
David S. Knopman
Articles
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3 weeks ago |
nature.com | Christopher Schwarz |Matthew L. Senjem |Prashanthi Vemuri |Leah Forsberg |David Jones |Hugo Botha | +7 more
AbstractDementia with Lewy bodies (DLB) frequently coexists with Alzheimer’s disease pathology, yet the pattern of cortical microstructural injury and its relationship with amyloid, tau, and cerebrovascular pathologies remains unclear.
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1 month ago |
nature.com | Cyril Pottier |Fahri Küçükali |Matt Baker |Gregory Jenkins |Cristina T. Vicente |Wouter De Coster | +55 more
AbstractFrontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) is a fatal neurodegenerative disorder with only a limited number of risk loci identified.
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Jan 16, 2025 |
nature.com | Farwa Ali |Michelle M. Mielke |Clifford R. Jack |David S. Knopman |Prashanthi Vemuri |Ronald Petersen | +1 more
AbstractDeclining gait performance is seen in aging individuals, due to neural and systemic factors. Plasma biomarkers provide an accessible way to assess evolving brain changes; non-specific neurodegeneration (NfL, GFAP) or evolving Alzheimer’s disease (Aβ 42/40 ratio, P-Tau181). In a population-based cohort of older adults, we evaluate the hypothesis that plasma biomarkers of neurodegeneration and Alzheimer’s Disease pathology are associated with worse gait performance.
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Jan 13, 2025 |
nature.com | Michael Fang |David S. Knopman |Keenan A. Walker |Rebecca Gottesman |Elizabeth Selvin
AbstractUnderstanding the lifetime risk of dementia can inform public health planning and improve patient engagement in prevention. Using data from a community-based, prospective cohort study (n = 15,043; 26.9% Black race, 55.1% women and 30.8% with at least one apolipoprotein E4 (APOE ε4) allele), we estimated the lifetime risk of dementia (from age 55 years to 95 years), with mortality treated as a competing event.
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Jan 8, 2025 |
alz-journals.onlinelibrary.wiley.com | Gil D. Rabinovici |Biomedical Imaging |David S. Knopman |Javier Arbizu
1 INTRODUCTION AND SCOPE Alzheimer's disease (AD) is defined neuropathologically by the deposition of extracellular plaques composed of aggregated forms of the amyloid-beta (Aβ) polypeptide and intraneuronal neurofibrillary tangles (NFTs) composed of aggregated hyperphosphorylated tau protein.1, 2 In the past 20 years, positron emission tomography (PET) radiotracers have been developed to image amyloid plaques and tau tangles in vivo.3-9 Currently, three fluorine-18-labeled amyloid...
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