线粒体
线粒体DNA
线粒体生物发生
帕金森病
线粒体融合
粒线体疾病
线粒体分裂
疾病
医学
移植
TFAM公司
氧化磷酸化
生物
生物信息学
细胞生物学
神经科学
病理
遗传学
基因
生物化学
内科学
作者
Pranay Wal,Ankita Wal,Himangi Vig,Danish Mahmood,Mohd Masih Uzzaman Khan
标识
DOI:10.34172/apb.2024.019
摘要
Purpose: Both aging and neurodegenerative illnesses are thought to be influenced by mitochondrial malfunction and free radical formation. Deformities of the energy metabolism, mitochondrial genome polymorphisms, nuclear DNA genetic abnormalities associated with mitochondria, modifications of mitochondrial fusion or fission, variations in shape and size, variations in transit, modified mobility of mitochondria, transcription defects, and the emergence of misfolded proteins associated with mitochondria are all linked to Parkinson's disease. Method: This review is a condensed compilation of data from research that have been published between the years of 2014 and 2022, using search engines like Google Scholar, PubMed, and Scopus. Result: Mitochondrial transplantation is a one-of-a-kind treatment for mitochondrial diseases and deficits in mitochondrial biogenesis. The replacement of malfunctioning mitochondria with transplanted viable mitochondria using innovative methodologies has shown promising outcomes as a cure for Parkinson's, involving tissue sparing coupled with enhanced energy generation and lower oxidative damage. Numerous mitochondria-targeted therapies, including mitochondrial gene therapy, redox therapy, and others, have been investigated for their effectiveness and potency. Conclusion: The development of innovative therapeutics for mitochondria-directed treatments in Parkinson's disease may be aided by optimising mitochondrial dynamics. Many neurological diseases have been studied in animal and cellular models, and it has been found that mitochondrial maintenance can slow the death of neuronal cells. It has been hypothesised that drug therapies for neurodegenerative diseases that focus on mitochondrial dysfunction will help to delay the onset of neuronal dysfunction.
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