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Dynamics of autophagy and mitophagy in neurons
Author(s) -
Holzbaur Erika L.F.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.402.4
Subject(s) - mitophagy , autophagy , parkin , neurodegeneration , optineurin , pink1 , microbiology and biotechnology , mitochondrion , neuroscience , biology , amyotrophic lateral sclerosis , parkinson's disease , disease , medicine , apoptosis , genetics , pathology
Neurons are large, polarized, and very long‐lived cells. In order to maintain cellular function over decades, neurons are highly dependent on homeostatic mechanisms such as autophagy. Autophagy is a cellular pathway for the degradation of aggregated proteins and dysfunctional organelles such as mitochondria, which are degraded by mitophagy. Mutations in proteins required for autophagy or mitophagy including PINK1, Parkin, Optineurin and TBK1 are sufficient to cause neurodegeneration, indicating the importance of this pathway to maintain neuronal function. We are using live cell imaging in cell models and in primary neurons to study the dynamics of autophagy and mitophagy, in order to define the underlying molecular mechanisms and to better understand how defects in this pathway lead to neurodegenerative diseases such as Amyotrophic lateral sclerosis (ALS) and Parkinson's disease. Support or Funding Information Supported by a Javits Neuroscience Investigator Award to E. Holzbaur (NIH R37 NS060698)