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

Evan Fletcher, Sylvia Villeneuve, Pauline Maillard, Danielle J Harvey, Bruce R Reed, William Jagust, Charles DeCarli

Research output: Contribution to journalArticle

13 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)173-180
Number of pages8
JournalNeurobiology of Aging
Volume40
DOIs
StatePublished - Apr 1 2016

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Keywords

  • Alzheimer's
  • Atrophy
  • Longitudinal
  • Neurodegeneration
  • Normals
  • β-amyloid

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)
  • Aging
  • Developmental Biology
  • Geriatrics and Gerontology

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