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Loss of proteins regulating synaptic plasticity in normal aging of the human brain and in Alzheimer disease.

Abstract
Recent studies suggest that the cognitive impairment associated with normal aging is due to neuronal dysfunction rather than to loss of neurons or synapses. To characterize this dysfunction, molecular indices of neuronal function were quantified in autopsy samples of cerebral cortex. During normal aging, the most dramatic decline was found in levels of synaptic proteins involved in structural plasticity (remodeling) of axons and dendrites. Alzheimer disease, the most common cause of dementia in the elderly, was associated with an additional 81% decrease in levels of drebrin, a protein regulating postsynaptic plasticity. Disturbed mechanisms of plasticity may contribute to cognitive dysfunction during aging and in Alzheimer disease.
AuthorsK Hatanpää, K R Isaacs, T Shirao, D R Brady, S I Rapoport
JournalJournal of neuropathology and experimental neurology (J Neuropathol Exp Neurol) Vol. 58 Issue 6 Pg. 637-43 (Jun 1999) ISSN: 0022-3069 [Print] England
PMID10374754 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Nerve Tissue Proteins
Topics
  • Aged
  • Aged, 80 and over
  • Aging (metabolism)
  • Alzheimer Disease (metabolism)
  • Humans
  • Immunoblotting
  • Immunohistochemistry
  • Nerve Tissue Proteins (metabolism)
  • Neuronal Plasticity (physiology)
  • Synapses (physiology)

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