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The synapse in traumatic brain injury.

Aimun A B Jamjoom1, Jonathan Rhodes2, Peter J D Andrews2

  • 1Centre for Clinical Brain Sciences, Chancellor's Building, Edinburgh BioQuarter, University of Edinburgh, Edinburgh EH16 4SB, UK.

Brain : a Journal of Neurology
|November 13, 2020
PubMed
Summary

Traumatic brain injury (TBI) significantly impacts synapse structure and function, leading to synapse loss. Understanding these synaptic changes is crucial for developing new treatments for TBI and related dementia.

Keywords:
astrocyteinflammationmicrogliasynaptomesynaptopathy

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Area of Science:

  • Neuroscience
  • Pathophysiology
  • Traumatic Brain Injury Research

Background:

  • Traumatic brain injury (TBI) is a major global health concern, linked to long-term disability and dementia.
  • Traditional TBI research focused on neuronal damage, but recent findings emphasize synaptic alterations.
  • Synapse loss following TBI results from immediate mechanical injury and secondary injury processes.

Purpose of the Study:

  • To review the critical role of synapses in TBI pathophysiology.
  • To explore the interplay of secondary injury processes like excitotoxicity, inflammation, and oxidative stress at the synapse.
  • To examine the impact of traumatic axonal injury and tau spread on synapses.

Main Methods:

  • Review of current literature on TBI, synaptic function, and secondary injury mechanisms.
  • Analysis of the role of astrocytes in synapse loss and recovery after TBI.
  • Discussion of emerging technologies including synapse molecular imaging, fluid biomarkers, and therapeutics.

Main Results:

  • TBI initiates secondary injury cascades (excitotoxicity, inflammation, oxidative stress) that converge at the synapse, causing loss.
  • Traumatic axonal injury affects synapses and may contribute to tau pathology spread.
  • Astrocytes are key mediators of both synapse loss and potential recovery.

Conclusions:

  • Synaptic dysfunction is central to TBI pathophysiology, driven by multiple interacting secondary injury processes.
  • Emerging technologies like synaptome mapping offer promise for identifying TBI-vulnerable or resistant synapses.
  • Targeting synaptic mechanisms and astrocyte roles presents potential therapeutic avenues for TBI and dementia prevention.