LRRK2 at the interface of autophagosomes, endosomes and lysosomes

Over the past 20 years, substantial progress has been made in identifying the underlying genetics of Parkinson’s disease (PD). Of the known genes, LRRK2 is a major genetic contributor to PD. However, the exact function of LRRK2 remains to be elucidated. In this review, we discuss how familial forms...

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Main Authors: Roosen, Dorien A., Cookson, Mark R.
Format: Online
Language:English
Published: BioMed Central 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5142374/
id pubmed-5142374
recordtype oai_dc
spelling pubmed-51423742016-12-15 LRRK2 at the interface of autophagosomes, endosomes and lysosomes Roosen, Dorien A. Cookson, Mark R. Review Over the past 20 years, substantial progress has been made in identifying the underlying genetics of Parkinson’s disease (PD). Of the known genes, LRRK2 is a major genetic contributor to PD. However, the exact function of LRRK2 remains to be elucidated. In this review, we discuss how familial forms of PD have led us to hypothesize that alterations in endomembrane trafficking play a role in the pathobiology of PD. We will discuss the major observations that have been made to elucidate the role of LRRK2 in particular, including LRRK2 animal models and high-throughput proteomics approaches. Taken together, these studies strongly support a role of LRRK2 in vesicular dynamics. We also propose that targeting these pathways may not only be beneficial for developing therapeutics for LRRK2-driven PD, but also for other familial and sporadic cases. BioMed Central 2016-12-07 /pmc/articles/PMC5142374/ /pubmed/27927216 http://dx.doi.org/10.1186/s13024-016-0140-1 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Roosen, Dorien A.
Cookson, Mark R.
spellingShingle Roosen, Dorien A.
Cookson, Mark R.
LRRK2 at the interface of autophagosomes, endosomes and lysosomes
author_facet Roosen, Dorien A.
Cookson, Mark R.
author_sort Roosen, Dorien A.
title LRRK2 at the interface of autophagosomes, endosomes and lysosomes
title_short LRRK2 at the interface of autophagosomes, endosomes and lysosomes
title_full LRRK2 at the interface of autophagosomes, endosomes and lysosomes
title_fullStr LRRK2 at the interface of autophagosomes, endosomes and lysosomes
title_full_unstemmed LRRK2 at the interface of autophagosomes, endosomes and lysosomes
title_sort lrrk2 at the interface of autophagosomes, endosomes and lysosomes
description Over the past 20 years, substantial progress has been made in identifying the underlying genetics of Parkinson’s disease (PD). Of the known genes, LRRK2 is a major genetic contributor to PD. However, the exact function of LRRK2 remains to be elucidated. In this review, we discuss how familial forms of PD have led us to hypothesize that alterations in endomembrane trafficking play a role in the pathobiology of PD. We will discuss the major observations that have been made to elucidate the role of LRRK2 in particular, including LRRK2 animal models and high-throughput proteomics approaches. Taken together, these studies strongly support a role of LRRK2 in vesicular dynamics. We also propose that targeting these pathways may not only be beneficial for developing therapeutics for LRRK2-driven PD, but also for other familial and sporadic cases.
publisher BioMed Central
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5142374/
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