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Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

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Published on: October 6, 2017

Presenilins in synaptic function and disease.

Angela Ho1, Jie Shen

  • 1Department of Biology, Boston University, 5 Cummington Street, Boston MA 02215, USA.

Trends in Molecular Medicine
|July 29, 2011
PubMed
Summary
This summary is machine-generated.

Presenilin mutations cause familial Alzheimer's disease (FAD) by disrupting synaptic function and neuronal survival. This review explores presenilin's role in synaptic plasticity, calcium regulation, and FAD pathogenesis.

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Last Updated: May 30, 2026

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Presenilin genes are associated with ~90% of early-onset familial Alzheimer's disease (FAD) mutations.
  • The precise mechanisms by which these mutations lead to FAD remain under investigation.

Purpose of the Study:

  • To review recent advances in understanding presenilin's function in synaptic processes.
  • To elucidate the role of presenilin in calcium regulation and its link to neurological disease.
  • To identify key questions for future research in FAD.

Main Methods:

  • Genetic analysis in model organisms (Drosophila and mice).
  • Review of existing literature on presenilin function and FAD.
  • Analysis of presenilin's role in synaptic function, learning, memory, and neuronal survival.

Main Results:

  • Presenilin is crucial for synaptic function, learning, memory, and neuronal survival in adult brains.
  • FAD-linked presenilin mutations impair its normal physiological functions.
  • Presenilin regulates intracellular calcium homeostasis, impacting neurotransmitter release and long-term potentiation.

Conclusions:

  • Presenilin plays a critical role in maintaining neuronal health and synaptic plasticity.
  • Dysregulation of presenilin function, particularly calcium homeostasis, is implicated in FAD.
  • Further research is needed to fully understand presenilin's complex role in Alzheimer's disease pathogenesis.