ArticleBrain communications2026
Pontine pathology mediates common symptoms of blast-induced chronic mild traumatic brain injury.
Article in Brain communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Primary Blast-Induced Traumatic Brain Injury as a Risk Factor for (Cerebro)vascular Disorder: Clinical Manifestations, Blast Physics, Biomechanics, Pathobiology, and Critical Gaps.International journal of molecular sciences · 2026Review
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Authors and funding
25 authors.
Funding
Abstract
Diffuse mild traumatic brain injury (mTBI) often leads to persistent post-concussive symptoms (PCS) such as fragmented sleep, yet the brain loci and cellular mechanisms that link injury to disability remain obscure. We tested the hypothesis that repeated blast-induced mTBI provokes a chronic myelinopathy with accompanied microglial response in the pontine reticular formation, a brainstem region that modulates arousal and sleep, and that this pathology statistically mediates persistent PCS burden. Using spatially resolved single cell phenotyping in a mouse model of blast-mTBI, we found that only repeated mTBI established persistent activation of disease-associated microglia and phagocytosis of myelin in the pontine reticular formation. Parallel studies in veterans with repeated blast-mTBI revealed identical microglial nodules on neuropathological exam up to two decades after documented blast injury, while diffusion tensor imaging confirmed a dose-dependent pontine myelin disruption that statistically mediated sleep disturbance and broad PCS. Together, these data identify pontine white matter pathology as both a biomarker and mechanistic driver of chronic PCS after repeated diffuse mTBI, highlighting brainstem microglia and oligodendrocytes as rational therapeutic targets.
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