title: Alzheimer's-type neuropathology in the precuneus is not increased relative to other areas of neocortex across a range of cognitive impairment.
abstract: We studied Alzheimer's disease (AD) pathology in the precuneus and surrounding brain areas. Anatomically, the precuneus corresponds to the medial portion of human cerebral cortical Brodmann Area 7. This study utilized patients from the University of Kentucky Alzheimer's Disease Center autopsy cohort. Data from 47 brains were used comprising patients of differing antemortem cognitive impairment severities, each with longitudinal clinical data and extensive neuropathological data. We assessed whether the precuneus and surrounding areas are differentially vulnerable to AD-type pathological lesions (diffuse amyloid plaques, neuritic amyloid plaques, and neurofibrillary tangles). Eleven areas of brain were evaluated for each case: amygdala, hippocampal CA1, subiculum, entorhinal cortex, frontal cortex, superior and middle temporal gyri, inferior parietal lobule, occipital cortex, posterior cingulate gyrus, Brodmann Area 31, and the precuneus proper. Like other areas of neocortex, the precuneus demonstrated increased diffuse and neuritic amyloid plaques early in the evolution in AD, and increased neurofibrillary tangles late in AD. Correcting for the antemortem cognitive status of the patients, there was no evidence of an increase in the density of AD-type pathology in the precuneus or neighboring areas relative to other areas of cerebral neocortex. Our results are not consistent with the idea that the precuneus is involved in a special way with plaques or tangles relative to other areas of neocortex.
authors.affiliation: Department of Pathology and Division of Neuropathology, University of Kentucky Medical Center, Sanders-Brown Center on Aging and Alzheimer's Disease Center, University of Kentucky, Lexington, KY 40536, USA. pnels2@email.uky.edu
authors.forename: Peter T
authors.initials: PT
authors.lastname: Nelson
authors.forename: Erin L
authors.initials: EL
authors.lastname: Abner
authors.forename: Stephen W
authors.initials: SW
authors.lastname: Scheff
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Schmitt
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Kryscio
authors.forename: Gregory A
authors.initials: GA
authors.lastname: Jicha
authors.forename: Charles D
authors.initials: CD
authors.lastname: Smith
authors.forename: Ela
authors.initials: E
authors.lastname: Patel
authors.forename: William R
authors.initials: WR
authors.lastname: Markesbery
mesh_terms: D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000473:pathology* / Q000503:physiopathology; D000679:Amygdala / Q000473:pathology / Q000503:physiopathology; D001931:Brain Mapping; D003072:Cognition Disorders / Q000175:diagnosis / Q000473:pathology* / Q000503:physiopathology; D018450:Disease Progression; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D019579:Neocortex / Q000473:pathology* / Q000503:physiopathology; D009410:Nerve Degeneration / Q000473:pathology* / Q000503:physiopathology; D016874:Neurofibrillary Tangles / Q000473:pathology; D009474:Neurons / Q000473:pathology*; D010296:Parietal Lobe / Q000473:pathology* / Q000503:physiopathology; D058225:Plaque, Amyloid / Q000473:pathology