Disease-associated tau impairs mitophagy by inhibiting Parkin translocation to mitochondria

ABSTRACT: Accumulation of the protein tau characterises Alzheimer's disease and other tauopathies, including familial forms of frontotemporal dementia (FTD) that carry pathogenic tau mutations. Another hallmark feature of these diseases is the accumulation of dysfunctional mitochondria. Although disease-associated tau is known to impair several aspects of mitochondrial function, it is still unclear whether it also directly impinges on mitochondrial quality control, specifically Parkin-dependent mitophagy. Using the mito-QC mitophagy reporter, we found that both human wild-type (hTau) and FTD mutant tau (hP301L) inhibited mitophagy in neuroblastoma cells, by reducing mitochondrial translocation of Parkin. In the C. elegans nervous system, hTau expression reduced mitophagy, whereas hP301L expression c

SUBMITTER: Prof. Jurgen Gotz 

PROVIDER: S-SCDT-EMBOJ-2018-99360 | biostudies-other |

REPOSITORIES: biostudies-other