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Quantitative synaptic alterations in the human neocortex during normal aging

E Masliah1, M Mallory, L Hansen

  • 1Department of Neurosciences, University of California, San Diego, La Jolla 92093-0624.

Neurology
|January 1, 1993
PubMed
Summary
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Synaptic density in the frontal cortex decreases with age, independent of beta-amyloid plaques. Older adults show a 20% reduction in presynaptic terminals, suggesting age-related synapse loss contributes to Alzheimer's disease pathology.

Area of Science:

  • Neuroscience
  • Aging Research
  • Neuropathology

Background:

  • Synaptic loss is a hallmark of Alzheimer's disease (AD).
  • The relationship between normal aging, synaptic density, and amyloid deposition is not fully understood.

Purpose of the Study:

  • To investigate the correlation between aging, synaptic population density, and beta-amyloid plaques in the human frontal cortex.
  • To determine if age-related synaptic loss is associated with amyloid deposition in non-demented individuals.

Main Methods:

  • Quantification of synaptic population density using double-immunolabeling for beta/A4 amyloid and synaptophysin.
  • Analysis of frontal cortex sections from 25 individuals aged 16-98 without dementia.
  • Microscopic examination of synaptic changes in relation to amyloid plaques.

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Main Results:

  • A significant inverse correlation was found between presynaptic terminal (PT) counts and age (r = -0.7, p < 0.001).
  • Individuals over 60 years old exhibited a 20% average decrease in PT density compared to younger individuals.
  • No significant correlation was observed between age and amyloid plaque number, or between synaptic density and amyloid plaque number.

Conclusions:

  • Age-dependent synaptic loss occurs in the neocortex, potentially contributing to AD.
  • This age-related synaptic loss appears largely independent of beta-amyloid deposition.
  • Focal synapse loss and altered bouton morphology were observed in mature plaques in aged individuals.