Mitochondrial degradation of amyloidogenic proteins - A new perspective for neurodegenerative diseases

Janin Lautenschäger; Gabriele S Kaminski Schierle

doi:10.1016/j.pneurobio.2019.101660

Mitochondrial degradation of amyloidogenic proteins - A new perspective for neurodegenerative diseases

Prog Neurobiol. 2019 Oct:181:101660. doi: 10.1016/j.pneurobio.2019.101660. Epub 2019 Jul 10.

Authors

Janin Lautenschäger¹, Gabriele S Kaminski Schierle²

Affiliations

¹ Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, West Cambridge Site, Philippa Fawcett Drive, Cambridge, CB3 0AS, UK. Electronic address: janin.lautenschlaeger@gmail.com.
² Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, West Cambridge Site, Philippa Fawcett Drive, Cambridge, CB3 0AS, UK.

PMID: 31301323
DOI: 10.1016/j.pneurobio.2019.101660

Abstract

This perspective article outlines mechanisms of mitochondrial import and protein degradation and how these have been linked to alpha-synuclein and Amyloid beta (Aβ) homeostasis. Our aim is to underpin and stimulate the debate on the recent conception of mitochondria as protein degrading organelles, which suggests that mitochondria are more directly involved in neurodegenerative diseases than previously assumed.

Keywords: Alpha-synuclein; Alzheimer’s disease; Amyloid beta; HtrA2; Huntingtin; Mitochondrial degradation; Neurodegeneration; Omi; Parkinson’s disease; PreP; SOD1.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Amyloid beta-Peptides / metabolism*
Animals
Humans
Mitochondria / metabolism*
Neurodegenerative Diseases / metabolism*
alpha-Synuclein / metabolism*

Substances

Amyloid beta-Peptides
alpha-Synuclein

Abstract

Publication types

MeSH terms

Substances

Grants and funding