subjects: Microbiology (medical), Pediatrics, medicine.medical_specialty, Tuberculosis, business.industry, Transmission (medicine), Cross-sectional study, 030503 health policy & services, Disease, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, Infectious Diseases, Pulmonary tuberculosis, Family medicine, Health care, medicine, Residence, 030212 general & internal medicine, Rural area, 0305 other medical science, business
Abstract: Background: Tuberculosis is one of the leading infectious diseases in Ethiopia. Emergence of MDR TB worsened the countries strategies towards the control of the diseases. Delay in seeking health care may worsen the disease, increase the risk of death and aggravate tuberculosis transmission in the community. Objective: This study was aimed at determining delay in seeking health care and analyzes factors influencing the delay from onset of symptoms of pulmonary tuberculosis until the presentation of modern health facilities. Methods: Institution based cross-sectional studies were conducted in randomly selected TB clinics, which deliver both diagnosis and treatment for TB in North Wollo health departments. Delay has analyzed from a period between onset of TB symptoms to first visit of any health provider (health seeking period). Respondents have interviewed on the same date of diagnosis using a semi-structured questionnaire. Binary logistic regression analysis applied to analyze the factors of delays. Results: Five hundred and twenty eight pulmonary TB patients aged 18 years and above enrolled in the study. Among these, 56.6% were males, 58.7% were married and 64% residing in rural areas. The median age was 33.5 (IQR=21) years. The median patient delay was 36 days and 62.3% of patients seek their first consultations after 30 days cut-off point. Long distance, rural residence, seeking treatment from traditional healers and poor knowledge about TB were associated factors that predict patient delay. Conclusion: A substantial proportion of long patients delay observed in seeking health care after 30 days cut-off point. Local authorities should collaborate, intensified awareness raising efforts to reduce high prevalence of patient delay in seeking health care.
Published: 2017

Catalog

Books, media, physical & digital resources

See catalog results

Searchworks

Select search scope, currently: Articles Catalog books, media & more in Jio Institute collections Articles journal articles & other e-resources

Search

Search Constraints

Refine your results

Search Limiters

Topic

Publication Year Range

Language

Publication Type

Journal

Region

Database

Publisher

356 results on '"Cash, D"'

Search Results

Catalog

Select search scope, currently: Articles

Catalog

books, media & more in Jio Institute collections

Articles

journal articles & other e-resources