13 results match your criteria: "From the Massachusetts General Hospital (R.F.B.); Washington University School of Medicine (S.E.S.).[Affiliation]"

Associations Between Self and Study Partner Report of Cognitive Decline With Regional Tau in a Multicohort Study.

Neurology

June 2024

From the Department of Neurology (M.F.J., H.K., R.F.B., G.A.M., P.V., D.M.R., K.A.J., R.A.S., R.E.A.), and Department of Radiology (M.F.J., K.A.J.), Massachusetts General Hospital, and Center for Alzheimer Research and Treatment (T.R., M.E.F., R.F.B., G.A.M., P.V., D.M.R., K.A.J., R.A.S., R.E.A.), Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.

Article Synopsis
  • This study investigates the relationship between self-reported cognitive decline and tau deposition in individuals with preclinical Alzheimer disease (AD), building on prior findings about β-amyloid (Aβ) status.
  • The research involved 675 cognitively unimpaired participants who completed assessments to examine the connections between tau levels and cognitive function, while accounting for factors like age and education.
  • Results indicated that higher tau levels in both the medial temporal lobe and neocortex were linked to increased cognitive function scores reported by both participants and their study partners, particularly in those with elevated Aβ levels.
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Background: Men with cerebral amyloid angiopathy (CAA) may have an earlier onset of intracerebral hemorrhage and a more hemorrhagic disease course compared to women. In this cohort study, we investigated sex differences in histopathological markers associated with amyloid-β burden and hemorrhage in cognitively impaired individuals and patients with CAA, using neuropathological data from two autopsy databases.

Methods: First, we investigated presence of parenchymal (Thal score) and vascular amyloid-β (CAA severity score) in cognitively impaired individuals from the National Alzheimer's Coordinating Center (NACC) neuropathology database.

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Associations Between Age at Menopause, Vascular Risk, and 3-Year Cognitive Change in the Canadian Longitudinal Study on Aging.

Neurology

May 2024

From the Hurvitz Brain Sciences Program (M.W.A., C.-Y.W., W.S., M.M., S.E.B., J.S.R.), Sunnybrook Research Institute; Rehabilitation Sciences Institute (M.W.A., J.S.R.), Department of Pharmacology & Toxicology (C.-Y.W., W.S.), University of Toronto, Ontario, Canada; Department of Neurology (G.T.C., R.F.B.), Massachusetts General Hospital, Harvard Medical School, Boston; Department of Psychology (T.P.), University of British Columbia, Vancouver, Canada; Center for Alzheimer Research and Treatment (CART) (R.F.B.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Melbourne School of Psychological Sciences (R.F.B.), University of Melbourne, Parkville, Victoria, Australia; Department of Neurology (P.P.), University of North Carolina at Chapel Hill School of Medicine; Division of Neurology (M.M., S.E.B., J.S.R.), Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto; Campbell Family Mental Health Research Institute (L.A.M.G.), The Centre for Addition and Mental Health; Department of Psychiatry (L.A.M.G.), Temerty Faculty of Medicine, Dalla Lana School of Public Health (G.E.), and Department of Psychology (G.E.), University of Toronto; Rotman Research Institute (G.E.), Baycrest Hospital; and Harquail Centre for Neuromodulation (J.S.R.), Sunnybrook Health Sciences Centre, University of Toronto, Ontario, Canada.

Background And Objectives: Mounting evidence supports sex differences in Alzheimer disease (AD) risk. Vascular and hormonal factors may together contribute to AD risk in female adults. We investigated whether age at menopause, vascular risk, and history of hormone therapy (HT) containing estrogens together influence cognition over a 3-year follow-up period.

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Association of Pathologic and Volumetric Biomarker Changes With Cognitive Decline in Clinically Normal Adults.

Neurology

December 2023

From the Department of Radiology (B.J.H., H.I.L.J., N.J.G., J.A.B., J.S.S., J.S., H.-S.Y., M.N., J.C.P., G.E.F., K.A.J.), Massachusetts General Hospital, the Gordon Center for Medical Imaging, Boston; Department of Neurology (B.J.H.), Cliniques Universitaires Saint-Luc, Brussels, Belgium; Faculty of Health, Medicine and Life Sciences (H.I.L.J.), School for Mental Health and Neuroscience, Alzheimer Centre Limburg, Maastricht University, the Netherlands; Department of Neurology (A.P.S., R.F.B., M.E.F., M.P., Y.T.Q., P.V., J.P.C., G.A.M., R.A., K.P., D.M.R., R.A.S., K.A.J.), Massachusetts General Hospital; Center for Alzheimer Research and Treatment (R.F.B., P.V., G.A.M., R.A., K.P., D.M.R., R.A.S., K.A.J.), Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston; Melbourne School of Psychological Sciences (R.F.B.), University of Melbourne, Australia; and Department of Psychiatry (J.G.), and Department of Biostatistics (B.C.H.), Massachusetts General Hospital, Harvard Medical School, Boston.

Article Synopsis
  • The study investigated the relationship between hippocampal volume (HV) atrophy, β-amyloid (Aβ), tau, and cognitive decline in older adults without dementia.
  • Faster HV atrophy was found to correlate with quicker cognitive decline, accounting for 10% of the variance in cognitive impairment beyond Aβ and tau measures.
  • Overall, combining data from various imaging biomarkers explained 45% of the variance in cognitive decline over a 10-year period.
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Association of β-Amyloid and Vascular Risk on Longitudinal Patterns of Brain Atrophy.

Neurology

July 2022

From the Department of Psychiatry (J.S.R.), Department of Neurology (J.P., M.S., H.-S.Y., O.H., S.H., A.P.S., R.F.B., D.R., K.A.J., R.A.S., J.P.C.), Department of Radiology (A.P.S., K.A.J., R.A.S.), Athinoula A. Martinos Center for Biomedical Imaging, and Department of Radiology (K.A.J.), Massachusetts General Hospital, Harvard Medical School, Boston; Department of Medicine (J.S.R.), Division of Neurology, Sunnybrook Health Sciences Centre, and Rehabilitation Sciences Institute (J.S.R.), University of Toronto; Harquail Centre for Neuromodulation (J.S.R.), Hurvitz Brain Sciences Program, Sunnybrook Research Institute, Toronto, Ontario, Canada; Banner Alzheimer's Institute (J.P.), Phoenix, AZ; Department of Neurology (H.-S.Y., D.R., K.A.J., R.A.S., J.P.C.), Center for Alzheimer Research and Treatment, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Florey Institute (R.F.B.), and Melbourne School of Psychological Sciences (R.F.B.), University of Melbourne, Australia; and Department of Neurology (T.H.), Icahn School of Medicine at Mount Sinai, New York, NY.

Background And Objectives: Vascular risk factors and elevated β-amyloid (Aβ) are commonly observed together among older adults. Here, we examined the interactive vs independent effects of systemic vascular risk and Aβ burden on longitudinal gray matter atrophy and how their co-occurrence may be related to cognitive decline in a cohort of clinically normal adults. A secondary goal was to examine whether vascular risk influences gray matter atrophy independently from markers of white matter injury.

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Predicting Abnormal Amyloid Burden: Can Machine Learning Become a Future Tool in Preventive Neurology?

Neurology

June 2022

From the Department of Neuroinflammation, UCL Queen Square Institute of Neurology (A.E.), and Centre for Medical Image Computing, Department of Computer Science (A.E.), University College London, UK; Department of Neurology (R.F.B.), Massachusetts General Hospital and Harvard Medical School; Center for Alzheimer Research and Treatment, Department of Neurology (R.F.B.), Brigham and Women's Hospital, Boston, MA; and Melbourne School of Psychological Science (R.F.B.), University of Melbourne, Victoria, Australia.

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Association of Emerging β-Amyloid and Tau Pathology With Early Cognitive Changes in Clinically Normal Older Adults.

Neurology

April 2022

From the Departments of Neurology (M.E.F., K.V.P., R.F.B., A.P.S., M.J.P., P.V., D.R.M., R.A.S.) and Radiology (H.I.L.J., B.J.H., K.A.J.), Massachusetts General Hospital, Harvard Medical School; Center for Alzheimer Research and Treatment (K.V.P., R.F.B., P.V., D.M.R., K.A.J., R.A.S.), Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Florey Institute of Neuroscience and Mental Health (R.F.B.); Melbourne School of Psychological Sciences (R.F.B.), University of Melbourne, Australia; Faculty of Health, Medicine and Life Sciences (H.I.L.J.), School for Mental Health and Neuroscience, Alzheimer Centre Limburg, Maastricht University, the Netherlands; and Cliniques Universitaires Saint-Luc (B.J.H.), Université Catholique de Louvain, Brussels, Belgium.

Background And Objectives: Alzheimer disease (AD) clinical trials are moving earlier in the disease process according to emerging signs of β-amyloid (Aβ) and tau pathology. If early treatment is the right time for intervention, it is critical to find the right test to optimize cognitive outcome measures for clinical trials. We sought to identify cognitive measures associated with the earliest detectable signs of emerging Aβ and tau pathology.

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Animal and human imaging research reported that the presence of cortical Alzheimer's Disease's (AD) neuropathology, beta-amyloid and neurofibrillary tau, is associated with altered neuronal activity and circuitry failure, together facilitating clinical progression. The locus coeruleus (LC), one of the initial subcortical regions harboring pretangle hyperphosphorylated tau, has widespread connections to the cortex modulating cognition. Here we investigate whether LC's in-vivo neuronal activity and functional connectivity (FC) are associated with cognitive decline in conjunction with beta-amyloid.

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Cognitive Heterogeneity in Alzheimer Clinical Trials: Harnessing Noise to Achieve Meaningfulness.

Neurology

June 2021

From the Department of Neurology (R.F.B.), Massachusetts General Hospital and Harvard Medical School; Center for Alzheimer Research and Treatment (R.F.B.), Department of Neurology, Brigham and Women's Hospital, Boston, MA; Melbourne School of Psychological Science (R.F.B.), University of Melbourne, VIC, Australia; and Department of Neurology (D.K.), Mayo Clinic, Rochester, MN.

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Comparing PET and MRI Biomarkers Predicting Cognitive Decline in Preclinical Alzheimer Disease.

Neurology

June 2021

From the Department of Radiology (D.V.M., J.A.B., H.I.L.J., J.S., J.S.S., Z.B.R., S.R.K., K.A.M., J.C.P., K.A.J., B.J.H.), Massachusetts General Hospital, Gordon Center for Medical Imaging and Athinoula A. Martinos Center for Biomedical Imaging, Boston; Faculty of Health, Medicine and Life Sciences (H.I.L.J.), School for Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, the Netherlands; Department of Neurology (R.F.B., P.V., K.V.P., D.M.R., R.A.S., K.A.J.), Massachusetts General Hospital, Harvard Medical School, Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston; The Florey Institute (R.F.B.) and Melbourne School of Psychological Science (R.F.B.), University of Melbourne, Victoria Australia; Department of Neurology (A.P.S., B.J.H.), Massachusetts General Hospital, Harvard Medical School, Boston; and Department of Neurology (B.J.H.), Cliniques Universitaires Saint-Luc, Brussels, Belgium.

Objective: To compare how structural MRI, fluorodeoxyglucose (FDG), and flortaucipir (FTP) PET signals predict cognitive decline in high-amyloid vs low-amyloid participants with the goal of determining which biomarker combination would result in the highest increase of statistical power for prevention trials.

Methods: In this prospective cohort study, we analyzed data from clinically normal adults from the Harvard Aging Brain Study with MRI, FDG, FTP, and Pittsburgh compound B (PiB)-PET acquired within a year and prospective cognitive evaluations over a mean 3-year follow-up. We focused analyses on predefined regions of interest: inferior temporal, isthmus cingulate, hippocampus, and entorhinal cortex.

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Defining the Lowest Threshold for Amyloid-PET to Predict Future Cognitive Decline and Amyloid Accumulation.

Neurology

January 2021

From the Departments of Neurology (M.E.F., S.J., A.P.S., M.J.P., D.M.R., K.V.P., R.A.B., K.A.J., R.A.S., R.F.B.) and Radiology (J.C.P., J.A.B., H.I.L.J., B.J.H., K.A.J.), Massachusetts General Hospital, Harvard Medical School; Department of Biostatistics (S.J., R.A.B.), Harvard T.H. Chan School of Public Health, Boston, MA; Division of Public Health Sciences (S.J.), Department of Surgery, Washington University School of Medicine in St. Louis, MO; Faculty of Health (H.I.L.J.), Medicine and Life Sciences, School for Mental Health and Neuroscience, Alzheimer Centre Limburg, Maastricht University, the Netherlands; Cliniques Universitaires Saint-Luc (B.J.H.), Université Catholique de Louvain, Brussels, Belgium; Center for Alzheimer Research and Treatment (D.M.R., K.V.P., R.A.S., R.F.B.), Brigham and Women's Hospital, Boston, MA; Department of Molecular Imaging & Therapy (V.L.V.), Austin Health, Melbourne, Australia; Department of Neuroscience (E.C.M.), Stanford University, Palo Alto, CA; Department of Biostatistics (R.A.B.), New York University School of Global Public Health, NY; Center for Alzheimer Research and Treatment, Brigham and Women's Hospital, Boston, MA; and Melbourne School of Psychological Sciences (R.F.B.), University of Melbourne, Australia.

Introduction: As clinical trials move toward earlier intervention, we sought to redefine the β-amyloid (Aβ)-PET threshold based on the lowest point in a baseline distribution that robustly predicts future Aβ accumulation and cognitive decline in 3 independent samples of clinically normal individuals.

Methods: Sequential Aβ cutoffs were tested to identify the lowest cutoff associated with future change in cognition (Preclinical Alzheimer Cognitive Composite [PACC]) and Aβ-PET in clinically normal participants from the Harvard Aging Brain Study (n = 342), Australian Imaging, Biomarker and Lifestyle study of aging (n = 157), and Alzheimer's Disease Neuroimaging Initiative (n = 356).

Results: Within samples, cutoffs derived from future Aβ-PET accumulation and PACC decline converged on the same inflection point, beyond which trajectories diverged from normal.

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Functional network integrity presages cognitive decline in preclinical Alzheimer disease.

Neurology

July 2017

From the Florey Institutes of Neuroscience and Mental Health (R.F.B.), Melbourne; Melbourne School of Psychological Science (R.F.B.), University of Melbourne, Australia; Department of Neurology (R.F.B., A.P.S., K.V.P., B.J.H., G.M., D.M.R., K.A.J., R.A.S., J.P.C.), Athinoula A. Martinos Center for Biomedical Imaging (A.P.S., T.H., B.J.H., J.S., K.A.J.) and Gordon Center for Medical Imaging, Division of Nuclear Medicine and Molecular Imaging (J.S., K.A.J.), Department of Radiology, Massachusetts General Hospital; Harvard Medical School (R.F.B., A.P.S., T.H., K.V.P., B.J.H., G.M., D.M.R., K.A.J., R.A.S., J.P.C.); Center for Alzheimer Research and Treatment, Department of Neurology (K.V.P., G.M., D.M.R., K.A.J., R.A.S., J.P.C.), Brigham and Women's Hospital, Boston, MA: and Department of Psychiatry (E.E.S.), University of Texas Southwestern Medical Center, Dallas.

Objective: To examine the utility of resting-state functional connectivity MRI (rs-fcMRI) measurements of network integrity as a predictor of future cognitive decline in preclinical Alzheimer disease (AD).

Methods: A total of 237 clinically normal older adults (aged 63-90 years, Clinical Dementia Rating 0) underwent baseline β-amyloid (Aβ) imaging with Pittsburgh compound B PET and structural and rs-fcMRI. We identified 7 networks for analysis, including 4 cognitive networks (default, salience, dorsal attention, and frontoparietal control) and 3 noncognitive networks (primary visual, extrastriate visual, motor).

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