Targeting Mitochondria as a Therapeutic Approach for Parkinson’s Disease

被引：0
作者：
Maryam Abrishamdar
Maryam Sadat Jalali
Yaghoob Farbood
机构：
[1] Ahvaz Jundishapur University of Medical Sciences,Department of Physiology, Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute
[2] Ahvaz Jundishapur University of Medical Sciences,Department of Physiology, Medicine Faculty, Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute
来源：
Cellular and Molecular Neurobiology | 2023年 / 43卷
关键词：
Parkinson’s disease; Mitochondrial dysfunction; Neurodegeneration;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Neurodegeneration is among the most critical challenges that involve modern societies and annually influences millions of patients worldwide. While the pathophysiology of Parkinson’s disease (PD) is complicated, the role of mitochondrial is demonstrated. The in vitro and in vivo models and genome-wide association studies in human cases proved that specific genes, including PINK1, Parkin, DJ-1, SNCA, and LRRK2, linked mitochondrial dysfunction with PD. Also, mitochondrial DNA (mtDNA) plays an essential role in the pathophysiology of PD. Targeting mitochondria as a therapeutic approach to inhibit or slow down PD formation and progression seems to be an exciting issue. The current review summarized known mutations associated with both mitochondrial dysfunction and PD. The significance of mtDNA in Parkinson's disease pathogenesis and potential PD therapeutic approaches targeting mitochondrial dysfunction was then discussed.
引用
收藏
页码：1499 / 1518
页数：19
相关论文
共 1895 条
[11]  
De Strooper B(2017)FACS-assisted CRISPR-Cas9 genome editing facilitates parkinson's disease modeling Stem Cell Rep 9 1664-1675
[12]  
Morais VA(2017)Exenatide once weekly versus placebo in parkinson’s disease: a randomised, double-blind, placebo-controlled trial Lancet (london, England) 390 640-643
[13]  
Aman Y(2012)Number of CAG repeats in POLG1 and its association with parkinson disease in the Norwegian population Mitochondrion 12 998-1000
[14]  
Ryan B(2007)Familial parkinsonism and ophthalmoplegia from a mutation in the mitochondrial DNA helicase twinkle Arch Neurol 64 132-141
[15]  
Torsetnes SB(2007)Brain neutral lipids mass is increased in alpha-synuclein gene-ablated mice J Neurochem 101 109-114
[16]  
Knapskog A-B(1998)Coenzyme Q10 attenuates the 1-methyl-4-phenyl-1,2,3, tetrahydropyridine (MPTP) induced loss of striatal dopamine and dopaminergic axons in aged mice Brain Res 783 1262-1264
[17]  
Watne LO(2006)Creatine supplementation in parkinson disease: a placebo-controlled randomized pilot trial Neurology 67 515-517
[18]  
McEwan WA(2006)High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and parkinson disease Nat Genet 38 1044-1066
[19]  
Fang EF(2013)The function of α-synuclein Neuron 79 154-157
[20]  
Ammal Kaidery N(2020)Alzheimer’s and parkinson's brain tissues have reduced expression of genes for mtDNA OXPHOS proteins, mitobiogenesis regulator PGC-1α protein and mtRNA stabilizing protein LRPPRC (LRP130) Mitochondrion 53 65-68
12345678910