Hostname: page-component-848d4c4894-5nwft Total loading time: 0 Render date: 2024-05-21T18:19:53.368Z Has data issue: false hasContentIssue false
  • English
  • Français

Canadian Collaborative Project on Genetic Susceptibility to MS, Phase 2: Rationale and Method

Published online by Cambridge University Press:  18 September 2015

A.D. Sadovnick ,
N.J. Risch ,
G.C. Ebers  and
the Canadian Collaborative Study Group
A.D. Sadovnick*
Affiliation:
Department of Medical Genetics, University of British Columbia, Vancouver
N.J. Risch
Affiliation:
Department of Genetics, Stanford University School of Medicine, California, U.S.A.
G.C. Ebers
Affiliation:
Department of Clinical Neurological Sciences, University of Western Ontario, London
*
GF401 Koerner Pavilion, VHHSSC-UBC, 2211 Wesbrook Mall, Vancouver, British Columbia, Canada V6T 2B5
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

Results from the Canadian Collaborative Project on Genetic Susceptibility to Multiple Sclerosis (MS)-Phase 1 (CCPGSMS-Phase 1) together with other family data published since 1982 have led to the following conclusions about the etiology of MS: (i) genetic and non-genetic (environmental) factors are involved in the etiology of MS on a population basis; (ii) the familial aggregation of MS is genetic; (iii) maternal factors do not influence the risk for siblings to develop MS; and (iv) MS appears to be oligogenic. The present paper describes the rationale and methodology for the CCPGSMS-Phase 2.

Methods:

The CCPGSMS-Phase 2 is a nation-wide collaborative effort involving all the 15 Canadian MS clinics. A series of structured questionnaires is administered to MS index cases, spouse controls and mothers of index cases and spouse controls (if available) by trained interviewers. Blood samples are taken for molecular genetic studies. This national effort is coordinated by the MS Clinics in Vancouver and London.

Results:

The CCPGSMS-Phase 2 is in progress so specific results are not available. The study is designed to (i) increase the database for genetic epidemiological/molecular genetic research and (ii) gather population-based data to further our understanding of the non-genetic factors in the etiology of MS.

Conclusions:

It is anticipated that the results from this study will impact on the eventual prevention, cure and treatment of MS.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 25 , Issue 3 , August 1998 , pp. 216 - 221
Copyright
Copyright © Canadian Neurological Sciences Federation 1998

References

REFERENCES

1.Ebers, GC, Sadovnick, AD, Risch, NJ and the Canadian Collaborative Study Group. Familial aggregation in multiple sclerosis is genetic. Nature 1995; 377: 150–151.Google ScholarPubMed
2.Sadovnick, AD, Ebers, GC, Dyment, D, et al. Evidence for the genetic basis of multiple sclerosis. Lancet 1996; 347: 1728–1730.CrossRefGoogle ScholarPubMed
3.Ebers, GC, Kukay, K, Bulman, DE, et al. A full genome search in multiple sclerosis. Nature Genet 1996; 13: 472–476.CrossRefGoogle ScholarPubMed
4.Ebers, GC, Bulman, DE, Sadovnick, AD, et al. A population-based twin study in multiple sclerosis. N Engl J Med 1986; 315: 1638–1642.CrossRefGoogle Scholar
5.Sadovnick, AD, Armstrong, H, Rice, GPA, et al. A population-based study of multiple sclerosis in twins: update. Ann Neurol 1993; 33: 281–285.CrossRefGoogle ScholarPubMed
6.Mumford, CJ, Wood, NW, Kellar-Wood, H, et al. The British Isles survey of multiple sclerosis in twins. Neurology 1994; 44: 11–15.CrossRefGoogle ScholarPubMed
7.Sadovnick, AD, Baird, PA, Ward, RH. Multiple sclerosis: Updated risks for relatives. Am J Med Genet 1988; 29: 533–541.CrossRefGoogle ScholarPubMed
8.Carton, H, Vlietinck, R, Debruyne, J, et al. Risks of multiple sclerosis in relatives of patients in Flanders, Belgium. J Neurol Neurosurg Psychiatry 1997; 62: 329–333.Google Scholar
9.Robertson, NM, Fraser, M, Deans, J, et al. Age-adjusted recurrence risks for relatives of patients with multiple sclerosis. Brain 1996; 119: 449–455.CrossRefGoogle ScholarPubMed
10.Sawcer, S, Jones, HB, Feakes, R, et al. A genome screen in multiple sclerosis reveals susceptibility on chromosome 6p21 and 17q22. Nature Genet 1996; 13: 464–468.CrossRefGoogle ScholarPubMed
11.The Multiple Sclerosis Genetics Group. Complete genomic screen for multiple sclerosis underscores a role for the major histocompatibility complex. Nature Genet 1996; 13: 469–471.CrossRefGoogle Scholar
12.Robertson, NP, O’Riordan, J, Clayton, D, et al. Conjugal multiple sclerosis. J Neurol 1995; 242: S8.Google Scholar
13.Sibley, WA, Bamford, CR, Clark, K. Triggering factors in multiple sclerosis. In: Poser, CM, Paty, DW, Scheinberg, L, et al., eds. The Diagnosis of Multiple Sclerosis. New York: Thieme-Stratton Inc., 1984; chap 2, 15.Google Scholar
14.Ebers, GC, Sadovnick, AD. Epidemiology. In: Paty, DE, Ebers, GC, eds. Multiple Sclerosis. Philadephia: FA Davis Company, 1997; chap 2, 16–17.Google Scholar
15.Poser, CM, Paty, DW, Scheinberg, L, et al. New diagnostic criteria for multiple sclerosis: Guidelines for research protocols. Ann Neurol 1983; 13: 227–231.CrossRefGoogle ScholarPubMed
16.Kurtzke, JF. Rating neurological impairment in multiple sclerosis: an expanded disability status scale (EDSS). Neurology 1983; 33: 1444–1452.CrossRefGoogle Scholar