Publication

Abstract : The mitochondria, apart from being known as the cell’s “powerhouse,” are crucial in the viability of nerve cells. Any damage to these cellular organelles can result in their cellular level dysfunction which includes rapidly multiplying reactive oxygen species (ROS) from the mitochondrial membrane, impaired calcium ion homeostasis, and disturbed mitochondrial dynamics by the formation of permeability transition pore in mitochondria. All these impaired biochemical changes lead to various neurological disorders such as progressive supranuclear palsy (PSP), Parkinson’s disease (PD), and Alzheimer’s disease (AD). Moreover, impaired mitochondrial functions are particularly prone to damage owing to prolonged lifespan and stretched length of the neurons. At the same time, neurons are highly dependent on ATP, and thus, the mitochondria play a central role in the pathogenesis pertaining to neuronal disorders. Dysfunction in the mitochondria is an early pathological hallmark of neurological disorders, and its early detection with the help of suitable biomarkers can lead to promising treatment in this area. Thus, the drugs which are targeting mitochondrial dysfunctions are the emerging area of research in connection with neurological disorders. This can be evidenced by the great opportunities for mitigation, diagnosis, and treatment of numerous human disorders that entail mitochondrial dysfunction at the nexus of their pathogenesis. Here, we throw light at the mitochondrial pathologies and indications of dysfunctional mitochondria in PD, AD, and PSP. There is also an insight into the possible therapeutic strategies highlighting the need for mitochondria-based medicine and made an attempt for claiming the prerequisite for the therapy of neurological diseases.