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

Kimmo Hatanpää, Krystyna R. Isaacs, Tomoaki Shirao, Daniel R. Brady, Stanley I. Rapoport

Research output: Contribution to journalArticle

148 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)637-643
Number of pages7
JournalJournal of neuropathology and experimental neurology
Issue number6
StatePublished - Jun 1999



  • Cytochrome oxidase
  • Drebrin
  • Energy metabolism
  • GAP-43
  • Neuron specific-enolase
  • Synaptophysin
  • β-tubulin

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

Cite this