Mechanisms of neuronal death in brain aging and alzheimer's disease: Role of endocrine‐mediated calcium dyshomeostasis

Philip W. Landfield, Olivier Thibault, Mary L. Mazzanti, Nada M. Porter, D. Steven Kerr

Research output: Contribution to journalArticlepeer-review

111 Scopus citations

Abstract

This paper reviews evidence that brain aging and Alzheimer's disease (AD) are somehow closely related and that the hippocampus (CA1) is highly vulnerable to cell loss under both conditions. In addition, two current lines of evidence on the mechanisms of hippocampal cell loss with aging are considered, including studies of neuronal calcium dysregulation and studies of cumulative glucocorticoid (GC) neurotoxicity. Moreover, recent electro‐physiological studies have shown that excess glucocorticoid activation of hippocampal neurons increases the influx of calcium through voltage‐activated calcium channels. Second messenger systems may mediate the steroid modulation of calcium channels. Therefore, it is hypothesized that excess glucocorticoid activation and neuronal calcium dysregulation may be two phases of a single process that increases the susceptibility of neurons to neurodegeneration during aging and Alzheimer's disease. © 1992 John Wiley & Sons, Inc.

Original languageEnglish
Pages (from-to)1247-1260
Number of pages14
JournalJournal of Neurobiology
Volume23
Issue number9
DOIs
StatePublished - Nov 1992

Keywords

  • Alzheimer's Disease
  • brain aging
  • calcium currents
  • calcium potentials
  • calcium regulation
  • glucocorticoids
  • hippocampus
  • neuron death

ASJC Scopus subject areas

  • General Neuroscience
  • Cellular and Molecular Neuroscience

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