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Hypoxia-Induced Neuroinflammation in Alzheimer’s Disease: Potential Neuroprotective Effects of Centella asiatica
Alzheimer’s disease (AD) is a neurodegenerative disorder that is characterised by the presence of extracellular beta-amyloid fibrillary plaques and intraneuronal neurofibrillary tau tangles in the brain. Recurring failures of drug candidates targeting these pathways have prompted research in AD mult...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8551388/ https://www.ncbi.nlm.nih.gov/pubmed/34721056 http://dx.doi.org/10.3389/fphys.2021.712317 |
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author | Hambali, Aqilah Kumar, Jaya Hashim, Nur Fariesha Md Maniam, Sandra Mehat, Muhammad Zulfadli Cheema, Manraj Singh Mustapha, Muzaimi Adenan, Mohd Ilham Stanslas, Johnson Hamid, Hafizah Abdul |
author_facet | Hambali, Aqilah Kumar, Jaya Hashim, Nur Fariesha Md Maniam, Sandra Mehat, Muhammad Zulfadli Cheema, Manraj Singh Mustapha, Muzaimi Adenan, Mohd Ilham Stanslas, Johnson Hamid, Hafizah Abdul |
author_sort | Hambali, Aqilah |
collection | PubMed |
description | Alzheimer’s disease (AD) is a neurodegenerative disorder that is characterised by the presence of extracellular beta-amyloid fibrillary plaques and intraneuronal neurofibrillary tau tangles in the brain. Recurring failures of drug candidates targeting these pathways have prompted research in AD multifactorial pathogenesis, including the role of neuroinflammation. Triggered by various factors, such as hypoxia, neuroinflammation is strongly linked to AD susceptibility and/or progression to dementia. Chronic hypoxia induces neuroinflammation by activating microglia, the resident immune cells in the brain, along with an increased in reactive oxygen species and pro-inflammatory cytokines, features that are common to many degenerative central nervous system (CNS) disorders. Hence, interests are emerging on therapeutic agents and plant derivatives for AD that target the hypoxia-neuroinflammation pathway. Centella asiatica is one of the natural products reported to show neuroprotective effects in various models of CNS diseases. Here, we review the complex hypoxia-induced neuroinflammation in the pathogenesis of AD and the potential application of Centella asiatica as a therapeutic agent in AD or dementia. |
format | Online Article Text |
id | pubmed-8551388 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-85513882021-10-29 Hypoxia-Induced Neuroinflammation in Alzheimer’s Disease: Potential Neuroprotective Effects of Centella asiatica Hambali, Aqilah Kumar, Jaya Hashim, Nur Fariesha Md Maniam, Sandra Mehat, Muhammad Zulfadli Cheema, Manraj Singh Mustapha, Muzaimi Adenan, Mohd Ilham Stanslas, Johnson Hamid, Hafizah Abdul Front Physiol Physiology Alzheimer’s disease (AD) is a neurodegenerative disorder that is characterised by the presence of extracellular beta-amyloid fibrillary plaques and intraneuronal neurofibrillary tau tangles in the brain. Recurring failures of drug candidates targeting these pathways have prompted research in AD multifactorial pathogenesis, including the role of neuroinflammation. Triggered by various factors, such as hypoxia, neuroinflammation is strongly linked to AD susceptibility and/or progression to dementia. Chronic hypoxia induces neuroinflammation by activating microglia, the resident immune cells in the brain, along with an increased in reactive oxygen species and pro-inflammatory cytokines, features that are common to many degenerative central nervous system (CNS) disorders. Hence, interests are emerging on therapeutic agents and plant derivatives for AD that target the hypoxia-neuroinflammation pathway. Centella asiatica is one of the natural products reported to show neuroprotective effects in various models of CNS diseases. Here, we review the complex hypoxia-induced neuroinflammation in the pathogenesis of AD and the potential application of Centella asiatica as a therapeutic agent in AD or dementia. Frontiers Media S.A. 2021-10-14 /pmc/articles/PMC8551388/ /pubmed/34721056 http://dx.doi.org/10.3389/fphys.2021.712317 Text en Copyright © 2021 Hambali, Kumar, Hashim, Maniam, Mehat, Cheema, Mustapha, Adenan, Stanslas and Hamid. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Physiology Hambali, Aqilah Kumar, Jaya Hashim, Nur Fariesha Md Maniam, Sandra Mehat, Muhammad Zulfadli Cheema, Manraj Singh Mustapha, Muzaimi Adenan, Mohd Ilham Stanslas, Johnson Hamid, Hafizah Abdul Hypoxia-Induced Neuroinflammation in Alzheimer’s Disease: Potential Neuroprotective Effects of Centella asiatica |
title | Hypoxia-Induced Neuroinflammation in Alzheimer’s Disease: Potential Neuroprotective Effects of Centella asiatica |
title_full | Hypoxia-Induced Neuroinflammation in Alzheimer’s Disease: Potential Neuroprotective Effects of Centella asiatica |
title_fullStr | Hypoxia-Induced Neuroinflammation in Alzheimer’s Disease: Potential Neuroprotective Effects of Centella asiatica |
title_full_unstemmed | Hypoxia-Induced Neuroinflammation in Alzheimer’s Disease: Potential Neuroprotective Effects of Centella asiatica |
title_short | Hypoxia-Induced Neuroinflammation in Alzheimer’s Disease: Potential Neuroprotective Effects of Centella asiatica |
title_sort | hypoxia-induced neuroinflammation in alzheimer’s disease: potential neuroprotective effects of centella asiatica |
topic | Physiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8551388/ https://www.ncbi.nlm.nih.gov/pubmed/34721056 http://dx.doi.org/10.3389/fphys.2021.712317 |
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