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