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1. Generation of a gene-corrected human isogenic iPSC line from an Alzheimer’s disease iPSC line carrying the PSEN1 H163R mutation

Author

Damián Hernández, Stephanie Morgan Schlicht, Jordan Elli Clarke, Maciej Daniszewski, Celeste M. Karch, Alison M. Goate, Alice Pébay, Sarah Adams, Ricardo Allegri, Aki Araki, Nicolas Barthelemy, Randall Bateman, Jacob Bechara, Tammie Benzinger, Sarah Berman, Courtney Bodge, Sus Brandon, William (Bill) Brooks, Jared Brosch, Jill Buck, Virginia Buckles, Kathleen Carter, Lisa Cash, Charlie Chen, Jasmeer Chhatwal, Patricio Chrem Mendez, Jasmin Chua, Helena Chui, Laura Courtney, Carlos Cruchaga, Gregory S Day, Chrismary DeLaCruz, Darcy Denner, Anna Diffenbacher, Aylin Dincer, Tamara Donahue, Jane Douglas, Duc Duong, Noelia Egido, Bianca Esposito, Anne Fagan, Marty Farlow, Becca Feldman, Colleen Fitzpatrick, Shaney Flores, Nick Fox, Erin Franklin, Nelly Joseph-Mathurin, Hisako Fujii, Samantha Gardener, Bernardino Ghetti, Alison Goate, Sarah Goldberg, Jill Goldman, Alyssa Gonzalez, Brian Gordon, Susanne Gr¨aber-Sultan, Neill Graff-Radford, Morgan Graham, Julia Gray, Emily Gremminger, Miguel Grilo, Alex Groves, Christian Haass, Lisa H¨asler, Jason Hassenstab, Cortaiga Hellm, Elizabeth Herries, Laura Hoechst-Swisher, Anna Hofmann, David Holtzman, Russ Hornbeck, Yakushev Igor, Ryoko Ihara, Takeshi Ikeuchi, Snezana Ikonomovic, Kenji Ishii, Clifford Jack, Gina Jerome, Erik Johnson, Mathias Jucker, Celeste Karch, Stephan K¨aser, Kensaku Kasuga, Sarah Keefe, William Klunk, Robert Koeppe, Deb Koudelis, Elke Kuder-Buletta, Christoph Laske, Allan Levey, Johannes Levin, Yan Li, Oscar Lopez, Jacob Marsh, Ralph Martins, Neal Scott Mason, Colin Masters, Kwasi Mawuenyega, Austin McCullough, Eric McDade, Arlene Mejia, Estrella Morenas-Rodriguez, John Morris, James Mountz, Cath Mummery, Neelesh Nadkarni, Akemi Nagamatsu, Katie Neimeyer, Yoshiki Niimi, James Noble, Joanne Norton, Brigitte Nuscher, Ulricke Obermüller, Antoinette O’Connor, Riddhi Patira, Richard Perrin, Lingyan Ping, Oliver Preische, Alan Renton, John Ringman, Stephen Salloway, Peter Schofield, Michio Senda, Nicholas T Seyfried, Kristine Shady, Hiroyuki Shimada, Wendy Sigurdson, Jennifer Smith, Lori Smith, Beth Snitz, Hamid Sohrabi, Sochenda Stephens, Kevin Taddei, Sarah Thompson, Jonathan V¨oglein, Peter Wang, Qing Wang, Elise Weamer, Chengjie Xiong, Jinbin Xu, and Xiong Xu

Subjects
Biology (General), QH301-705.5
Abstract

We report the generation of a gene-edited human induced pluripotent stem cell (iPSC) line from an Alzheimer’s disease patient-derived iPSC line harbouring the PSEN1 H163R mutation. This line demonstrates pluripotent stem cell morphology, expression of pluripotency markers, and maintains a normal karyotype.

Published
2024
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2. Predicting brain age from functional connectivity in symptomatic and preclinical Alzheimer disease

Author

Peter R. Millar, Patrick H. Luckett, Brian A. Gordon, Tammie L.S. Benzinger, Suzanne E. Schindler, Anne M. Fagan, Carlos Cruchaga, Randall J. Bateman, Ricardo Allegri, Mathias Jucker, Jae-Hong Lee, Hiroshi Mori, Stephen P Salloway, Igor Yakushev, John C. Morris, Beau M. Ances, Sarah Adams, MS, Ricardo Allegri, PhD, Aki Araki, Nicolas Barthelemy, PhD, Randall Bateman, MD, Jacob Bechara, BS, Tammie Benzinger, MD, PhD, Sarah Berman, MD, PhD, Courtney Bodge, PhD, Susan Brandon, BS, William (Bill) Brooks, MBBS,MPH, Jared Brosch, MD, PhD, Jill Buck, BSN, Virginia Buckles, PhD, Kathleen Carter, PhD, Lisa Cash, BFA, Charlie Chen, BA, Jasmeer Chhatwal, MD,PhD, Patricio Chrem Mendez, MD, Jasmin Chua, BS, Helena Chui, MD, Laura Courtney, BS, Carlos Cruchaga, PhD, Gregory S Day, MD, Chrismary DeLaCruz, BA, Darcy Denner, PhD, Anna Diffenbacher, MS, Aylin Dincer, BS, Tamara Donahue, MS, Jane Douglas, MPh, Duc Duong, BS, Noelia Egido, BS, Bianca Esposito, BS, Anne Fagan, PhD, Marty Farlow, MD, Becca Feldman, BS,BA, Colleen Fitzpatrick, MS, Shaney Flores, BS, Nick Fox, MD, Erin Franklin, MS, Nelly Joseph-Mathurin, PhD, Hisako Fujii, PhD, Samantha Gardener, PhD, Bernardino Ghetti, MD, Alison Goate, PhD, Sarah Goldberg, MS,LPC,NCC, Jill Goldman, MS,MPhil,CGC, Alyssa Gonzalez, BS, Brian Gordon, PhD, Susanne Gräber-Sultan, PhD, Neill Graff-Radford, MD, Morgan Graham, BA, Julia Gray, MS, Emily Gremminger, BA, Miguel Grilo, MD, Alex Groves, Christian Haass, PhD, Lisa Häsler, MSc, Jason Hassenstab, PhD, Cortaiga Hellm, BA, Elizabeth Herries, BA, Laura Hoechst-Swisher, MS, Anna Hofmann, MD, Anna Hofmann, David Holtzman, MD, Russ Hornbeck, MSCS, MPM, Yakushev Igor, MD, Ryoko Ihara, MD, Takeshi Ikeuchi, MD, Snezana Ikonomovic, MD, Kenji Ishii, MD, Clifford Jack, MD, Gina Jerome, MS, Erik Johnson, MD, PHD, Mathias Jucker, PhD, Celeste Karch, PhD, Stephan Käser, PHD, Kensaku Kasuga, MD, Sarah Keefe, BS, William Klunk, MD, PHD, Robert Koeppe, PHD, Deb Koudelis, MHS,RN, Elke Kuder-Buletta, RN, Christoph Laske, PhD, Allan Levey, MD, PHD, Johannes Levin, MD, Yan Li, PHD, Oscar Lopez, MD, MD, Jacob Marsh, BA, Ralph Martins, PhD, Neal Scott Mason, PhD, Colin Masters, MD, Kwasi Mawuenyega, PhD, Austin McCullough, PhD Candidate, Eric McDade, DO, Arlene Mejia, MD, Estrella Morenas-Rodriguez, MD, PhD, John Morris, MD, James Mountz, MD, Cath Mummery, PhD, N eelesh Nadkarni, MD, PhD, Akemi Nagamatsu, RN, Katie Neimeyer, MS, Yoshiki Niimi, MD, James Noble, MD, Joanne Norton, MSN, RN, PMHCNS-BC, Brigitte Nuscher, Ulricke Obermüller, Antoinette O'Connor, MRCPI, Riddhi Patira, MD, Richard Perrin, MD, PhD, Lingyan Ping, PhD, Oliver Preische, MD, Alan Renton, PhD, John Ringman, MD, Stephen Salloway, MD, Peter Schofield, PhD, Michio Senda, MD, PhD, Nicholas T Seyfried, D.Phil, Kristine Shady, BA, BS, Hiroyuki Shimada, MD, PhD, Wendy Sigurdson, RN, Jennifer Smith, PhD, Lori Smith, PA-C, Beth Snitz, PhD, Hamid Sohrabi, PhD, Sochenda Stephens, BS, CCRP, Kevin Taddei, BS, Sarah Thompson, PA-C, Jonathan Vöglein, MD, Peter Wang, PhD, Qing Wang, PhD, Elise Weamer, MPH, Chengjie Xiong, PhD, Jinbin Xu, PhD, and Xiong Xu, BS, MS

Subjects
Brain aging, Alzheimer disease, Resting-state functional connectivity, fMRI, Machine learning, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

“Brain-predicted age” quantifies apparent brain age compared to normative neuroimaging trajectories. Advanced brain-predicted age has been well established in symptomatic Alzheimer disease (AD), but is underexplored in preclinical AD. Prior brain-predicted age studies have typically used structural MRI, but resting-state functional connectivity (FC) remains underexplored. Our model predicted age from FC in 391 cognitively normal, amyloid-negative controls (ages 18–89). We applied the trained model to 145 amyloid-negative, 151 preclinical AD, and 156 symptomatic AD participants to test group differences. The model accurately predicted age in the training set. FC-predicted brain age gaps (FC-BAG) were significantly older in symptomatic AD and significantly younger in preclinical AD compared to controls. There was minimal correspondence between networks predictive of age and AD. Elevated FC-BAG may reflect network disruption during symptomatic AD. Reduced FC-BAG in preclinical AD was opposite to the expected direction, and may reflect a biphasic response to preclinical AD pathology or may be driven by inconsistency between age-related vs. AD-related networks. Overall, FC-predicted brain age may be a sensitive AD biomarker.

Published
2022
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3. Sweet Sorghum as Feedstock in Great Plains Corn Ethanol Plants: The Role of Biofuel Policy

Author

Richard Perrin, Lilyan Fulginiti, Subir Bairagi, and Ismail Dweikat

Subjects
rfs2, rin price, sweet sorghum syrup, Agriculture
Abstract

This research examines whether sweet sorghum, a crop considered more drought-tolerant and suitable for semi-arid areas than corn, could result in an economically viable sweet sorghum ethanol pathway in the Great Plains. We find that that if the D5ÐD6 RIN price spread exceeds the $0.35/gal recently experienced, the benefits of the pathway would be equivalent to about $90/acre of sweet sorghum, or $0.38/gal of ethanol. Because of sparse cultivation potential, only four the six existing plants in the NebraskaÐColorado High Plains area might expect transportation costs to be low enough for economic feasibility.

Published
2018
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4. Relationships between big‐five personality factors and Alzheimer's disease pathology in autosomal dominant Alzheimer's disease

Author

Andrew J. Aschenbrenner, Jennifer Petros, Eric McDade, Guoqiao Wang, David A. Balota, Tammie LS Benzinger, Carlos Cruchaga, Alison Goate, Chengjie Xiong, Richard Perrin, Anne M. Fagan, Neill Graff‐Radford, Bernardino Ghetti, Johannes Levin, Endy Weidinger, Peter Schofield, Susanne Gräber, Jae‐Hong Lee, Jasmeer P. Chhatwal, John C. Morris, Randall Bateman, Jason Hassenstab, and for the Dominantly Inherited Alzheimer Network

Subjects
Neurology. Diseases of the nervous system, RC346-429, Geriatrics, RC952-954.6
Abstract

Abstract Introduction Changes in personality characteristics are associated with the onset of symptoms in Alzheimer's disease (AD) and may even precede clinical diagnosis. However, personality changes caused by disease progression can be difficult to separate from changes that occur with normal aging. The Dominantly Inherited Alzheimer Network (DIAN) provides a unique cohort in which to relate measures of personality traits to in vivo markers of disease in a much younger sample than in typical late onset AD. Methods Personality traits measured with the International Personality Item Pool at baseline from DIAN participants were analyzed as a function of estimated years to onset of clinical symptoms and well‐established AD biomarkers. Results Both neuroticism and conscientiousness were correlated with years to symptom onset and markers of tau pathology in the cerebrospinal fluid. Self‐reported conscientiousness and both neuroticism and conscientiousness ratings from a collateral source were correlated with longitudinal rates of cognitive decline such that participants who were rated as higher on neuroticism and lower on conscientiousness exhibited accelerated rates of cognitive decline. Discussion Personality traits are correlated with the accumulation of AD pathology and time to symptom onset, suggesting that AD progression can influence an individual's personality characteristics. Together these findings suggest that measuring neuroticism and conscientiousness may hold utility in tracking disease progression in AD.

Published
2020
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5. A 66-Year-Old Woman with a Progressive, Longitudinally Extensive, Tract Specific, Myelopathy

Author

Elizabeth O’Keefe, Katherine E. Schwetye, John Nazarian, Richard Perrin, Robert E. Schmidt, and Robert Bucelli

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

A 66-year-old woman presented with progressive lancinating pain and sensory deficits attributable to a myelopathy of unclear etiology. Spinal cord magnetic resonance imaging showed a longitudinally extensive T2-hyperintense lesion of the dorsal columns. Comprehensive serum, urine, and cerebrospinal fluid analyses failed to identify an etiology. Empiric intravenous methylprednisolone and intravenous immunoglobulin were of no benefit and serial screens for an occult malignancy were negative. She developed dysesthesias and allodynia affecting her entire body and lost the use of her arms and legs due to severe sensory ataxia that was steadily progressive from onset. She opted against additional aggressive medical management of her condition and passed away on hospice eleven months after symptom onset. Autopsy revealed findings most consistent with polyphasic spinal cord ischemia affecting the dorsal and lateral white matter tracts and, to a lesser extent, adjacent gray matter. The underlying etiology for the progressive vasculopathy remains unknown. Spinal cord ischemia affecting the posterior spinal cord is rare and to our knowledge this case represents the only instance of a progressive spinal cord tractopathy attributable to chronic spinal cord ischemia.

Published
2016
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6. Parenchymal border macrophages regulate the flow dynamics of the cerebrospinal fluid

Author

Antoine, Drieu, Siling, Du, Steffen E, Storck, Justin, Rustenhoven, Zachary, Papadopoulos, Taitea, Dykstra, Fenghe, Zhong, Kyungdeok, Kim, Susan, Blackburn, Tornike, Mamuladze, Oscar, Harari, Celeste M, Karch, Randall J, Bateman, Richard, Perrin, Martin, Farlow, Jasmeer, Chhatwal, Song, Hu, Gwendalyn J, Randolph, Igor, Smirnov, and Ulricke, Obermüller

Subjects
Central Nervous System, Extracellular Matrix Proteins, Aging, Multidisciplinary, Macrophages, Brain, Endocytosis, Article, Mice, Interferon-gamma, Meninges, Phagocytosis, Alzheimer Disease, Animals, Humans, Rheology, Parenchymal Tissue, Cerebrospinal Fluid
Abstract

Macrophages are important players for the maintenance of tissue homeostasis(1). Perivascular and leptomeningeal macrophages reside in close proximity to the central nervous system (CNS) parenchyma(2), and their role in CNS physiology has not been well enough studied to date. Given their continuous interaction with the cerebrospinal fluid (CSF) and strategic positioning, we refer to these cells collectively as parenchymal border macrophages (PBMs). Here, we demonstrate that PBMs regulate CSF flow dynamics. We identify a subpopulation of PBMs expressing high levels of CD163 and Lyve1 (scavenger receptor proteins), located in close proximity to the brain arterial tree, and show that Lyve1+ PBMs regulate arterial motion that drives CSF flow. Pharmacological or genetic depletion of PBMs led to accumulation of extracellular matrix proteins, obstructing CSF access to perivascular spaces hence impairing CNS perfusion and clearance. Aging-associated alterations in PBMs and impairment of CSF dynamics were restored upon intracisternal injection of macrophage colony-stimulating growth factor (M-CSF). Human single-nuclei RNA sequencing data obtained from Alzheimer’s disease (AD) patients and healthy controls point to changes in phagocytosis/endocytosis and interferon-gamma (IFNγ) signaling on PBMs, pathways that are corroborated in a mouse AD model. Collectively, our results identify PBMs as novel cellular regulators of CSF flow dynamics, which could potentially be targeted pharmacologically to alleviate brain clearance deficits associated with aging and AD.

Published
2022
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7. Amyloid and Tau Pathology Associations With Personality Traits, Neuropsychiatric Symptoms, and Cognitive Lifestyle in the Preclinical Phases of Sporadic and Autosomal Dominant Alzheimer’s Disease

Author

Alexa Pichet Binette, Étienne Vachon-Presseau, John Morris, Randall Bateman, Tammie Benzinger, D. Louis Collins, Judes Poirier, John C.S. Breitner, Sylvia Villeneuve, Ricardo Allegri, Fatima Amtashar, Randy Bateman, Sarah Berman, Courtney Bodge, Susan Brandon, William (Bill) Brooks, Jill Buck, Virginia Buckles, Sochenda Chea, Jasmeer Chhatwal, Patricio Chrem, Helena Chui, Jake Cinco, Jack Clifford, Carlos Cruchaga, Mirelle D‘Mello, Tamara Donahue, Jane Douglas, Noelia Edigo, Nilufer Erekin-Taner, Anne Fagan, Marty Farlow, Angela Farrar, Howard Feldman, Gigi Flynn, Nick Fox, Erin Franklin, Hisako Fujii, Cortaiga Gant, Samantha Gardener, Bernardino Ghetti, Alison Goate, Jill Goldman, Brian Gordon, Neill Graff-Radford, Julia Gray, Jenny Gurney, Jason Hassenstab, Mie Hirohara, David Holtzman, Russ Hornbeck, Siri Houeland DiBari, Takeshi Ikeuchi, Snezana Ikonomovic, Gina Jerome, Mathias Jucker, Celeste Karch, Kensaku Kasuga, Takeshi Kawarabayashi, William (Bill) Klunk, Robert Koeppe, Elke Kuder-Buletta, Christoph Laske, Jae-Hong Lee, Johannes Levin, Daniel Marcus, Ralph Martins, Neal Scott Mason, Colin Masters, Denise Maue-Dreyfus, Eric McDade, Lucy Montoya, Hiroshi Mori, Akem Nagamatsu, Katie Neimeyer, James Noble, Joanne Norton, Richard Perrin, Marc Raichle, John Ringman, Jee Hoon Roh, Stephen Salloway, Peter Schofield, Hiroyuki Shimada, Tomoyo Shiroto, Mikio Shoji, Wendy Sigurdson, Hamid Sohrabi, Paige Sparks, Kazushi Suzuki, Laura Swisher, Kevin Taddei, Jen Wang, Peter Wang, Mike Weiner, Mary Wolfsberger, Chengjie Xiong, Xiong Xu, Angela Tam, Anne Labonté, Anne-Marie Faubert, Axel Mathieu, Cécile Madjar, Charles Edouard Carrier, Christian Dansereau, Christina Kazazian, Claude Lepage, Cynthia Picard, David Maillet, Diane Michaud, Doris Couture, Doris Dea, Claudio Cuello, Alan Barkun, Alan Evans, Blandine Courcot, Christine Tardif, Clément Debacker, Clifford R. Jack, David Fontaine, David S. Knopman, Gerhard Maultaup, Jamie Near, Jeannie-Marie Leoutsakos, Jean-Robert Maltais, Jason Brandt, Jens Pruessner, John C. Morris, Laksanun Cheewakriengkrai, Lisa-Marie Münter, Louis Collins, Mallar Chakravarty, Mark A. Sager, Marina Dauar-Tedeschi, Mark Eisenberg, Natasha Rajah, Paul Aisen, Joanne Toussaint, Pedro Rosa-Neto, Pierre Bellec, Penelope Kostopoulos, Pierre Etienne, Pierre N. Tariot, Pierre Orban, Reisa A. Sperling, Rick Hoge, Ronald G. Thomas, Serge Gauthier, Suzanne Craft, Thomas J. Montine, Vasavan Nair, Véronique Bohbot, Vinod Venugopalan, Vladimir Fonov, Yasser Ituria-Medina, Zaven S. Khachaturian, Eduard Teigner, Elena Anthal, Elsa Yu, Fabiola Ferdinand, Galina Pogossova, Ginette Mayrand, Guerda Duclair, Guylaine Gagné, Holly Newbold-Fox, Illana Leppert, Isabelle Vallée, Jacob W. Vogel, Jennifer Tremblay-Mercier, Joanne Frenette, Josée Frappier, Justin Kat, Justin Miron, Karen Wan, Laura Mahar, Leopoldina Carmo, Louise Théroux, Mahsa Dadar, Marianne Dufour, Marie-Elyse Lafaille-Magnan, Melissa Appleby, Mélissa Savard, Miranda Tuwaig, Mirela Petkova, Pierre Rioux, Pierre-François Meyer, Rana El-Khoury, Renee Gordon, Renuka Giles, Samir Das, Seqian Wang, Shirin Tabrizi, Sulantha Mathotaarachchi, Sylvie Dubuc, Tanya Lee, Thomas Beaudry, Valérie Gervais, Véronique Pagé, Julie Gonneaud, Gülebru Ayranci, Tharick A. Pascoal, René Desautels, Fatiha Benbouhoud, Eunice Farah Saint-Fort, Sander C.J. Verfaillie, Sarah Farzin, Alyssa Salaciak, Stephanie Tullo, Etienne Vachon-Presseau, Leslie-Ann Daoust, Theresa Köbe, Nathan Spreng, Melissa McSweeney, Nathalie Nilsson, Morteza Pishnamazi, and Christophe Bedetti

Subjects
0301 basic medicine, Oncology, medicine.medical_specialty, tau Proteins, Disease, Article, 03 medical and health sciences, Cognition, 0302 clinical medicine, Alzheimer Disease, Internal medicine, mental disorders, medicine, Humans, Dementia, Big Five personality traits, Family history, Life Style, Biological Psychiatry, Aged, Amyloid beta-Peptides, Extraversion and introversion, business.industry, medicine.disease, Neuroticism, 3. Good health, 030104 developmental biology, Positron-Emission Tomography, Cohort, Alzheimer's disease, business, 030217 neurology & neurosurgery
Abstract

Background Major prevention trials for Alzheimer’s disease (AD) are now focusing on multidomain lifestyle interventions. However, the exact combination of behavioral factors related to AD pathology remains unclear. In 2 cohorts of cognitively unimpaired individuals at risk of AD, we examined which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (years of education or lifetime cognitive activity) related to the pathological hallmarks of AD, amyloid-β, and tau deposits. Methods A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. Separately, we studied 117 mutation carriers from the DIAN (Dominant Inherited Alzheimer Network) study group cohort with amyloid positron emission tomography and behavioral data. Using partial least squares analysis, we identified latent variables relating amyloid or tau pathology with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle. Results In PREVENT-AD, lower neuroticism, neuropsychiatric burden, and higher education were associated with less amyloid deposition (p = .014). Lower neuroticism and neuropsychiatric features, along with higher measures of openness and extraversion, were related to less tau deposition (p = .006). In DIAN, lower neuropsychiatric burden and higher education were also associated with less amyloid (p = .005). The combination of these factors accounted for up to 14% of AD pathology. Conclusions In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. These results may suggest potential pathways by which multidomain interventions might help delay AD onset or progression.

Published
2021
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8. Plasma glial fibrillary acidic protein in autosomal dominant Alzheimer’s disease: associations with β-amyloid-PET, neurodegeneration and cognition

Author

Pratishtha Chatterjee, Lisa Vermunt, Brian Gordon, Steve Pedrini, Lynn Boonkamp, Nicola Armstrong, Chengjie Xiong, Abhay Singh, Yan Li, Hamid Sohrabi, Kevin Taddei, Mark Molloy, Tammie Benzinger, John Morris, Celeste Karch, Sarah Berman, Jasmeer Chhatwal, Carlos Cruchaga, Neill Graff-Radford, Gregory Day, Martin Farlow, Nick Fox, Alison Goate, Jason Hassenstab, Jae-Hong Lee, Johannes Levin, Eric McDade, Hiroshi Mori, Richard Perrin, Raquel Sánchez-Valle, Peter Schofield, Allan Levey, Mathias Jucker, Colin Masters, Anne Fagan, Randall Bateman, Ralph Martins, and Charlotte Teunissen

Abstract

Glial fibrillary acidic protein (GFAP) is a promising candidate blood-based biomarker for Alzheimer’s disease (AD) diagnosis and prognostication. The timing of its disease-associated changes, its clinical correlates, and biofluid-type dependency will influence its clinical utility. We evaluated plasma, serum, and CSF GFAP in families with autosomal dominant AD (ADAD), leveraging the predictable age at symptom onset to determine changes by stage of disease. Plasma GFAP elevations appear a decade before expected symptom onset, after β-amyloid accumulation and prior to neurodegeneration and cognitive decline. Plasma GFAP distinguished β-amyloid-positive from β-amyloid-negative ADAD participants and showed a stronger relationship with β-amyloid load in asymptomatic than symptomatic ADAD. Higher plasma GFAP was associated with the degree and rate of neurodegeneration and cognitive impairment. Serum GFAP showed similar relationships, but these were less pronounced for CSF GFAP. Our findings support a role for plasma GFAP as a clinical biomarker for β-amyloid-associated cognitive deterioration in AD.

Published
2022
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9. Vitamin D Supplementation in COVID-19 Patients: A Clinical Case Series

Author

Richard Perrin, Miriam A. Smith, Kim C Ohaegbulam, Pranavkumar Patel, and Mohamed Swalih

Subjects
Male, vitamin D, Comorbidity, 030204 cardiovascular system & hematology, Calcitriol receptor, law.invention, chemistry.chemical_compound, 0302 clinical medicine, Randomized controlled trial, law, Pharmacology (medical), 030212 general & internal medicine, Cholecalciferol, Vitamins, General Medicine, Middle Aged, Ergocalciferol, C-Reactive Protein, Treatment Outcome, Ergocalciferols, Female, Coronavirus Infections, CRP, medicine.drug, Adult, medicine.medical_specialty, Pneumonia, Viral, vitamin D deficiency, Proinflammatory cytokine, Betacoronavirus, 03 medical and health sciences, Immune system, Internal medicine, medicine, Vitamin D and neurology, Humans, Pandemics, Therapeutic Innovation, Pharmacology, IL-6, SARS-CoV-2, business.industry, Oxygen Inhalation Therapy, COVID-19, Length of Stay, Vitamin D Deficiency, medicine.disease, chemistry, Dietary Supplements, Receptors, Calcitriol, ARDS, business
Abstract

Background Coronavirus disease 2019 (COVID-19) has infected more than 4.4 million people and caused more than 300,000 deaths partly through acute respiratory distress syndrome with propensity to affect African American and Hispanic communities disproportionately. Patients with worse outcomes have exhibited higher blood plasma levels of proinflammatory cytokines. Activation of the vitamin D receptor expressed on immune cells has been shown to directly reduce the secretion of inflammatory cytokines, such as interleukin-6, and indirectly affect C-reactive protein. Areas of uncertainty The significance of the vitamin D pathway in patients diagnosed with COVID-19. Therapeutic innovation Vitamin D supplementation in patients after diagnosis of COVID-19. Patients and pharmacological interventions We report 4 vitamin D deficient patients diagnosed with COVID-19 in April 2020 who were provided with either cholecalciferol of 1000 IU daily (standard dose) or ergocalciferol 50,000 IU daily for 5 days (high dose) as part of supplementation. Clinical outcomes Patients that received a high dose of vitamin D supplementation achieved normalization of vitamin D levels and improved clinical recovery evidenced by shorter lengths of stay, lower oxygen requirements, and a reduction in inflammatory marker status. Conclusions Vitamin D supplementation may serve as a viable alternative for curtailing acute respiratory distress syndrome in patients in underserved communities where resources to expensive and sought-after medications may be scarce. Randomized clinical trials will serve as an appropriate vessel to validate the efficacy of the therapeutic regimen and dissection of the pathway.

Published
2020
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11. Theoretician, advocate and candidate in California State government

Author

Bancroft Library. Oral History Center, Morris, Gabrielle S., Graves, Richard Perrin, Bancroft Library. Oral History Center, Morris, Gabrielle S., and Graves, Richard Perrin

Abstract

Graduate studies and work as research associate in Bureau of Public Administration, University of California, Berkeley; influence of Prof. Samuel C. May; acquaintance with Earl Warren as district attoney of Alameda County, California, and governor; work as executive director of League of California Cities, 1933-1953; director of California civil defense program under governors Olson and Warren; views on Japanese relocation; 1954 campaign as Democratic nominee for governor of California. Appended: copies of letters, clippings and other documentary material., California Audiovisual Preservation Project (CAVPP)

Published
1973

12. Isolation of Escherichia coli O157:H7 from Intact Colon Fecal Samples of Swine

Author

Ingrid Feder, F. Morgan Wallace, Jeffrey T. Gray, Pina Fratamico, Paula J. Fedorka-Cray, Rachel A. Pearce, Jeffrey E. Call, Richard Perrine, and John B. Luchansky

Subjects
Escherichia coli O157, H7, feces, swine, dispatch, United States, Medicine, Infectious and parasitic diseases, RC109-216
Abstract

Escherichia coli O157:H7 was recovered from colon fecal samples of pigs. Polymerase chain reaction confirmed two genotypes: isolates harboring the eaeA, stx1, and stx2 genes and isolates harboring the eaeA, stx1, and hly933 genes. We demonstrate that swine in the United States can harbor potentially pathogenic E. coli O157:H7.

Published
2003
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13. A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease

Author

Barthélemy, Nicolas R, Li, Yan, Morris, John C, Neimeyer, Katie, Noble, James, Norton, Joanne, Perrin, Richard, Raichle, Marc, Renton, Alan, Ringman, John, Roh, Jee Hoon, Salloway, Stephen, Schofield, Peter, Karch, Celeste M, Shimada, Hiroyuki, Sigurdson, Wendy, Sohrabi, Hamid, Sparks, Paige, Suzuki, Kazushi, Taddei, Kevin, Wang, Peter, Xiong, Chengjie, Xu, Xiong, Allegri, Ricardo, Mendez, Patricio Chrem, Berman, Sarah B, Ikeuchi, Takeshi, Mori, Hiroshi, Shoji, Mikio, Joseph-Mathurin, Nelly, Farlow, Martin, Chhatwal, Jasmeer, Graff-Radford, Neill R, Schofield, Peter R, Masters, Colin L, Martins, Ralph N, O'Connor, Antoinette, Gordon, Brian A, Fox, Nick C, Levin, Johannes, Jucker, Mathias, Gabelle, Audrey, Lehmann, Sylvain, Sato, Chihiro, Bateman, Randall J, McDade, Eric, Network, Dominantly Inherited Alzheimer, Hassenstab, Jason, Bateman, Randy, Bechara, Jacob, Benzinger, Tammie, Berman, Sarah, Bodge, Courtney, Brandon, Susan, Brooks, William Bill, Buck, Jill, Buckles, Virginia, Chea, Sochenda, Benzinger, Tammie L S, Chrem Mendez, Patricio, Chui, Helena, Cinco, Jake, Clifford, Jack, Cruchaga, Carlos, Donahue, Tamara, Douglas, Jane, Edigo, Noelia, Erekin-Taner, Nilufer, Fagan, Anne, Fitzpatrick, Colleen, Flynn, Gigi, Fox, Nick, Franklin, Erin, Fujii, Hisako, Gant, Cortaiga, Gardener, Samantha, Ghetti, Bernardino, Fagan, Anne M, Goate, Alison, Goldman, Jill, Gordon, Brian, Graff-Radford, Neill, Gray, Julia, Groves, Alexander, Hoechst-Swisher, Laura, Holtzman, David, Hornbeck, Russ, Perrin, Richard J, DiBari, Siri Houeland, Ikonomovic, Snezana, Jerome, Gina, Karch, Celeste, Kasuga, Kensaku, Kawarabayashi, Takeshi, Klunk, William Bill, Koeppe, Robert, Kuder-Buletta, Elke, Goate, Alison M, Laske, Christoph, Lee, Jae-Hong, Martins, Ralph, Mason, Neal Scott, Masters, Colin, Maue-Dreyfus, Denise, Morris, John, Nagamatsu, Akem, Washington University School of Medicine in St. Louis, Washington University in Saint Louis (WUSTL), Icahn School of Medicine at Mount Sinai [New York] (MSSM), Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia [Buenos Aires] (FLENI), FLENI, University of Pittsburgh School of Medicine, Pennsylvania Commonwealth System of Higher Education (PCSHE), Niigata University, Osaka City University (OCU), Hirosaki University, The University of Tokyo (UTokyo), Columbia University [New York], Indiana University - Purdue University Indianapolis (IUPUI), Indiana University System, Harvard Medical School [Boston] (HMS), Mayo Clinic [Jacksonville], Brown University, Neuroscience Research Australia (NeuRA), University of New South Wales [Sydney] (UNSW), The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Edith Cowan University (ECU), Commonwealth Scientific and Industrial Research Organisation [Canberra] (CSIRO)-Planning and Transport Research Centre (PATREC), University College of London [London] (UCL), German Research Center for Neurodegenerative Diseases - Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Ludwig-Maximilians-Universität München (LMU), Munich Cluster for systems neurology [Munich] (SyNergy), Technische Universität Munchen - Université Technique de Munich [Munich, Allemagne] (TUM)-Ludwig-Maximilians-Universität München (LMU), University of Tübingen, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), BioCampus Montpellier (BCM), Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Dominantly Inherited Alzheimer Network: Ricardo Allegri, Randy Bateman, Jacob Bechara, Tammie Benzinger, Sarah Berman, Courtney Bodge, Susan Brandon, William Bill Brooks, Jill Buck, Virginia Buckles, Sochenda Chea, Jasmeer Chhatwal, Patricio Chrem Mendez, Helena Chui, Jake Cinco, Jack Clifford, Carlos Cruchaga, Tamara Donahue, Jane Douglas, Noelia Edigo, Nilufer Erekin-Taner, Anne Fagan, Martin Farlow, Colleen Fitzpatrick, Gigi Flynn, Nick Fox, Erin Franklin, Hisako Fujii, Cortaiga Gant, Samantha Gardener, Bernardino Ghetti, Alison Goate, Jill Goldman, Brian Gordon, Neill Graff-Radford, Julia Gray, Alexander Groves, Jason Hassenstab, Laura Hoechst-Swisher, David Holtzman, Russ Hornbeck, Siri Houeland DiBari, Takeshi Ikeuchi, Snezana Ikonomovic, Gina Jerome, Mathias Jucker, Celeste Karch, Kensaku Kasuga, Takeshi Kawarabayashi, William Bill Klunk, Robert Koeppe, Elke Kuder-Buletta, Christoph Laske, Jae-Hong Lee, Johannes Levin, Ralph Martins, Neal Scott Mason, Colin Masters, Denise Maue-Dreyfus, Eric McDade, Hiroshi Mori, John Morris, Akem Nagamatsu, Katie Neimeyer, James Noble, Joanne Norton, Richard Perrin, Marc Raichle, Alan Renton, John Ringman, Jee Hoon Roh, Stephen Salloway, Peter Schofield, Hiroyuki Shimada, Wendy Sigurdson, Hamid Sohrabi, Paige Sparks, Kazushi Suzuki, Kevin Taddei, Peter Wang, Chengjie Xiong, Xiong Xu, Technische Universität München [München] (TUM)-Ludwig-Maximilians-Universität München (LMU), BioCampus (BCM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), and Michel-Avella, Amandine

Subjects
0301 basic medicine, Male, [SDV]Life Sciences [q-bio], Inheritance Patterns, genetics [Alzheimer Disease], Plaque, Amyloid, Disease, 0302 clinical medicine, Cerebrospinal fluid, Cognition, pathology [Brain], Phosphorylation, biology, Neurodegeneration, Brain, General Medicine, Middle Aged, Magnetic Resonance Imaging, 3. Good health, [SDV] Life Sciences [q-bio], cerebrospinal fluid [Alzheimer Disease], 030220 oncology & carcinogenesis, Disease Progression, Female, Alzheimer's disease, metabolism [Alzheimer Disease], Adult, Amyloid, genetics [Inheritance Patterns], Tau protein, Neuroimaging, tau Proteins, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Atrophy, Alzheimer Disease, Fluorodeoxyglucose F18, mental disorders, medicine, Humans, ddc:610, pathology [Plaque, Amyloid], chemistry [Fluorodeoxyglucose F18], metabolism [Amyloid], Aged, medicine.disease, metabolism [tau Proteins], 030104 developmental biology, cerebrospinal fluid [tau Proteins], Solubility, biology.protein, diagnostic imaging [Alzheimer Disease], Neuroscience
Abstract

International audience; Development of tau-based therapies for Alzheimer's disease requires an understanding of the timing of disease-related changes in tau. We quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer's disease. We identified a pattern of tau staging where site-specific phosphorylation changes occur at different periods of disease progression and follow distinct trajectories over time. These tau phosphorylation state changes are uniquely associated with structural, metabolic, neurodegenerative and clinical markers of disease, and some (p-tau217 and p-tau181) begin with the initial increases in aggregate amyloid-β as early as two decades before the development of aggregated tau pathology. Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset. These findings provide insights into the pathways linking tau, amyloid-β and neurodegeneration, and may facilitate clinical trials of tau-based treatments.

Published
2020
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