Subfield-specific increase in brain growth protein in postmortem hippocampus of Alzheimer's patients

J. L. Rekart, B. Quinn, M. M. Mesulam, Aryeh Routtenberg*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

36 Scopus citations

Abstract

The neuropathology of Alzheimer's disease (AD) reflects a precarious balance between neurodegenerative phenomena and reactive events of neuroplasticity. This latter aspect of AD neuropathology has received less attention than it deserves and its contribution to memory loss is therefore not well understood. To monitor neuroplastic-related events we studied the distribution of the plasticity-associated, brain growth protein GAP-43 in AD subjects and age-matched controls. In tissue from AD patients, we observed a consistent elevation of GAP-43 in a subfield of the hippocampus, stratum lacunosum moleculare. This subfield contains inputs from multiple brain regions and is known to regulate declarative memory function. Levels of potentially aberrant sprouting, as marked by elevated growth protein, were positively correlated with the severity of AD suggesting that increased expression of GAP-43 leads to a miswiring of circuits critical for memory function. Our findings suggest a mechanism, aberrant neuroplasticity, that in concert with neurodegeneration may importantly contribute to the memory loss in AD.

Original languageEnglish (US)
Pages (from-to)579-584
Number of pages6
JournalNeuroscience
Volume126
Issue number3
DOIs
StatePublished - Jun 23 2004

Keywords

  • 43 kDa
  • AChE
  • AD
  • Alzheimer's disease
  • CA1
  • GAP-43
  • GAP-43: growth-associated protein
  • IR
  • OML
  • SLM
  • SR
  • acetylcholinesterase
  • cornu ammonis 1
  • immunoreactivity
  • memory
  • outer molecular layer
  • reactive synaptogenesis
  • stratum lacunosum moleculare
  • stratum radiatum

ASJC Scopus subject areas

  • Neuroscience(all)

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