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• W2141102146 abstract "Traumatic brain injury (TBI) occurs in response to an acute insult to the head and is recognized as a major risk factor for Alzheimer's disease (AD). Indeed, recent studies have suggested a pathological overlap between TBI and AD, with both conditions exhibiting amyloid-beta (Aβ) deposits, tauopathy, and neuroinflammation. Additional studies involving animal models of AD indicate that some AD-related genotypic determinants may be critical factors enhancing temporal and phenotypic symptoms of TBI. Thus in the present study, we examined sub-acute effects of moderate TBI delivered by a gas-driven shock tube device in Aβ depositing Tg2576 mice. Three days later, significant increases in b-amyloid deposition, glycogen synthase-3 (GSK-3) activation, phospho-tau, and pro-inflammatory cytokines were observed. Importantly, peripheral treatment with the naturally occurring flavonoid, luteolin, significantly abolished these accelerated pathologies. This study lays the groundwork for a safe and natural compound that could prevent or treat TBI with minimal or no deleterious side effects in combat personnel and others at risk or who have experienced TBI." @default.
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• W2141102146 date "2014-01-09" @default.
• W2141102146 modified "2023-10-14" @default.
• W2141102146 title "Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury" @default.
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• W2141102146 doi "https://doi.org/10.3390/ijms15010895" @default.
• W2141102146 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3907845" @default.
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