3 results match your criteria: "Broad Institute (P.L.D.)[Affiliation]"
Neurology
June 2018
From Rush Alzheimer's Disease Center (S.O., A.S.B., L.Y., J.F., C.G., J.A.S., D.A.B.) and Departments of Neurological Sciences (A.S.B., L.Y., J.A.S., D.A.B.) and Pathology (J.F., J.A.S.), Rush University Medical Center, Chicago, IL; Shariati Hospital (S.O.), Tehran University of Medical Sciences, Iran; Department of Geriatrics (J.F.), University of Sao Paulo Medical School, Brazil; University Hospital (V.H.), University of Western Ontario, London, Canada; Broad Institute (P.L.D.J.), Cambridge, MA; Center for Translational & Systems Neuroimmunology (P.L.D.J.), Department of Neurology, Columbia University Medical Center, New York, NY.
Objective: To examine the association of the ε2ε4 genotype with incident Alzheimer disease (AD), mild cognitive impairment (MCI), cognitive decline, and AD pathology in older adults.
Methods: We used data from 2,151 older adults of European ancestry who were free of dementia at baseline and underwent structured annual clinical evaluation in a longitudinal study for incident AD and MCI, and cognitive decline. Postmortem examination in decedents documented pathologic AD and quantified β-amyloid and neurofibrillary tangles.
Neurology
February 2016
From the Rush Alzheimer's Disease Center (A.S.B., L.Y., P.A.B., J.A.S., D.A.B.), Neurological Science (A.S.B., L.Y., J.A.S., D.A.B.), Behavioral Sciences (P.A.B.), Pathology (Neuropathology) (J.A.S.), Rush University Medical Center, Chicago, IL; Program in Translational NeuroPsychiatric Genomics (P.L.D.), Institute for the Neurosciences, Departments of Neurology and Psychiatry, Brigham and Women's Hospital, Boston; Harvard Medical School (P.L.D.), Boston; and Program in Medical and Population Genetics, Broad Institute (P.L.D.), Cambridge, MA.
Objectives: We tested whether brain-derived neurotrophic factor (BDNF) gene expression levels are associated with cognitive decline in older adults.
Methods: Five hundred thirty-five older participants underwent annual cognitive assessments and brain autopsy at death. BDNF gene expression was measured in the dorsolateral prefrontal cortex.
Neurology
March 2015
From the Rush Alzheimer's Disease Center (L.Y., J.Y., D.A.B., J.A.S.), the Department of Neurological Sciences (L.Y., J.Y., D.A.B., J.A.S.), and the Department of Pathology (J.A.S.), Rush University Medical Center, Chicago, IL; Program in Translational NeuroPsychiatric Genomics (P.L.D.), Institute for the Neurosciences, Departments of Neurology and Psychiatry, Brigham and Women's Hospital, Boston; Harvard Medical School (P.L.D.), Boston; Program in Medical and Population Genetics, Broad Institute (P.L.D.), Cambridge, MA; and the Department of Pathology and Laboratory Medicine (J.Q.T.), Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania, Philadelphia.
Objective: To determine the independent association of the TMEM106B variants with transactive response DNA binding protein 43 (TDP-43) pathology in older persons without frontotemporal lobar degeneration (FTLD) and to explore functional pathways that link the risk variants to the pathology, including a GRN mRNA pathway.
Methods: Data came from 544 autopsied participants without FTLD in 2 community-based studies of aging. Participants underwent uniform neuropathologic evaluations, including TDP-43 cytoplasmic inclusions.