Neuroinflammation Interactions with Mitochondria: Implications for Alzheimer’s Disease

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Vic Shao-Chih Chiang
Vic Shao-Chih Chiang

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GJMR Volume 21 Issue A3

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Neuroinflammation Interactions with Mitochondria: Implications for Alzheimer’s Disease Banner

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The objective of our study was to evaluate, in a population of Togolese People Living With HIV(PLWHIV), the agreement between three scores derived from the general population namely the Framingham score, the Systematic Coronary Risk Evaluation (SCORE), the evaluation of the cardiovascular risk (CVR) according to the World Health Organization.
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The mitochondria are the powerhouses of the body, which is paramount for the central nervous system given their high energy expenditure. This high dependence on the mitochondria renders mitochondrial dysfunctions to impair the central nervous system, as seen in neurodegenerative diseases. This article concentrates on the neurodgenerative disease, Alzheimer’s disease and the well-established neuroinflammation pathophysiology, from a mitochondrial perspective. I first focused on the energy production functions of the mitochondria, and the mitochondrial DNA, imperative for mitochondrial function. For instance in their aberrations in Alzheimer’s disease, and in vitro experiments with inflammatory markers that drove damages to the mitochondria DNA. Subsequently, I discussed about mitochondrial biogenesis using expression studies with correlated changes in Alzheimer’s disease and stem cells whereby mitochondria are critical regulators of their fate, pertinent to Alzheimer’s disease. Finally, I accentuated on emerging technologies that enable disentangling the abstruse nature of mitochondria, and some uprising areas of mitochondria research deserving attention from the lens of Alzheimer’s disease. Overall, there is a plausible link between Alzheimer’s disease, neuroinflammation, and mitochondrial mechanisms, but current studies are limited to causally address this question. I presented several improvements and strategies that could be taken to advance the understanding of this relationship in future studies.

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No external funding was declared for this work.

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The authors declare no conflict of interest.

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No ethics committee approval was required for this article type.

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Vic Shao-Chih Chiang. 2021. \u201cNeuroinflammation Interactions with Mitochondria: Implications for Alzheimer’s Disease\u201d. Global Journal of Medical Research - A: Neurology & Nervous System GJMR-A Volume 21 (GJMR Volume 21 Issue A3): .

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Correlating neuroinflammation with mitochondrial functions in Alzheimer’s research.
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Crossref Journal DOI 10.17406/gjmra

Print ISSN 0975-5888

e-ISSN 2249-4618

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GJMR-A Classification: NLMC Code: WW 400
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v1.2

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July 31, 2021

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English

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The mitochondria are the powerhouses of the body, which is paramount for the central nervous system given their high energy expenditure. This high dependence on the mitochondria renders mitochondrial dysfunctions to impair the central nervous system, as seen in neurodegenerative diseases. This article concentrates on the neurodgenerative disease, Alzheimer’s disease and the well-established neuroinflammation pathophysiology, from a mitochondrial perspective. I first focused on the energy production functions of the mitochondria, and the mitochondrial DNA, imperative for mitochondrial function. For instance in their aberrations in Alzheimer’s disease, and in vitro experiments with inflammatory markers that drove damages to the mitochondria DNA. Subsequently, I discussed about mitochondrial biogenesis using expression studies with correlated changes in Alzheimer’s disease and stem cells whereby mitochondria are critical regulators of their fate, pertinent to Alzheimer’s disease. Finally, I accentuated on emerging technologies that enable disentangling the abstruse nature of mitochondria, and some uprising areas of mitochondria research deserving attention from the lens of Alzheimer’s disease. Overall, there is a plausible link between Alzheimer’s disease, neuroinflammation, and mitochondrial mechanisms, but current studies are limited to causally address this question. I presented several improvements and strategies that could be taken to advance the understanding of this relationship in future studies.

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Neuroinflammation Interactions with Mitochondria: Implications for Alzheimer’s Disease

Vic Shao-Chih Chiang
Vic Shao-Chih Chiang

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