Crosslink between mutations in mitochondrial genes and brain disorders: implications for mitochondrial-targeted therapeutic interventions

At the present, association of mitochondrial dysfunction and progression of neurological disorders has gained significant attention. Defects in mitochondrial network dynamics, point mutations, deletions, and interaction of pathogenomic proteins with mitochondria are some of the possible underlying mechanisms involved in these neurological disorders. Mitochondrial genetics, defects in mitochondrial oxidative phosphorylation machinery, and reactive oxygen species production might share common crosstalk in the progression of these neurological disorders. It is of significant interests to explore and develop therapeutic strategies aimed at correcting mitochondrial abnormalities. This review provided insights on mitochondrial dysfunction/mutations involved in the progression of Alzheimer's disease, Huntington's disease, and epilepsy with a special focus on Parkinson's disease pathology. Along with the deleterious effects of mitochondrial mutations in aforesaid neurological disorders, this paper unraveled the available therapeutic strategy, specifically aiming to improve mitochondrial dysfunction, drugs targeting mitochondrial proteins, gene therapies aimed at correcting mutant mtDNA, peptidebased approaches, and lipophilic cations.

Automated summary

The association between mitochondrial dysfunction and progression of neurological disorders has gained significant attention. Possible mechanisms involved in these disorders include defects in mitochondrial network dynamics, point mutations, deletions, and interaction of pathogenomic proteins with mitochondria. Shared crosstalk between mitochondrial genetics, defects in mitochondrial oxidative phosphorylation machinery, and reactive oxygen species production might contribute to the progression of these disorders. Exploring and developing therapeutic strategies to correct mitochondrial abnormalities is of great interest.