Search

Your search keyword '"Q Trojanowski, J"' showing total 3 results
Start Over Author "Q Trojanowski, J" Search Limiters Available in Library Collection
3 results on '"Q Trojanowski, J"'

1. Genetic risk for neurodegenerative disorders, and its overlap with cognitive ability and physical function

Author

Hagenaars, Sp, Radaković, R, Crockford, C, Fawns-Ritchie, C, Gale, Cr, Deary, Ij, J B, J Kwok, Dobson-Stone, C, R Schofield, P, Gmhalliday, R Hodges, J, Piguet, O, Bartley, L, Thompson, E, Hernaândez, I, Ruiz, A, Mboada, Borroni, B, Padovani, A, Cruchaga, C, J Cairns, N, Benussi, L, Binetti, G, Ghidoni, R, Forloni, G, Albani, D, Galimberti, D, Fenoglio, C, Serpente, M, Scarpini, E, Clarimoân, J, Lleoâ, A, Blesa, R, Mlandqvist, Waldoè, Nilsson, K, Nilsson, C, I R, A Mackenzie, G-Y, R Hsiung, Dma, Mann, Grafman, J, Cmmorris, Attems, J, D Griffiths, T, G McKeith, I, J Thomas, A, Pietrini, P, D Huey, E, Emwassermann, Baborie, A, Jaros, E, Tierney, Mc, Pastor, P, Razquin, C, Ortega-Cubero, S, Alonso, E, Perneczky, R, Diehl-Schmid, J, Alexopoulos, P, Kurz, A, Rainero, I, Rubino, E, Pinessi, L, Rogaeva, E, P St George-Hyslop, Rossi, G, Tagliavini, F, Giaccone, G, B Rowe, J, Cmschlachetzki, J, Uphill, J, Collinge, J, Mead, S, Danek, A, Vmvan, Deerlin, Mgrossman, Q Trojanowski, J, J van der Zee, C Van Broeckhoven, F Cappa, S, Leber, I, Hannequin, D, Golfier, V, Mvercelletto, Brice, A, Nacmias, B, Sorbi, S, Bagnoli, S, Piaceri, I, E Nielsen, J, E Hjermind, L, Mriemenschneider, Mmayhaus, Ibach, B, Gasparoni, G, Pichler, S, Wgu, Rossor, Mn, C Fox, N, D Warren, J, Spillantini, Mg, R Morris, H, Rizzu, P, Heutink, P, S Snowden, J, Rollinson, S, Richardson, A, Gerhard, A, C Bruni, A, Maletta, R, Frangipane, F, Cupidi, C, Bernardi, L, Manfossi, Mgallo, Conidi, Me, Smirne, N, Rademakers, R, Baker, M, Dwdickson, R Graff-Radford, N, C Petersen, R, Knopman, D, A Josephs, K, F Boeve, B, E Parisi, J, Wwseeley, L Miller, B, Amkarydas, Rosen, H, C van Swieten, J, E G, P Dopper, Seelaar, H, Y A, L Pijnenburg, Scheltens, P, Logroscino, G, Capozzo, R, Novelli, V, A Puca, A, Franceschi, M, Postiglione, A, Milan, G, Sorrentino, P, Mkristiansen, H-H, Chiang, Graff, C, Pasquier, F, Rollin, A, Deramecourt, V, Lebouvier, T, Kapogiannis, D, Ferrucci, L, Pickering-Brown, S, B Singleton, A, Hardy, J, and Momeni., P

Subjects
Genetics and Molecular Biology (all), Multifactorial Inheritance, Peak Expiratory Flow Rate, Disease, Physical function, Alzheimer's Disease, Biochemistry, Motor Neuron Diseases, 0302 clinical medicine, Cognition, Learning and Memory, Biochemistry, Genetics and Molecular Biology (all), Agricultural and Biological Sciences (all), Forced Expiratory Volume, Medicine and Health Sciences, Amyotrophic lateral sclerosis, Genetic risk, Cognitive Impairment, 0303 health sciences, Cognitive Neurology, Neurodegenerative Diseases, Middle Aged, Mental Status and Dementia Tests, Neurology, Frontotemporal Dementia, Clinical psychology, Frontotemporal dementia, Research Article, Adult, Cognitive Neuroscience, Risk Assessment, 03 medical and health sciences, Memory, Alzheimer Disease, Mental Health and Psychiatry, mental disorders, medicine, Genetics, Humans, Effects of sleep deprivation on cognitive performance, Muscle Strength, Genetic Association Studies, 030304 developmental biology, Aged, business.industry, Amyotrophic Lateral Sclerosis, Biology and Life Sciences, medicine.disease, United Kingdom, Physical Fitness, Genetics of Disease, Cognitive Science, Polygenic risk score, Dementia, business, 030217 neurology & neurosurgery, Neuroscience, Genome-Wide Association Study
Abstract

INTRODUCTIONIt is unclear whether polygenic risk for neurodegenerative disease is associated with cognitive performance and physical health.METHODSThis study tested whether polygenic scores for Alzheimer’s disease (AD), Amyotrophic Lateral Sclerosis (ALS), or frontotemporal dementia (FTD) are associated with cognitive performance and physical health. Group-based analyses were performed to compare associations with cognitive and physical function outcomes in the top and bottom 10% for the three neurodegenerative polygenic risk scores.RESULTSHigher polygenic risk scores for AD, ALS, and FTD were associated with lower cognitive performance. Higher polygenic risk scores for FTD was also associated with increased forced expiratory volume in 1s and peak expiratory flow. A significant group difference was observed on the symbol digit substitution task between individuals with high polygenic risk for FTD and high polygenic risk for ALS.DISCUSSIONOur results suggest overlap between polygenic risk for neurodegenerative disorders, cognitive function and physical health.

Published
2018

2. CSF Biomarker and PIB-PET-Derived Beta-Amyloid Signature Predicts Metabolic, Gray Matter, and Cognitive Changes in Nondemented Subjects

Author

Leslie M. Shaw, John Q. Trojanowski J, Philip S. Insel, William J. Jagust, Michael Ewers, Paul S. Aisen, Michael Weiner, Norbert Schuff, and Ronald C. Petersen

Subjects
Pathology, medicine.medical_specialty, Amyloid, Cognitive Neuroscience, Precuneus, Temporal lobe, Cellular and Molecular Neuroscience, Cerebrospinal fluid, Atrophy, medicine, Humans, Dementia, Cognitive Dysfunction, Cognitive decline, Aged, Aged, 80 and over, Amyloid beta-Peptides, Aniline Compounds, medicine.diagnostic_test, Brain, Articles, Middle Aged, medicine.disease, Thiazoles, Early Diagnosis, medicine.anatomical_structure, Positron emission tomography, Positron-Emission Tomography, Radiopharmaceuticals, Psychology, Biomarkers
Abstract

Beta-amyloid (Aβ) is a histopathological hallmark of Alzheimer’s disease dementia, but high levels of Aβ in the brain can also be found in a substantial proportion of nondemented subjects. Here we investigated which 2-year rate of brain and cognitive changes are present in nondemented subjects with high and low Aβ levels, as assessed with cerebrospinal fluid and molecular positron emission tomography (PET)–based biomarkers of Aβ. In subjects with mild cognitive impairment, increased brain Aβ levels were associated with significantly faster cognitive decline, progression of gray matter atrophy within temporal and parietal brain regions, and a trend for a faster decline in parietal Fludeoxyglucose (FDG)-PET metabolism. Changes in gray matter and FDG-PET mediated the association between Aβ and cognitive decline. In contrast, elderly cognitively healthy controls (HC) with high Aβ levels showed only a faster medial temporal lobe and precuneus volume decline compared with HC with low Aβ. In conclusion, the current results suggest not only that both functional and volumetric brain changes are associated with high Aβ years before the onset of dementia but also that HC with substantial Aβ levels show higher Aβ pathology resistance, lack other pathologies that condition neurotoxic effects of Aβ, or accumulated Aβ for a shorter time period.

Published
2011
Full Text
View/download PDF

3. Distinct FTDP-17 missense mutations in tau produce tau aggregates and other pathological phenotypes in transfected CHO cells.

Author

V, Vogelsberg-Ragaglia, J, Bruce, C, Richter-Landsberg, B, Zhang, M, Hong, Q, Trojanowski J, and M, Lee V

Abstract

Multiple tau gene mutations are pathogenic for hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), with filamentous tau aggregates as the major lesions in the CNS of these patients. Recent studies have shown that bacterially expressed recombinant tau proteins with FTDP-17 missense mutations cause functional impairments, i.e., a reduced ability of mutant tau to bind to or promote the assembly of microtubules. To investigate the biological consequences of FTDP-17 tau mutants and assess their ability to form filamentous aggregates, we engineered Chinese hamster ovary cell lines to stably express tau harboring one or several different FTDP-17 mutations and showed that different tau mutants produced distinct pathological phenotypes. For example, delta K, but not several other single tau mutants (e.g., V337 M, P301L, R406W), developed insoluble amorphous and fibrillar aggregates, whereas a triple tau mutant (VPR) containing V337M, P301L, and R406W substitutions also formed similar aggregates. Furthermore, the aggregates increased in size over time in culture. Significantly, the formation of aggregated delta K and VPR tau protein correlated with reduced affinity of these mutants to bind microtubules. Reduced phosphorylation and altered proteolysis was also observed in R406W and delta K tau mutants. Thus, distinct pathological phenotypes, including the formation of insoluble filamentous tau aggregates, result from the expression of different FTDP-17 tau mutants in transfected Chinese hamster ovary cells and implies that these missense mutations cause diverse neurodegenerative FTDP-17 syndromes by multiple mechanisms.

Published
2000

Catalog

Books, media, physical & digital resources
See catalog results