International Journal of Molecular Sciences | |
Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury | |
Darrell Sawmiller1  Song Li3  Md Shahaduzzaman2  Adam J. Smith2  Demian Obregon1  Brian Giunta3  Cesar V. Borlongan2  Paul R. Sanberg2  | |
[1] James A. Haley Veteran’s Administration Hospital, Tampa, FL 33612, USA;Center of Excellence for Aging and Brain Repair, Department of Neurosurgery and Brain Repair, Morsani College of Medicine, University of South Florida, Tampa, FL 33613, USA; E-Mails:;Department of Psychiatry, Morsani College of Medicine, University of South Florida, Tampa, FL 33613, USA; E-Mails: | |
关键词: traumatic brain injury; Alzheimer’s disease; amyloidogenesis; tauopathy; GSK; neuroinflammation; luteolin; | |
DOI : 10.3390/ijms15010895 | |
来源: mdpi | |
【 摘 要 】
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.
【 授权许可】
CC BY
© 2014 by the authors; licensee MDPI, Basel, Switzerland
【 预 览 】
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