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Difference between revisions of "Lang 2022 Cell Mol Life Sci"

From Bioblast
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|title=Lang M, Grünewald A, Pramstaller PP, Hicks AA, Pichler I (2022) A genome on shaky ground: exploring the impact of mitochondrial DNA integrity on Parkinson's disease by highlighting the use of cybrid models. https://doi.org/10.1007/s00018-022-04304-3
|title=Lang M, Grünewald A, Pramstaller PP, Hicks AA, Pichler I (2022) A genome on shaky ground: exploring the impact of mitochondrial DNA integrity on Parkinson's disease by highlighting the use of cybrid models. https://doi.org/10.1007/s00018-022-04304-3
|info=Cell Mol Life Sci 79:283. [https://pubmed.ncbi.nlm.nih.gov/35513611 PMID: 35513611]
|info=Cell Mol Life Sci 79:283. [https://pubmed.ncbi.nlm.nih.gov/35513611 PMID: 35513611]
|authors=Lang M, Grünewald A, Pramstaller PP, Hicks AA, Pichler I
|authors=Lang Martin, Gruenewald Anne, Pramstaller Peter P, Hicks Andrew A, Pichler Irene
|year=2022
|year=2022
|journal=Cell Mol Life Sci
|journal=Cell Mol Life Sci
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|editor=[[Plangger M]]
|editor=[[Plangger M]]
}}
}}
{{Labeling}}
{{Labeling
|area=mtDNA;mt-genetics
|diseases=Parkinson's
}}

Revision as of 13:40, 22 June 2022

Publications in the MiPMap
Lang M, Grünewald A, Pramstaller PP, Hicks AA, Pichler I (2022) A genome on shaky ground: exploring the impact of mitochondrial DNA integrity on Parkinson's disease by highlighting the use of cybrid models. https://doi.org/10.1007/s00018-022-04304-3

» Cell Mol Life Sci 79:283. PMID: 35513611

Lang Martin, Gruenewald Anne, Pramstaller Peter P, Hicks Andrew A, Pichler Irene (2022) Cell Mol Life Sci

Abstract: Mitochondria play important roles in the regulation of key cellular processes, including energy metabolism, oxidative stress response, and signaling towards cell death or survival, and are distinguished by carrying their own genome (mtDNA). Mitochondrial dysfunction has emerged as a prominent cellular mechanism involved in neurodegeneration, including Parkinson's disease (PD), a neurodegenerative movement disorder, characterized by progressive loss of dopaminergic neurons and the occurrence of proteinaceous Lewy body inclusions. The contribution of mtDNA variants to PD pathogenesis has long been debated and is still not clearly answered. Cytoplasmic hybrid (cybrid) cell models provided evidence for a contribution of mtDNA variants to the PD phenotype. However, conclusive evidence of mtDNA mutations as genetic cause of PD is still lacking. Several models have shown a role of somatic, rather than inherited mtDNA variants in the impairment of mitochondrial function and neurodegeneration. Accordingly, several nuclear genes driving inherited forms of PD are linked to mtDNA quality control mechanisms, and idiopathic as well as familial PD tissues present increased mtDNA damage. In this review, we highlight the use of cybrids in this PD research field and summarize various aspects of how and to what extent mtDNA variants may contribute to the etiology of PD. Keywords: Cybrids, Mitochondria, Mitochondrial genome, Parkinson’s disease, mtDNA Bioblast editor: Plangger M


Labels: MiParea: mtDNA;mt-genetics  Pathology: Parkinson's