Prominent hippocampal CA3 gene expression profile in neurocognitive aging

Rebecca P. Haberman, Carlo Colantuoni, Amy M. Stocker, Alexandra C. Schmidt, Jan T. Pedersen, Michela Gallagher

Research output: Contribution to journalArticle

Abstract

Research in aging laboratory animals has characterized physiological and cellular alterations in medial temporal lobe structures, particularly the hippocampus, that are central to age-related memory deficits. The current study compares molecular alterations across hippocampal subregions in a rat model that closely mirrors individual differences in neurocognitive features of aging humans, including both impaired memory and preserved function. Using mRNA profiling of the CA1, CA3 and dentate gyrus subregions, we have distinguished between genes and pathways related to chronological age and those associated with impaired or preserved cognitive outcomes in healthy aged Long-Evans rats. The CA3 profile exhibited the most prominent gene expression differences related to cognitive status and of the three subregions, best distinguished preserved from impaired function among the aged animals. Within this profile differential expression of synaptic plasticity and neurodegenerative disease-related genes suggests recruitment of adaptive mechanisms to maintain function and structural integrity in aged unimpaired rats that does not occur in aged impaired animals.

Original languageEnglish (US)
Pages (from-to)1678-1692
Number of pages15
JournalNeurobiology of Aging
Volume32
Issue number9
DOIs
StatePublished - Sep 1 2011

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Keywords

  • Hippocampus
  • Preserved cognition
  • Spatial memory
  • Synaptic plasticity

ASJC Scopus subject areas

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

Cite this

Haberman, R. P., Colantuoni, C., Stocker, A. M., Schmidt, A. C., Pedersen, J. T., & Gallagher, M. (2011). Prominent hippocampal CA3 gene expression profile in neurocognitive aging. Neurobiology of Aging, 32(9), 1678-1692. https://doi.org/10.1016/j.neurobiolaging.2009.10.005