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Related Experiment Video

Updated: Sep 15, 2025

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Increased Synapse Elimination by Inflammatory Cells Contributes to Long-lasting Post-Stroke Memory Dysfunction in Old

Zahra Shabani1,2, Peipei Pan1,2, Qifeng Li1,2

  • 1Center for Cerebrovascular Research, University of California, San Francisco.

Biorxiv : the Preprint Server for Biology
|July 15, 2025
PubMed
Summary

Older mice experience long-term memory loss after stroke due to increased synapse removal by inflammatory cells, particularly astrocytes. Activating alpha7-nicotinic acetylcholine receptors (nAchRs) may mitigate this memory deficit.

Keywords:
AgingMemory dysfunctionNeuroinflammationStrokeSynapse elimination

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Area of Science:

  • Neuroscience
  • Immunology
  • Gerontology

Background:

  • Post-stroke memory dysfunction is more prevalent in older individuals.
  • Brain astrocytes and microglia contribute to synapse removal during stroke, impacting neurobehavioral outcomes.

Purpose of the Study:

  • To investigate the association between memory dysfunction in aged mice and increased synapse removal by inflammatory cells post-stroke.
  • To evaluate the therapeutic potential of activating alpha7-nicotinic acetylcholine receptors (nAchRs) in mitigating stroke-induced memory deficits.

Main Methods:

  • Ischemic stroke was induced in young and old mice.
  • Memory function was assessed using Y-maze and novel object recognition (NOR) tests.
  • Synapse removal, neuroinflammation, and neuronal changes were analyzed; alpha7-nAchR activation was tested in a separate cohort.

Main Results:

  • Old mice exhibited significant long-term memory dysfunction, larger infarct volumes, and heightened neuroinflammation compared to young mice.
  • Increased synapse engulfment by microglia/macrophages and astrocytes was observed in old mice, with astrocytes playing a more prominent role.
  • Activation of alpha7-nAchRs reduced synapse removal by inflammatory cells in the hippocampus.

Conclusions:

  • Increased synapse removal by inflammatory cells, especially astrocytes, contributes to long-lasting memory deficits in aged mice post-stroke.
  • Targeting neuroinflammation via alpha7-nAchR activation shows promise for reducing synapse loss and improving memory function after stroke.