Insights into LRRK2 function and dysfunction from transgenic and knockout rodent models.

Mutations in the LRRK2 (leucine-rich repeat kinase 2) gene on chromosome 12 cause autosomal dominant PD (Parkinson's disease), which is indistinguishable from sporadic forms of the disease. Numerous attempts have therefore been made to model PD in rodents via the transgenic expression of LRRK2...

Full description

Bibliographic Details
Main Authors: Sloan, M, Alegre-Abarrategui, J, Wade-Martins, R
Format: Journal article
Language:English
Published: 2012
_version_ 1797068414011834368
author Sloan, M
Alegre-Abarrategui, J
Wade-Martins, R
author_facet Sloan, M
Alegre-Abarrategui, J
Wade-Martins, R
author_sort Sloan, M
collection OXFORD
description Mutations in the LRRK2 (leucine-rich repeat kinase 2) gene on chromosome 12 cause autosomal dominant PD (Parkinson's disease), which is indistinguishable from sporadic forms of the disease. Numerous attempts have therefore been made to model PD in rodents via the transgenic expression of LRRK2 and its mutant variants and to elucidate the function of LRRK2 by knocking out rodent Lrrk2. Although these models often only partially recapitulate PD pathology, they have helped to elucidate both the normal and pathological function of LRRK2. In particular, LRRK2 has been suggested to play roles in cytoskeletal dynamics, synaptic machinery, dopamine homoeostasis and autophagic processes. Our understanding of how these pathways are affected, their contribution towards PD development and their interaction with one another is still incomplete, however. The present review summarizes the findings from LRRK2 rodent models and draws potential connections between the apparently disparate cellular processes altered, in order to better understand the underlying mechanisms of LRRK2 dysfunction and illuminate future therapeutic interventions.
first_indexed 2024-03-06T22:10:26Z
format Journal article
id oxford-uuid:519cf75f-9a60-4406-bc24-e9c35cacdcc4
institution University of Oxford
language English
last_indexed 2024-03-06T22:10:26Z
publishDate 2012
record_format dspace
spelling oxford-uuid:519cf75f-9a60-4406-bc24-e9c35cacdcc42022-03-26T16:20:37ZInsights into LRRK2 function and dysfunction from transgenic and knockout rodent models.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:519cf75f-9a60-4406-bc24-e9c35cacdcc4EnglishSymplectic Elements at Oxford2012Sloan, MAlegre-Abarrategui, JWade-Martins, RMutations in the LRRK2 (leucine-rich repeat kinase 2) gene on chromosome 12 cause autosomal dominant PD (Parkinson's disease), which is indistinguishable from sporadic forms of the disease. Numerous attempts have therefore been made to model PD in rodents via the transgenic expression of LRRK2 and its mutant variants and to elucidate the function of LRRK2 by knocking out rodent Lrrk2. Although these models often only partially recapitulate PD pathology, they have helped to elucidate both the normal and pathological function of LRRK2. In particular, LRRK2 has been suggested to play roles in cytoskeletal dynamics, synaptic machinery, dopamine homoeostasis and autophagic processes. Our understanding of how these pathways are affected, their contribution towards PD development and their interaction with one another is still incomplete, however. The present review summarizes the findings from LRRK2 rodent models and draws potential connections between the apparently disparate cellular processes altered, in order to better understand the underlying mechanisms of LRRK2 dysfunction and illuminate future therapeutic interventions.
spellingShingle Sloan, M
Alegre-Abarrategui, J
Wade-Martins, R
Insights into LRRK2 function and dysfunction from transgenic and knockout rodent models.
title Insights into LRRK2 function and dysfunction from transgenic and knockout rodent models.
title_full Insights into LRRK2 function and dysfunction from transgenic and knockout rodent models.
title_fullStr Insights into LRRK2 function and dysfunction from transgenic and knockout rodent models.
title_full_unstemmed Insights into LRRK2 function and dysfunction from transgenic and knockout rodent models.
title_short Insights into LRRK2 function and dysfunction from transgenic and knockout rodent models.
title_sort insights into lrrk2 function and dysfunction from transgenic and knockout rodent models
work_keys_str_mv AT sloanm insightsintolrrk2functionanddysfunctionfromtransgenicandknockoutrodentmodels
AT alegreabarrateguij insightsintolrrk2functionanddysfunctionfromtransgenicandknockoutrodentmodels
AT wademartinsr insightsintolrrk2functionanddysfunctionfromtransgenicandknockoutrodentmodels