Neurological disorders, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis, constitute a heterogeneous group of conditions that collectively impose a substantial burden on global healthcare systems. These disorders are characterized by progressive neuronal degeneration, synaptic dysfunction, and irreversible impairment of cognitive and motor functions. Despite differences in clinical presentation and etiology, accumulating evidence suggests that they share common molecular and cellular mechanisms, among which oxidative stress and mitochondrial dysfunction play central and interdependent roles. Advances in molecular neuroscience and cellular bioenergetics have highlighted that neuronal survival is critically dependent on mitochondrial integrity, given the essential functions of mitochondria in ATP production, intracellular calcium buffering, and regulation of programmed cell death pathways.
Dilara Aliyeva*1, Irada Aliyeva2, Gulnara Valiyeva1, Asiya Aghayeva1, Azada Rustamzada1, Sabina Mashadiyeva-Bayramova2 (Wed,) studied this question.