Neurodegenerative disorders associated with genes of mitochondria

Abstract

Background Over the last decade, aggregating evidences suggested that there is a causative link between mutation in gene associated with mitochondrial dysfunction and development of several neurodegenerative disorders. Main text Recent structural and functional studies associated with mitochondrial genes have shown that mitochondrial abnormalities possibly lead to mitochondrial dysfunction. Several studies on animal models of neurodegenerative diseases and mitochondrial genes have provided compelling evidence that mitochondria is involved in the initiation as well as progression of diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Huntington’s disease (HD), and Friedreich ataxia (FA). Conclusion In this mini-review, we have discussed the different etiologic and pathogenesis connected with the mitochondrial dysfunction and relevant neurodegenerative diseases that underlie the dominant part of mitochondrial genes in the disease development and its progress.

P5B-ATPases in the mammalian polyamine transport system and their role in disease

“…Alongside maintaining healthy lysosomal functionality, ATP13A2 also plays a role in maintaining mitochondrial function. ATP13A2-deficient models exhibit mitochondrial dysfunction such as reduced membrane potential and ATP production, increased mitochondrial mass, fragmentation and reactive oxygen species (ROS) production [119]. Rotenone, a pesticide and mitochondrial complex I inhibitor that is an environmental Parkinson's disease risk factor, leads to mitochondrial ROS and toxicity causing cell death that can be attenuated upon ATP13A2-mediated PA transport [120].…”

Human Bone Marrow-Derived Mesenchymal Stem Cell Applications in Neurodegenerative Disease Treatment and Integrated Omics Analysis for Successful Stem Cell Therapy

“…To date, many studies on NDDs have shown different features of neurodegeneration, such as cell viability reduction, genetic mutations, gene expression alterations, and cellular function impairment [95][96][97]. To understand the different cellular processes in NDDs, cell health has been evaluated using several methods, including morphological analysis, viability assays, metabolic assays, and gene expression analysis [98][99][100], because cell quality directly affects cell functionality [101,102].…”

Phytochemicals: A Promising Alternative for the Prevention of Alzheimer’s Disease

“…In the ageing brain, misfolded protein accumulates and leads to metabolic loss, oxidative stress-induced damage, and synapse dysfunction. In AD, oxidative damage is indicated by high levels of DNA oxidation products such as 8-hydroxydeoxyguanosine in the brain cell nucleus and mitochondria [6][7][8].…”