摘要
Neuronal death is associated with mitochondrial dysfunction caused by mutations in mitochondrial DNA.Mitochondrial DNA becomes damaged when processes such as replica-tion,repair,and nucleotide synthesis are compromised.This extensive accumulation of damaged mitochondrial DNA subsequently disrupts the normal function of mitochondria,lead-ing to aging,degeneration,or even death of neurons.Mitochondrial dysfunction stands as a pivotal factor in the development of neurodegenerative diseases,including Parkinson’s dis-ease,Alzheimer’s disease,Huntington’s disease,and amyotrophic lateral sclerosis.Recog-nizing the intricate nature of their pathogenesis,there is an urgent need for more effective therapeutic interventions.In recent years,mitochondrial DNA editing tools such as zinc finger nucleases,double-stranded DNA deaminase toxin A-derived cytosine base editors,and tran-scription activator-like effector ligand deaminases have emerged.Their emergence will revo-lutionize the research and treatment of mitochondrial diseases.In this review,we summarize the advancements in mitochondrial base editing technology and anticipate its utilization in neurodegenerative diseases,offering insights that may inform preventive strategies and ther-apeutic interventions for disease phenotypes.
