| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From the Departments of Neurology (A.S., B.T., D.P., W.T., J.P., T.D., A.Sz.), Pharmacology (P.P.W.), and Metabolic Diseases (M.T.M.), Jagiellonian University, Krakow, Poland and Department of Neurology (D.A.F.), University of Michigan, Ann Arbor, MI.
* To whom correspondence should be addressed. E-mail: slowik{at}cm-uj.krakow.pl.
Abstract-- Background: The human paraoxonase (PON) gene family consists of three members, PON1, PON2, and PON3, located adjacent to each other on chromosome 7. PON catalytic activity may be influenced by frequent amino acid variants. Chronic exposure to certain chemicals or to environmental factors causing enhanced lipid peroxidation metabolized by paraoxonases may be a risk factor for sporadic ALS (sALS). Objective: The aim of this study was to examine the association between PON1 Q192R, PON1 L55M, and PON2 C311S functional polymorphisms and the risk of sALS in a Polish population. Methods: The authors included 185 patients with a definite or probable diagnosis of sALS (El Escorial Criteria) and 437 healthy controls of similar age and gender. The paraoxonase polymorphisms were studied by PCR and restriction enzyme digestion. Results: Using logistic regression analyses, the C allele of the C311S polymorphism was associated with sALS in dominant and additive models, whereas the R allele of the Q192R polymorphism was associated with sALS in recessive, additive, and dominant models. The authors compared the distribution of haplotypes between cases and controls. The R-C haplotype was overrepresented among cases (odds ratio 3.44, 95% CI: 1.55 to 7.62, p = 0.002). Conclusions: Frequent amino acid variants in the paraoxonase 1 and paraoxonase 2 genes are associated with sporadic ALS in a Polish population.
This article has been cited by other articles:
|
|
 |
|
  P. N. Valdmanis, E. Kabashi, A. Dyck, P. Hince, J. Lee, P. Dion, M. D'Amour, F. Souchon, J. -P. Bouchard, F. Salachas, et al. Association of paraoxonase gene cluster polymorphisms with ALS in France, Quebec, and Sweden Neurology, August 12, 2008; 71(7): 514 - 520. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. -M. Wills, J. E. Landers, H. Zhang, R. J. Richter, A. J. Caraganis, M. E. Cudkowicz, C. E. Furlong, and R. H. Brown Jr Paraoxonase 1 (PON1) organophosphate hydrolysis is not reduced in ALS Neurology, March 18, 2008; 70(12): 929 - 934. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.C. Schymick, K. Talbot, and B.J. Traynor Genetics of sporadic amyotrophic lateral sclerosis Hum. Mol. Genet., October 15, 2007; 16(R2): R233 - R242. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. A. Sutedja, J. H. Veldink, K. Fischer, H. Kromhout, J.H.J. Wokke, M. H.B. Huisman, D. J.J. Heederik, and L. H. Van den Berg Lifetime occupation, education, smoking, and risk of ALS Neurology, October 9, 2007; 69(15): 1508 - 1514. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Cronin, M. J Greenway, J. H M Prehn, and O. Hardiman Paraoxonase promoter and intronic variants modify risk of sporadic amyotrophic lateral sclerosis J. Neurol. Neurosurg. Psychiatry, September 1, 2007; 78(9): 984 - 986. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Kasperaviciute, M. E. Weale, K. V. Shianna, G. T. Banks, C. L. Simpson, V. K. Hansen, M. R. Turner, C. E. Shaw, A. Al-Chalabi, H. S. Pall, et al. Large-scale pathways-based association study in amyotrophic lateral sclerosis Brain, September 1, 2007; 130(9): 2292 - 2301. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. E. Shaw and A. Al-Chalabi Susceptibility genes in sporadic ALS: separating the wheat from the chaff by international collaboration. Neurology, September 12, 2006; 67(5): 738 - 739. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
