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Communication

Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury

by
Darrell Sawmiller
1,2,*,
Song Li
2,3,
Md Shahaduzzaman
4,
Adam J. Smith
4,
Demian Obregon
1,2,
Brian Giunta
2,
Cesar V. Borlongan
4,
Paul R. Sanberg
4 and
Jun Tan
1,2
1
James A. Haley Veteran's Administration Hospital, Tampa, FL 33612, USA
2
Department of Psychiatry, Morsani College of Medicine, University of South Florida, Tampa, FL 33613, USA
3
Department of Biophysics, School of Physics and Optoelectronic Technology, Dalian University of Technology, Dalian 116024, China
4
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
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2014, 15(1), 895-904; https://doi.org/10.3390/ijms15010895
Submission received: 29 October 2013 / Revised: 3 January 2014 / Accepted: 6 January 2014 / Published: 9 January 2014
(This article belongs to the Special Issue Pathology and Treatment of Central Nervous System Diseases)
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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.
Keywords: traumatic brain injury; Alzheimer’s disease; amyloidogenesis; tauopathy; GSK; neuroinflammation; luteolin traumatic brain injury; Alzheimer’s disease; amyloidogenesis; tauopathy; GSK; neuroinflammation; luteolin

Share and Cite

MDPI and ACS Style

Sawmiller, D.; Li, S.; Shahaduzzaman, M.; Smith, A.J.; Obregon, D.; Giunta, B.; Borlongan, C.V.; Sanberg, P.R.; Tan, J. Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury. Int. J. Mol. Sci. 2014, 15, 895-904. https://doi.org/10.3390/ijms15010895

AMA Style

Sawmiller D, Li S, Shahaduzzaman M, Smith AJ, Obregon D, Giunta B, Borlongan CV, Sanberg PR, Tan J. Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury. International Journal of Molecular Sciences. 2014; 15(1):895-904. https://doi.org/10.3390/ijms15010895

Chicago/Turabian Style

Sawmiller, Darrell, Song Li, Md Shahaduzzaman, Adam J. Smith, Demian Obregon, Brian Giunta, Cesar V. Borlongan, Paul R. Sanberg, and Jun Tan. 2014. "Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury" International Journal of Molecular Sciences 15, no. 1: 895-904. https://doi.org/10.3390/ijms15010895

APA Style

Sawmiller, D., Li, S., Shahaduzzaman, M., Smith, A. J., Obregon, D., Giunta, B., Borlongan, C. V., Sanberg, P. R., & Tan, J. (2014). Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury. International Journal of Molecular Sciences, 15(1), 895-904. https://doi.org/10.3390/ijms15010895

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