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Updated: Jan 15, 2026

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Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury
Published on: January 20, 2023
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Synaptic Pathology in Traumatic Brain Injury and Therapeutic Insights.
Poojith Nuthalapati1,2, Sophie E Holmes1,3, Hamada H Altalib1,2,3
1Department of Neurology, Yale School of Medicine, New Haven, CT 06510, USA.
International Journal of Molecular Sciences
|October 16, 2025
Summary
Traumatic brain injury (TBI) causes progressive synaptic dysfunction across acute, subacute, and chronic phases. Understanding these stages is key to developing targeted therapies for neurological deficits.
Area of Science:
- Neuroscience
- Neuropathology
- Trauma Research
Background:
- Traumatic brain injury (TBI) initiates a complex cascade of neuropathological events.
- Synaptic integrity is significantly disrupted post-TBI, leading to neurological sequelae.
Purpose of the Study:
- To review the distinct phases of synaptic dysfunction and loss following TBI.
- To elucidate the contribution of synaptic alterations to neurological deficits.
Main Methods:
- Review of literature on TBI-induced neuropathology.
- Analysis of synaptic changes during acute, subacute, and chronic phases post-TBI.
Main Results:
- Acute phase: Excitotoxicity, dendritic spine loss, mitochondrial dysfunction.
- Subacute phase: Continued excitotoxicity, neuroinflammation, autophagy.
- Chronic phase: Reduced synaptic density, structural remodeling, cognitive/mood deficits, epilepsy.
Conclusions:
- Synaptic dysfunction progresses through distinct phases post-TBI.
- Targeted interventions addressing phase-specific mechanisms are crucial.
- Future therapies should focus on synaptic repair and neurotransmitter modulation.
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