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Open Access Green as soon as Postprint is submitted to ZB.
A cybrid cell model for the assessment of the link between mitochondrial deficits and sporadic Parkinson's disease.
Methods Mol. Biol. 1265, 415-424 (2015)
Parkinson's disease (PD) is a multifactorial and clinically complex age-related movement disorder. The cause of its most common form (sporadic PD, sPD) is unknown, but one prominent causal factor is mitochondrial dysfunction. Although several genetic- and toxin-based models have been developed along the last decades to mimic the pathological cascade of PD, cellular models that reliably recapitulate the pathological features of the neurons that degenerate in PD are scarce. We describe here the generation of cytoplasmic hybrid cells (or cybrids) as a cellular model of sPD. This approach consists on the fusion of platelets harboring mtDNA from sPD patients with cells in which the endogenous mtDNA has been depleted (Rho0 cells). The sPD cybrid model has been successful in recapitulating most of the hallmarks of sPD, constituting now a validated model for addressing the link between mitochondrial dysfunction and sPD pathology.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Alpha-synuclein Oligomers ; Cellular Models ; Cybrids ; Mitochondria ; Mitochondrial Impairment ; Mtdna ; Neurodegeneration ; Oxidative Stress ; Parkinson's Disease ; Rho Cells
ISSN (print) / ISBN
1064-3745
e-ISSN
1940-6029
Conference Title
Mitochondrial Medicine
Journal
Methods in Molecular Biology
Quellenangaben
Volume: 1265,
Pages: 415-424
Publisher
Springer
Publishing Place
Berlin [u.a.]
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)