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Dopamine and cortical iPSC-derived neurons with different Parkinsonian mutations show variation in lysosomal and mitochondrial dysfunction: implications for protein deposition versus selective cell loss
Output Details
Description
Mutations that cause Parkinson's disease give diverse pathological phenotypes. Those with PRKN loss of function mutations have significantly earlier selective vulnerability of dopamine neurons, those with SNCA mutations have increased alpha-synuclein deposition, while those with LRRK2 mutations have additional deposition of tau. Direct comparison of cell models with these mutations aim to clarify the relative cellular dysfunctions associated with these different pathological phenotypes.
Identifier (DOI)
10.1101/2024.10.07.617117