A role for calcineurin in Alzheimer's disease

Lindsay C. Reese, Giulio Taglialatela

Research output: Contribution to journalReview article

58 Scopus citations

Abstract

Alzheimer's disease (AD) is an incurable age-related neurodegenerative disorder characterized by profound memory dysfunction. This bellwether symptom suggests involvement of the hippocampus -- a brain region responsible for memory formation -- and coincidentally an area heavily burdened by hyperphosphorylated tau and neuritic plaques of amyloid beta (Aβ). Recent evidence suggests that pre-fibrillar soluble Aβ underlies an early, progressive loss of synapses that is a hallmark of AD. One of the downstream effects of soluble Aβ aggregates is the activation of the phosphatase calcineurin (CaN). This review details the evidence of CaN hyperactivity in 'normal' aging, models of AD, and actual disease pathogenesis; elaborates on how this could manifest as memory impairment, neuroinflammation, hyperphosphorylated tau, and neuronal death.

Original languageEnglish (US)
Pages (from-to)685-692
Number of pages8
JournalCurrent Neuropharmacology
Volume9
Issue number4
StatePublished - Dec 1 2011

Keywords

  • Alzheimers
  • Amyloid beta
  • Calcineurin
  • Calcium

ASJC Scopus subject areas

  • Pharmacology
  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Pharmacology (medical)

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