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

作　　者：Jaspreet Kalra 

机构地区：[1]Department of Pharmacology,ISF College of Pharmacy,Ghal Kalan,Moga,Punjab,India [2]Department of Molecular Physiology and Biological Physics,University of Virginia,Charlottesville,VA,USA

出　　处：《Neural Regeneration Research》2023年第1期94-101,共8页中国神经再生研究（英文版）

摘　　要：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,peptide-based approaches,and lipophilic cations.

关 键 词：adenosine-triphosphate deficiency mitochondrial fission/fusion mitochondrial mutations neurodegenerative disorders oxidative phosphorylation therapeutic interventions 

分 类 号：R743[医药卫生—神经病学与精神病学]