This invention provides methods to predict the likelihood of suicidal or self-destructive behavior in a patient during treatment. The method employs the detection of a polymorphism in the SLC6A3 gene at Exon 9 A59G or a surrogate marker, by various methods. Also provided are methods of treatment based on the presence or absence of this polymorphism or surrogate marker. Also provided are kits to use in the methods of the invention.
Biomarkers For The Prediction Of Responsiveness To Clozapine Treatment
Yunsheng He - Waltham MA, US Elisabeth Marie Leroy - Boston MA, US
Assignee:
NOVARTIS AG - Basel
International Classification:
A61K 31/5513 C12Q 1/68
US Classification:
514220, 435 6
Abstract:
This invention provides methods to predict the likelihood of suicidal or self-destructive behaviour in a patient during treatment. The method employs the detection of a VNTR polymorphism in the 3′-UTR of the dopamine transporter gene (SLC6A3). Patients with nine or fewer repeats are considered poor responders to clozapine. Nine or fewer repeats in the SLC6A3 gene have been correlated with poor expression of the SLC6A3 gene. Also provided are methods of treatment based on the presence or absence of this polymorphism or surrogate markers thereof. Also provided are kits to use in the methods of the invention.
Cloning Of A Gene Mutation For Parkinson's Disease
Christian Lavedan - North Potomac MD, US Elisabeth Leroy - Washington DC, US Robert L. Nussbaum - Chevy Chase MD, US William G. Johnson - Short Hills NJ, US Roger C. Duvoisin - Sante Fe NM, US
Assignee:
The United States of America as represented by the Secretary of the Department of Health and Human Services - Washington DC
International Classification:
C12Q 1/68 C07H 21/04 C12N 5/00 C12N 15/00
US Classification:
435 6, 435 691, 4353201, 435325, 536 231, 536 235
Abstract:
Parkinson's disease (PD) is a common neurodegenrative disorder with a lifetime incidence of approximately 2 percent. It was recently reported that a PD susceptibility gene is located on the long arm of human chromosome four. The present invention reports the subsequent identification of a mutation in the alpha synuclein gene, which codes for a presynaptic protein thought to be involved in neuronal plasticity. The finding of a specific molecular alteration which is causative for PD will permit the detailed understanding of the pathophysiology of the disorder, which will lead to potential therapetuic interventions, as well as a means for diagnosing individuals having an increased risk of developing the disease.