TY - JOUR
T1 - Trumping neurodegeneration
T2 - Targeting common pathways regulated by autosomal recessive Parkinson's disease genes
AU - Scott, Laura
AU - Dawson, Valina L.
AU - Dawson, Ted M.
N1 - Funding Information:
Supported by NIH/NINDS grant P50 NS38377 and the JPB Foundation . T.M.D. is the Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases. X.B., V.L.D. and T.M.D. acknowledge the joint participation by the Adrienne Helis Malvin Medical Research Foundation through its direct engagement in the continuous active conduct of medical research in conjunction with the Johns Hopkins Hospital and the Johns Hopkins University School of Medicine and the Foundation's Parkinson's Disease Program M-2014.
Funding Information:
Supported by NIH/NINDS grant P50 NS38377 and the JPB Foundation. T.M.D. is the Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases. X.B., V.L.D. and T.M.D. acknowledge the joint participation by the Adrienne Helis Malvin Medical Research Foundation through its direct engagement in the continuous active conduct of medical research in conjunction with the Johns Hopkins Hospital and the Johns Hopkins University School of Medicine and the Foundation's Parkinson's Disease Program M-2014.
Publisher Copyright:
© 2017 Elsevier Inc.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2017/12
Y1 - 2017/12
N2 - Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the progressive loss of dopaminergic (DA) neurons. Most PD cases are sporadic; however, rare familial forms have been identified. Autosomal recessive PD (ARPD) results from mutations in Parkin, PINK1, DJ-1, and ATP13A2, while rare, atypical juvenile ARPD result from mutations in FBXO7, DNAJC6, SYNJ1, and PLA2G6. Studying these genes and their function has revealed mitochondrial quality control, protein degradation processes, and oxidative stress responses as common pathways underlying PD pathogenesis. Understanding how aberrancy in these common processes leads to neurodegeneration has provided the field with numerous targets that may be therapeutically relevant to the development of disease-modifying treatments.
AB - Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the progressive loss of dopaminergic (DA) neurons. Most PD cases are sporadic; however, rare familial forms have been identified. Autosomal recessive PD (ARPD) results from mutations in Parkin, PINK1, DJ-1, and ATP13A2, while rare, atypical juvenile ARPD result from mutations in FBXO7, DNAJC6, SYNJ1, and PLA2G6. Studying these genes and their function has revealed mitochondrial quality control, protein degradation processes, and oxidative stress responses as common pathways underlying PD pathogenesis. Understanding how aberrancy in these common processes leads to neurodegeneration has provided the field with numerous targets that may be therapeutically relevant to the development of disease-modifying treatments.
KW - Autosomal recessive Parkinson's disease
KW - Mitochondria
KW - Oxidative stress
KW - PINK1
KW - Parkin
KW - Protein degradation
UR - http://www.scopus.com/inward/record.url?scp=85018169957&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85018169957&partnerID=8YFLogxK
U2 - 10.1016/j.expneurol.2017.04.008
DO - 10.1016/j.expneurol.2017.04.008
M3 - Review article
C2 - 28445716
AN - SCOPUS:85018169957
VL - 298
SP - 191
EP - 201
JO - Experimental Neurology
JF - Experimental Neurology
SN - 0014-4886
ER -