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Nemil Bhatt1, Nicha Puangmalai2, Cynthia Jerez2

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Repetitive mild traumatic brain injuries (TBI) can spread toxic tau protein aggregates, causing cognitive deficits and neuroinflammation. This study reveals how TBI-derived tau polymorphs initiate and propagate tau pathology, linking TBI to neurodegenerative diseases.

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Area of Science:

  • Neuroscience
  • Pathology
  • Traumatic Brain Injury Research

Background:

  • Tau protein misfolding and aggregation into neurofibrillary tangles are hallmarks of tauopathies.
  • Traumatic brain injury (TBI) is a risk factor for tauopathy onset and progression.
  • Mechanisms of TBI-derived tau polymorph dissemination are not well understood.

Purpose of the Study:

  • To investigate if TBI-derived tau polymorphs can initiate pathological tau formation.
  • To determine if different TBI types lead to distinct tau pathogenic trajectories.
  • To elucidate the role of neuroinflammation in TBI-induced tauopathy.

Main Methods:

  • Wild-type mice were injected with TBI-derived tau polymorphs from sham, single-blast (SB), or repeated-blast (RB) conditions.
  • Cognitive and motor functions were assessed using behavioral assays at 2 and 8 months post-injection.
  • Tau aggregation, glial activation, inflammasome formation, and TBI biomarkers were analyzed.

Main Results:

  • Repeated-blast TBI-derived tau polymorphs (RB-BDTPs) induced significant cognitive and motor deficits.
  • RB-BDTPs promoted toxic tau aggregate formation in the hippocampus, which spread to cortical layers over time.
  • RB-BDTP exposure increased glial activation, NLRP3 inflammasome formation, and S100B aggregation, indicating neuroinflammation.

Conclusions:

  • TBI-BDTPs can initiate and propagate tau pathology, contributing to tauopathies.
  • Neuroinflammation, including glial activation and inflammasome formation, is closely linked to TBI-induced tau pathology.
  • This study enhances understanding of the interplay between TBI, tauopathy, and neuroinflammation.