β-amyloid, hippocampal atrophy and their relation to longitudinal brain change in cognitively normal individuals.

Titleβ-amyloid, hippocampal atrophy and their relation to longitudinal brain change in cognitively normal individuals.
Publication TypeJournal Article
Year of Publication2016
AuthorsFletcher E, Villeneuve S, Maillard P, Harvey D, Reed B, Jagust W, DeCarli C
JournalNeurobiol Aging
Volume40
Pagination173-80
Date Published2016 Apr
ISSN1558-1497
KeywordsAged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Atrophy, Cerebral Amyloid Angiopathy, Cognition, Cohort Studies, Female, Hippocampus, Humans, Magnetic Resonance Imaging, Male, Regression Analysis
Abstract

Recent literature has examined baseline hippocampal volume and extent of brain amyloidosis to test potential synergistic effects on worsening cognition and extent of brain atrophy. Use of hippocampal volume in prior studies was based on the notion that limbic circuit degeneration is an early manifestation of the Alzheimer's Disease (AD) pathophysiology. To clarify these interactions early in the AD process, we tested the effects of amyloid and baseline normalized hippocampal volume on longitudinal brain atrophy rates in a group of cognitively normal individuals. Results showed that the combination of elevated β-amyloid and baseline hippocampal atrophy is associated with increased rates specific to the limbic circuit and splenium. Importantly, this atrophy pattern emerged from a voxelwise analysis, corroborated by regression models over region of interests in native space. The results are broadly consistent with previous studies of the effects of amyloid and baseline hippocampal atrophy in normals, while pointing to accelerated atrophy of AD-vulnerable regions detectable at the preclinical stage.

DOI10.1016/j.neurobiolaging.2016.01.133
Alternate JournalNeurobiol. Aging
PubMed ID26973117
PubMed Central IDPMC4792128
Grant ListR01 AG042292 / AG / NIA NIH HHS / United States
R01 AG047827 / AG / NIA NIH HHS / United States
R01 AG021028 / AG / NIA NIH HHS / United States
P30 AG010129 / AG / NIA NIH HHS / United States
P30 AG10129 / AG / NIA NIH HHS / United States