Aging-Related Calcium Dysregulation in Rat Entorhinal Neurons Homologous with the Human Entorhinal Neurons in which Alzheimer's Disease Neurofibrillary Tangles First Appear

John C. Gant, Inga Kadish, Kuey Chu Chen, Olivier Thibault, Eric M. Blalock, Nada M. Porter, Philip W. Landfield

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Aging is the leading risk factor for idiopathic Alzheimer's disease (AD), indicating that normal aging processes promote AD and likely are present in the neurons in which AD pathogenesis originates. In AD, neurofibrillary tangles (NFTs) appear first in entorhinal cortex, implying that aging processes in entorhinal neurons promote NFT pathogenesis. Using electrophysiology and immunohistochemistry, we find pronounced aging-related Ca 2 + dysregulation in rat entorhinal neurons homologous with the human neurons in which NFTs originate. Considering that humans recapitulate many aspects of animal brain aging, these results support the hypothesis that aging-related Ca 2 + dysregulation occurs in human entorhinal neurons and promotes NFT pathogenesis.

Original languageEnglish
Pages (from-to)1371-1378
Number of pages8
JournalJournal of Alzheimer's Disease
Volume66
Issue number4
DOIs
StatePublished - 2018

Bibliographical note

Funding Information:
This work was supported by NIH grants AG004542, AG052050, and AG037868.

Publisher Copyright:
© 2018 - IOS Press and the authors. All rights reserved.

Keywords

  • Afterhyperpolarization
  • FKBP
  • aging models
  • calcium-dependent
  • cytoskeleton
  • hippocampus
  • neurofibrillary progression
  • ryanodine receptor

ASJC Scopus subject areas

  • Neuroscience (all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

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