Role of Mitochondrial Medicine in Neuropsychiatric Disorders

: Mitochondria are important cytoplasmic organelles that provide cellular energy, regulate intracellular calcium levels, change a cell's reduction-oxidation potential, and control cell death. A growing body of evidence suggests that mitochondria play a key role in neurodegenerative illnesses like Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis, and Friedreich ataxia. Excessive free radical generation, reduced ATP production, mitochondrial permeability transition, mitochondrial DNA lesions, altered mitochondrial dynamics, and apoptosis are all common symptoms of mitochondrial dysfunction in neurodegenerative disorders. Though this field of research is still in its inchoate stage, mitochondrial medicine as an emerging treatment method targeting mitochondrial dysfunction in neurodegenerative illnesses has proven to have significant potential. This article discusses how mitochondrial dysfunction contributes to neurodegenerative disorders. In addition, we also discussed the recent progression of manifold mitochondrial therapies including blockade of mitochondrial permeability transition, gene therapy, and therapies with antioxidants which indicates mitochondrial medicine is a promising approach for the treatment of neurodegenerative disorders in near future. AD patients’ brains 16 . The production of mPTP is triggered by CypD's interaction with Aβ. This shows that aberrant amyloid buildup reduces the efficiency of the mitochondrial oxidative phosphorylation mechanism, resulting in lower ATP generation and higher ROS levels 15,16 . By genetically depleting CypD or utilizing a CypD inhibitor, the synthesis of the mPTP can be blocked which may, in turn, prevent the detrimental effects of AD. In mouse models, genetic depletion of CypD has been found to diminish mitochondrial swelling, oxidative stress, and apoptosis 15 . CypD deficient mice who overexpressed APP and Aβ, better regulated their mitochondrial functions including production of ATP and complex IV activity 17 . The same results were observed in AD-affected mice which confirms that depletion of CypD levels in AD patients is a potential therapeutic strategy 15 . Mitochondrial mitochondria from huntingtin knock-in more in respiration and mPTP opening from mutant huntingtin-induced caused by mutant huntingtin with Vit E effectively preserved complex II function and oxidative damage E supplementation reduced the start and progression of neuropathology in a SOD1 transgenic ALS mice model 58 . A Vit E-rich diet has been linked to a lower incidence of Parkinson's disease 59,60 . It has been suggested that combining vitamin E with vitamin C can slow the progression of PD 61 . However, there are conflicting data on the effectiveness of vitamin E and vitamin C as treatments for neurodegenerative illnesses. Zhang's recent study on the influence of vitamin E and vitamin C intake on the risk of Parkinson's disease found no reduction in the incidence of the ailment 62 . He theorized that the protective effect of high dietary Vit E levels could be attributed to other active chemicals in the food rather than Vit E. Several other studies found that giving Vit E or Vit C alone or in combination did not affect the progression or risk of AD and PD 63,64,65,66 . Furthermore, a few case-controlled studies found no benefit from vitamin therapy in ALS patients or animal models 67 . Excessive doses of vitamin E (>150 IU/day) may increase the mortality of recipients 68.