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Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury
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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Molecular Diversity Preservation International (MDPI)
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907845/ https://www.ncbi.nlm.nih.gov/pubmed/24413756 http://dx.doi.org/10.3390/ijms15010895 |
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author | Sawmiller, Darrell Li, Song Shahaduzzaman, Md Smith, Adam J. Obregon, Demian Giunta, Brian Borlongan, Cesar V. Sanberg, Paul R. Tan, Jun |
author_facet | Sawmiller, Darrell Li, Song Shahaduzzaman, Md Smith, Adam J. Obregon, Demian Giunta, Brian Borlongan, Cesar V. Sanberg, Paul R. Tan, Jun |
author_sort | Sawmiller, Darrell |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3907845 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Molecular Diversity Preservation International (MDPI) |
record_format | MEDLINE/PubMed |
spelling | pubmed-39078452014-01-31 Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury Sawmiller, Darrell Li, Song Shahaduzzaman, Md Smith, Adam J. Obregon, Demian Giunta, Brian Borlongan, Cesar V. Sanberg, Paul R. Tan, Jun Int J Mol Sci Communication 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. Molecular Diversity Preservation International (MDPI) 2014-01-09 /pmc/articles/PMC3907845/ /pubmed/24413756 http://dx.doi.org/10.3390/ijms15010895 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Communication Sawmiller, Darrell Li, Song Shahaduzzaman, Md Smith, Adam J. Obregon, Demian Giunta, Brian Borlongan, Cesar V. Sanberg, Paul R. Tan, Jun Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury |
title | Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury |
title_full | Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury |
title_fullStr | Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury |
title_full_unstemmed | Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury |
title_short | Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury |
title_sort | luteolin reduces alzheimer’s disease pathologies induced by traumatic brain injury |
topic | Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907845/ https://www.ncbi.nlm.nih.gov/pubmed/24413756 http://dx.doi.org/10.3390/ijms15010895 |
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