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D-Serine in the aging hippocampus.

Jean-Marie Billard1

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D-serine levels decrease with age, impairing memory by affecting N-methyl-D-aspartate receptors (NMDAR). Supplementation and preventing oxidative stress can restore NMDAR function and memory in aging brains.

Keywords:
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Area of Science:

  • Neuroscience
  • Aging Research
  • Synaptic Plasticity

Background:

  • Memory formation depends on synaptic plasticity, regulated by N-methyl-D-aspartate receptors (NMDARs).
  • NMDAR function requires glutamate and the co-agonist D-serine.
  • Age-related cognitive decline is linked to impaired synaptic plasticity and memory deficits.

Purpose of the Study:

  • To review recent studies on D-serine's role in age-related changes in hippocampal plasticity and memory.
  • To investigate the mechanisms behind impaired D-serine efficacy in aging.

Main Methods:

  • Review of experimental evidence on NMDAR function, D-serine levels, and serine racemase (SR) expression in aging models.
  • Comparison of healthy aging (LOU/C rats) versus typical aging models.
  • Assessment of the effects of N-acetyl-cysteine (NAC) on oxidative stress and D-serine pathways.

Main Results:

  • Aging reduces endogenous D-serine levels due to decreased serine racemase (SR) expression, impairing NMDAR function and memory.
  • Healthy aging models (LOU/C rats) maintain SR expression and D-serine levels, without memory deficits.
  • Oxidative stress in aging appears to negatively impact the D-serine pathway; NAC treatment preserves D-serine levels and NMDAR function.

Conclusions:

  • Reduced D-serine levels and SR expression contribute to age-related memory deficits.
  • Oxidative stress is implicated in the decline of the D-serine pathway during aging.
  • Targeting the D-serine pathway and mitigating oxidative stress may offer therapeutic strategies for age-related cognitive impairment.