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Curr Opin Neurobiol. 2018 Feb;48:52-58. doi: 10.1016/j.conb.2017.09.005. Epub 2017 Oct 10.

Endo-lysosomal dysfunction: a converging mechanism in neurodegenerative diseases.

Author information

1
Gladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
2
Biotechnology Research and Training Center, University of North Carolina at Pembroke, Pembroke, NC, USA.
3
Gladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: xu.chen@gladstone.ucsf.edu.
4
Gladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: li.gan@gladstone.ucsf.edu.

Abstract

Endo-lysosomal pathways are essential in maintaining protein homeostasis in the cell. Numerous genes in the endo-lysosomal pathways have been found to associate with neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and frontotemporal dementia (FTD). Mutations of these genes lead to dysfunction in multiple steps of the endo-lysosomal network: autophagy, endocytic trafficking and lysosomal degradation, resulting in accumulation of pathogenic proteins. Although the exact pathogenic mechanism varies for different disease-associated genes, dysfunction of the endo-lysosomal pathways represents a converging mechanism shared by these diseases. Therefore, strategies that correct or compensate for endo-lysosomal dysfunction may be promising therapeutic approaches to treat neurodegenerative diseases.

PMID:
29028540
DOI:
10.1016/j.conb.2017.09.005

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