Wal Pranay, Wal Ankita, Vig Himangi, Mahmood Danish, Khan Mohd Masih Uzzaman
Pharmacy Department, PSIT- Pranveer Singh Institute of Technology, (PHARMACY) Kanpur-Agra-Delhi National Highway (NH-2), Bhauti-Kanpur-209305.
Department of Pharmacology and Toxicology, Unaizah College of Pharmacy, Unaizah 51911, Saudi Arabia.
Adv Pharm Bull. 2024 Mar;14(1):147-160. doi: 10.34172/apb.2024.019. Epub 2023 Oct 14.
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.
This review is a condensed compilation of data from research that has been published between the years of 2014 and 2022, using search engines like Google Scholar, PubMed, and Scopus.
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.
The development of innovative therapeutics for mitochondria-directed treatments in Parkinson's disease may be aided by optimizing 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 hypothesized that drug therapies for neurodegenerative diseases that focus on mitochondrial dysfunction will help to delay the onset of neuronal dysfunction.
衰老和神经退行性疾病均被认为受线粒体功能障碍和自由基形成的影响。能量代谢畸形、线粒体基因组多态性、与线粒体相关的核DNA遗传异常、线粒体融合或裂变的改变、形状和大小的变化、转运变化、线粒体移动性改变、转录缺陷以及与线粒体相关的错误折叠蛋白的出现均与帕金森病有关。
本综述是对2014年至2022年间发表的研究数据的精简汇编,使用了谷歌学术、PubMed和Scopus等搜索引擎。
线粒体移植是一种针对线粒体疾病和线粒体生物发生缺陷的独特治疗方法。使用创新方法用移植的有活力的线粒体替代功能失调的线粒体,作为帕金森病的一种治疗方法已显示出有前景的结果,包括组织保留、增强能量生成和降低氧化损伤。已经研究了许多针对线粒体的疗法,包括线粒体基因疗法、氧化还原疗法等的有效性和效力。
优化线粒体动力学可能有助于开发用于帕金森病线粒体定向治疗的创新疗法。在动物和细胞模型中对许多神经疾病进行了研究,发现线粒体维持可以减缓神经元细胞的死亡。据推测,专注于线粒体功能障碍的神经退行性疾病药物疗法将有助于延缓神经元功能障碍的发作。