Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 15, Issue 1, Pages 895-904Publisher
MDPI
DOI: 10.3390/ijms15010895
Keywords
traumatic brain injury; tauopathy; neuroinflammation; luteolin; amyloidogenesis; GSK; Alzheimer's disease
Funding
- Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development, Medical Research Service - DoD TATRC [W81XWH-11-1-0634]
- Veterans Affairs [I01BX001143] Funding Source: NIH RePORTER
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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 (A beta) 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 A beta 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.
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