Research
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.
MicroRNAs as Potential Regulators of Docosahexaenoic Acid Benefits in Alzheimer’s Disease
Alzheimer’s disease (AD) is a highly prevalent neurodegenerative disease that imposes a prodigious burden on the society. Docosahexaenoic acids (DHA) are known to be beneficial in AD, in part through their anti-inflammatory properties. MicroRNAs (miRs) are important regulators of brain functions and this regulation becomes disrupted in AD. Objectives: The purpose of this article is to propose the involvement of miRs in the antiinflammatory effects of DHA on AD. Methods: The literature surrounding this topic is extensively researched: miR involvement in the pathophysiology of AD, the mechanism of action of DHA, the effects of DHA on miRs and potential future therapeutic strategies for AD involving miRs. Results: AD results in a disrupted miR network that relates to inflammation, but the altered miRs vary between studies. The effects of DHA on AD are generally positive but the mechanism remains enigmatic. Emerging studies demonstrate that one of the potential mechanisms of action of DHA is modulation of miRs.
