Crosstalk of the Neuronal Microenvironment in the Pathophysiology of Alzheimer's Disease and Prospective Intervention Strategies Advancing Mitochondrial Dynamics: A Comprehensive Review

Abstract

Mitochondria play a fundamental role in cell bioenergetics and respiratory processes, both of which are necessary for the myriad of metabolic responses that sustain cellular vitality. Mitochondrial dysfunction in neuronal cells facilitates the generation of reactive oxygen species, which are simply known as ROS, by a cellular irregularity called oxidative stress when there is an imbalance between the production of ROS and the body’s capacity to neutralize them. Thus, a reduction in the energy supply in the form of ATP can lead to damage to cellular components such as DNA, RNA, proteins, and lipids. Mitochondrial dynamics, including fission and fusion, can also be affected by this cellular occurrence. Alzheimer’s disease, a neurodegenerative disease that begins with the assembly of pathogenic proteins and neurofibrillary tangles, or NFTs, highlights significant oxidative stress across the body, which is incidentally linked to the vulnerable regions of the brain affected by the condition. AD shows oxidative harm at levels that are distant from those of coercive controls, inferring the involvement of additional factors (biological or genetic). Practically harmful mitochondria, which seem more useful in generating reactive oxygen species known as ROS but less productive in generating energy storehouses such as ATP, are early and recognizable indicators of diseases that damage mainly the hippocampus area in the brain, in which new memories form.