Skip Navigation

Brain 2005 128(12):2760-2762; doi:10.1093/brain/awh676
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (27)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Brice, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brice, A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Scientific Commentary

Genetics of Parkinson's disease: LRRK2 on the rise

The first 150 words of the full text of this article appear below.

Our view of the pathogenic mechanisms of Parkinson's disease has greatly changed over the past decade with the identification of several genes implicated in Mendelian forms of this disorder (Corti et al., 2005Go; Gasser et al., 2005Go). Parkin, DJ-1 and PINK1 are responsible for autosomal recessive forms, usually with early onset, that are not associated with Lewy bodies. {alpha}-Synuclein was considered to be the major gene responsible for autosomal dominant forms until late 2004, when the LRRK2 gene was identified (Paisan-Ruiz et al., 2004Go; Zimprich et al., 2004aGo). Despite their rarity, the discovery of {alpha}-synuclein mutations or multiplications led to the demonstration that {alpha}-synuclein is the major component of Lewy bodies, and clearly illustrated the gene dosage effect resulting from gene multiplications; duplications of the {alpha}-synuclein gene are responsible for a late-onset typical Parkinson's disease (Chartier-Harlin et al., 2004Go; . . . [Full Text of this Article]

Alexis Brice1,2,3,4

1 INSERM U679 (former U289), 2 Département de Génétique, Cytogénétique et Embryologie, 3 Fédération de Neurologie and 4 Faculté de Médecine Pierre et Marie Curie, Groupe hospitalier Pitié-Salpêtrière, AP-HP, 47 boulevard de l'Hôpital, 75013, Paris, France

E-mail: brice@ccr.jussieu.fr


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
NeurologyHome page
S. Lesage, S. Belarbi, A. Troiano, C. Condroyer, N. Hecham, P. Pollak, E. Lohman, T. Benhassine, F. Ysmail-Dahlouk, A. Durr, et al.
Is the common LRRK2 G2019S mutation related to dyskinesias in North African Parkinson disease?
Neurology, November 4, 2008; 71(19): 1550 - 1552.
[Full Text] [PDF]


Home page
NeurologyHome page
C. Marras and A. Lang
Invited Article: Changing concepts in Parkinson disease: Moving beyond the Decade of the Brain
Neurology, May 20, 2008; 70(21): 1996 - 2003.
[Abstract] [Full Text] [PDF]


Home page
NeurologyHome page
A. Orr-Urtreger, C. Shifrin, U. Rozovski, S. Rosner, D. Bercovich, T. Gurevich, H. Yagev-More, A. Bar-Shira, and N. Giladi
The LRRK2 G2019S mutation in Ashkenazi Jews with Parkinson disease: Is there a gender effect?
Neurology, October 16, 2007; 69(16): 1595 - 1602.
[Abstract] [Full Text] [PDF]


Home page
Arch NeurolHome page
S. Lesage, S. Janin, E. Lohmann, A.-L. Leutenegger, L. Leclere, F. Viallet, P. Pollak, F. Durif, S. Thobois, V. Layet, et al.
LRRK2 Exon 41 Mutations in Sporadic Parkinson Disease in Europeans
Arch Neurol, March 1, 2007; 64(3): 425 - 430.
[Abstract] [Full Text] [PDF]


Home page
Arch NeurolHome page
L. Ishihara, L. Warren, R. Gibson, R. Amouri, S. Lesage, A. Durr, M. Tazir, Z. K. Wszolek, R. J. Uitti, W. C. Nichols, et al.
Clinical Features of Parkinson Disease Patients With Homozygous Leucine-Rich Repeat Kinase 2 G2019S Mutations.
Arch Neurol, September 1, 2006; 63(9): 1250 - 1254.
[Abstract] [Full Text] [PDF]


Home page
NeurologyHome page
C. P. Zabetian, H. Morino, H. Ujike, M. Yamamoto, M. Oda, H. Maruyama, Y. Izumi, R. Kaji, A. Griffith, B. C. Leis, et al.
Identification and haplotype analysis of LRRK2 G2019S in Japanese patients with Parkinson disease
Neurology, August 22, 2006; 67(4): 697 - 699.
[Abstract] [Full Text] [PDF]


Home page
NEJMHome page
S. Lesage, A. Durr, M. Tazir, E. Lohmann, A.-L. Leutenegger, S. Janin, P. Pollak, A. Brice, and the French Parkinson's Disease Genetics Study Grou
LRRK2 G2019S as a Cause of Parkinson's Disease in North African Arabs
N. Engl. J. Med., January 26, 2006; 354(4): 422 - 423.
[Full Text] [PDF]