المؤلفون: Parinaz Massoumzadeh, Randall J. Bateman, John C. Morris, Colin L. Masters, Hiroshi Mori, Eric McDade, Peter R. Schofield, Carlos Cruchaga, Mathias Jucker, Richard J. Perrin, Tammie L.S. Benzinger, Jasmeer P. Chhatwal, Jonathan Vöglein, Jason Hassenstab, Elizabeth A. Grant, Chengjie Xiong, Neill R. Graff-Radford, Jingqin Luo, Marilyn S. Albert, Folasade Agboola, Anne M. Fagan, Bernardino Ghetti, Sterling C. Johnson

المصدر: Neurology 95(23), e3104-e3116 (2020). doi:10.1212/WNL.0000000000010747
Neurology

مصطلحات موضوعية: 0301 basic medicine, Oncology, Male, physiopathology [Cognitive Dysfunction], pathology [Cognitive Dysfunction], diagnostic imaging [Cognitive Dysfunction], 2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole, Hippocampus, cerebrospinal fluid [Amyloid beta-Peptides], chemistry.chemical_compound, pathology [Alzheimer Disease], metabolism [Cognitive Dysfunction], 0302 clinical medicine, diagnostic imaging [Cerebral Cortex], Cognitive decline, skin and connective tissue diseases, Cerebral Cortex, Aged, 80 and over, diagnostic imaging [Hippocampus], Aniline Compounds, medicine.diagnostic_test, Age Factors, Middle Aged, amyloid beta-protein (1-42), Magnetic Resonance Imaging, Biomarker (medicine), Female, Alzheimer's disease, metabolism [Alzheimer Disease], metabolism [Biomarkers], Adult, medicine.medical_specialty, Adolescent, metabolism [Amyloid beta-Peptides], Prodromal Symptoms, Standardized uptake value, MAPT protein, human, tau Proteins, Neuropathology, physiopathology [Alzheimer Disease], Article, 03 medical and health sciences, Young Adult, Alzheimer Disease, Internal medicine, medicine, Humans, Cognitive Dysfunction, ddc:610, cerebrospinal fluid [Peptide Fragments], Aged, Amyloid beta-Peptides, business.industry, Magnetic resonance imaging, amyloid beta-protein (1-40), medicine.disease, Peptide Fragments, Thiazoles, 030104 developmental biology, Cross-Sectional Studies, pathology [Hippocampus], chemistry, cerebrospinal fluid [tau Proteins], Positron-Emission Tomography, pathology [Cerebral Cortex], sense organs, Neurology (clinical), business, Pittsburgh compound B, diagnostic imaging [Alzheimer Disease], 030217 neurology & neurosurgery, Biomarkers

الوصف: ObjectiveTo determine the ordering of changes in Alzheimer disease (AD) biomarkers among cognitively normal individuals.MethodsCross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [11C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed. The age at which each marker exhibited an accelerated change (called the change point) was estimated and compared across the markers.ResultsAccelerated changes in CSF Aβ1-42 (Aβ42) occurred at 48.28 years of age and in Aβ42/Aβ40 ratio at 46.02 years, followed by PiB mean cortical standardized uptake value ratio (SUVR) with a change point at 54.47 years. CSF total tau (Tau) and tau phosphorylated at threonine 181 (Ptau) had a change point at ≈60 years, similar to those for MRI hippocampal volume and cortical thickness. The change point for a cognitive composite occurred at 62.41 years. The change points for CSF Aβ42 and Aβ42/Aβ40 ratio, albeit not significantly different from that for PiB SUVR, occurred significantly earlier than that for CSF Tau, Ptau, MRI markers, and the cognitive composite. Adjusted analyses confirmed that accelerated changes in CSF Tau, Ptau, MRI markers, and the cognitive composite occurred at ages not significantly different from each other.ConclusionsOur findings support the hypothesized early changes of amyloid in preclinical AD and suggest that changes in neuronal injury and neurodegeneration markers occur close in time to cognitive decline.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::accb5a8dcd4bb991084e13fdafa1e01cTest

المؤلفون: Kevin Taddei, Michael W. Weiner, Belinda M. Brown, Hamid R. Sohrabi, Jeremiah J. Peiffer, Colin L. Masters, Chengjie Xiong, Tammie L.S. Benzinger, Neill R. Graff-Radford, Christoph Laske, Peter R. Schofield, Virginia Buckles, Stephanie R. Rainey-Smith, James M. Noble, Jonathan Vöglein, Roger Clarnette, Anne M. Fagan, Martin N. Rossor, Ralph N. Martins, Samantha L. Gardener, Stephen Salloway, Nigel J. Cairns, John C. Morris, Randall J. Bateman, Tejal M. Shah, Kirk I. Erickson

المصدر: Alzheimer's & dementia : the journal of the Alzheimer's Association, vol 13, iss 11
Alzheimer's and dementia 13(11), 1197-1206 (2017). doi:10.1016/j.jalz.2017.03.008

مصطلحات موضوعية: 0301 basic medicine, Male, Pathology, Aging, Epidemiology, 2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole, genetics [Alzheimer Disease], Disease, cerebrospinal fluid [Amyloid beta-Peptides], Neurodegenerative, Alzheimer's Disease, Cohort Studies, Amyloid beta-Protein Precursor, 0302 clinical medicine, Cerebrospinal fluid, Surveys and Questionnaires, 2.1 Biological and endogenous factors, Cognitive decline, Aetiology, Aniline Compounds, biology, Health Policy, Brain, genetics [Presenilin-1], Middle Aged, amyloid beta-protein (1-42), Magnetic Resonance Imaging, Psychiatry and Mental health, genetics [Amyloid beta-Protein Precursor], Neurological, Female, Alzheimer's disease, Psychology, metabolism [Alzheimer Disease], Adult, medicine.medical_specialty, Amyloid, Genotype, Amyloid beta, Clinical Sciences, genetics [Mutation], genetics [Presenilin-2], tau Proteins, physiopathology [Alzheimer Disease], Presenilin, Article, 03 medical and health sciences, Cellular and Molecular Neuroscience, PSEN1 protein, human, Apolipoproteins E, Developmental Neuroscience, Alzheimer Disease, Internal medicine, mental disorders, Presenilin-2, medicine, Presenilin-1, Genetics, Acquired Cognitive Impairment, Dementia, Humans, ddc:610, cerebrospinal fluid [Peptide Fragments], diagnostic imaging [Brain], Exercise, metabolism [Amyloid], Amyloid beta-Peptides, PSEN2 protein, human, Physical activity, Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Amyloid β, medicine.disease, Peptide Fragments, Brain Disorders, Thiazoles, 030104 developmental biology, Endocrinology, Cross-Sectional Studies, cerebrospinal fluid [tau Proteins], metabolism [Brain], Geriatrics, Positron-Emission Tomography, Dominantly Inherited Alzheimer Network, Mutation, biology.protein, Linear Models, genetics [Apolipoproteins E], Neurology (clinical), Geriatrics and Gerontology, Tau, diagnostic imaging [Alzheimer Disease], physiology [Exercise], 030217 neurology & neurosurgery

الوصف: Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. Methods In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ 42, and CSF tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ 42 , or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fc8b74b9a8256ec014881f56da6ec51cTest
https://escholarship.org/uc/item/4x05j8kvTest