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The unresolved role of mitochondrial DNA in Parkinson's disease: An overview of published studies, their limitations, and future prospects.

Abstract：

:Parkinson's disease (PD), a progressive neurodegenerative disorder, has long been associated with mitochondrial dysfunction in both sporadic and familial forms of the disease. Mitochondria are crucial for maintaining cellular homeostasis, and their dysfunction is detrimental to dopaminergic neurons. These neurons are highly dependent on mitochondrial adenosine triphosphate (ATP) and degenerate in PD. Mitochondria contain their own genomes (mtDNA). The role of mtDNA has been investigated in PD on the premise that it encodes vital components of the ATP-generating oxidative phosphorylation (OXPHOS) complexes and accumulates somatic variation with age. However, the association between mtDNA variation and PD remains controversial. Herein, we provide an overview of previously published studies on the role of inherited as well as somatic (acquired) mtDNA changes in PD including point mutations, deletions and depletion. We outline limitations of previous investigations and the difficulties associated with studying mtDNA, which have left its role unresolved in the context of PD. Lastly, we highlight the potential for further research in this field and provide suggestions for future studies. Overall, the mitochondrial genome is indispensable for proper cellular function and its contribution to PD requires further, more extensive investigation.

journal_name

Neurochem Int

journal_title

Neurochemistry international

authors

Müller-Nedebock AC,Brennan RR,Venter M,Pienaar IS,van der Westhuizen FH,Elson JL,Ross OA,Bardien S

doi

10.1016/j.neuint.2019.104495

subject

Has Abstract

pub_date

2019-10-01 00:00:00

pages

104495

eissn

0197-0186

issn

1872-9754

pii

S0197-0186(19)30220-7

journal_volume

129

pub_type

杂志文章,评审

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