Therapeutic potential of NADH:in neurodegenerative diseases characterizde by mitochondrial dysfunction
Nicotinamide adenine dinucleotide(NADH)in its reduced form of is a key coenzyme in redox reac-tions,essential for maintaining energy homeostasis.NADH and its oxidized counterpart,NAD+,form a redox couple that regulates various biological processes,including calcium homeostasis,synaptic plasticity,anti-apopto-sis,and gene expression.The reduction of NAD+/NADH levels is closely linked to mitochondrial dysfunction,which plays a pivotal role in the cascade of various neurodegenerative disorders,including Parkinson's disease and Alzheimer's disease.Auditory neuropathy(AN)is recognized as a clinical biomarker in neurodegenerative disor-ders.Furthermore,mitochondrial dysfunction has been identified in patients with mutations in genes like OPA1 and AIFM1.However,effective treatments for these conditions are still lacking.Increasing evidence sug-gests that administratering NAD+or its precursors endogenously may potentially prevent and slow disease pro-gression by enhancing DNA repair and improving mitochondrial function.Therefore,this review concentrates on the metabolic pathways of NAD+/NADH production and their biological functions,and delves into the therapeu-tic potential and mechanisms of NADH in treating AN.