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Age of onset in siblings concordant for multiple sclerosis.

https://arctichealth.org/en/permalink/ahliterature226576
Source
Brain. 1991 Apr;114 ( Pt 2):937-50
Publication Type
Article
Date
Apr-1991
Author
D E Bulman
A D Sadovnick
G C Ebers
Author Affiliation
Multiple Sclerosis Clinic, University of Western Ontario, London, Canada.
Source
Brain. 1991 Apr;114 ( Pt 2):937-50
Date
Apr-1991
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
British Columbia
Diseases in Twins
Female
Humans
Male
Middle Aged
Multiple Sclerosis - genetics - physiopathology
Nuclear Family
Ontario
Regression Analysis
Time Factors
Twins, Monozygotic
Abstract
We have evaluated genetic and environmental influences in multiple sclerosis (MS) by comparing age of onset in 99 sibling pairs concordant for the disease. We used three methods of analysis: (1) comparison of mean differences in age of onset and year of onset, (2) linear regression of differences in age or year of onset vs difference in ages, and (3) intraclass correlation of age of onset which is also used for monozygotic twins concordant for MS. Comparison of the mean differences in age of onset or year of onset is found to be inappropriate and potentially misleading. No significant results were found in linear regression of the age of onset or year of onset vs differences in ages, although a trend towards onset at the same age is present. However, nontwin siblings show a significant intraclass correlation for age of onset (P less than 0.01) as is seen in genetic disorders. A stronger intraclass correlation in age of onset in concordant monozygotic twins vs concordant sibling pairs further suggests that age of onset is partly under genetic control, assuming common exposure to an environmental agent. The results give little support for common exposure to an environmental trigger in concordant MS sibling pairs. They are consistent with a mixture of random independent exposures and common exposures leading to the development of the disease, with the former predominating.
PubMed ID
2043958 View in PubMed
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Association between microchimerism and multiple sclerosis in Canadian twins.

https://arctichealth.org/en/permalink/ahliterature168314
Source
J Neuroimmunol. 2006 Oct;179(1-2):145-51
Publication Type
Article
Date
Oct-2006
Author
Cristen J Willer
Blanca M Herrera
Katie M E Morrison
A D Sadovnick
George C Ebers
Author Affiliation
Department of Clinical Neurology, University of Oxford, Oxford, UK.
Source
J Neuroimmunol. 2006 Oct;179(1-2):145-51
Date
Oct-2006
Language
English
Publication Type
Article
Keywords
Canada
Chimerism
Diseases in Twins
Female
Humans
Male
Multiple Sclerosis - genetics
Pedigree
Polymerase Chain Reaction
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Abstract
Microchimerism, the persistence of foreign cells thought to derive from previous pregnancies, has been associated with autoimmune diseases. A maternal parent-of-origin effect in MS remains unexplained. We tested for microchimerism in monozygotic and dizygotic twin-pairs with MS. Microchimerism was associated with MS in affected females from monozygotic concordant pairs when compared to both affected (p=0.020) and unaffected (p=0.025) females in monozygotic discordant pairs. Microchimerism was increased in affected females of dizygotic discordant pairs (p=0.059). The rate of microchimerism was significantly higher in affected twins than in unaffected co-twins (p=0.0059). These observations show an association in twins between the presence of microchimerism and having MS.
PubMed ID
16843535 View in PubMed
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Characterizing neuropsychiatric symptoms in subjects referred to dementia clinics.

https://arctichealth.org/en/permalink/ahliterature170506
Source
Neurology. 2006 Feb 28;66(4):523-8
Publication Type
Article
Date
Feb-28-2006
Author
K R Peters
K. Rockwood
S E Black
R. Bouchard
S. Gauthier
D. Hogan
A. Kertesz
I. Loy-English
B L Beattie
A D Sadovnick
H H Feldman
Author Affiliation
Department of Psychology, Trent University, Peterborough, Ontario, Canada.
Source
Neurology. 2006 Feb 28;66(4):523-8
Date
Feb-28-2006
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Canada
Cognition Disorders - classification - physiopathology
Cohort Studies
Dementia - classification - physiopathology
Educational Status
Female
Humans
Longitudinal Studies
Male
Mental Disorders - classification - physiopathology
Middle Aged
Neuropsychological Tests
Abstract
To characterize the neuropsychiatric symptoms (NPS) of subjects classified as not cognitively impaired (NCI), cognitively impaired-not demented (CIND), and dementia.
A Canadian Cohort Study of Cognitive Impairment and Related Dementias (ACCORD) is a longitudinal investigation of individuals referred to eight Canadian dementia centers for evaluation of cognitive impairment and neurobehavioral symptoms. Of the inception cohort of 804 subjects for whom the informant-based Neuropsychiatric Inventory (NPI) was completed at study entry, 35 were classified as NCI, 193 as CIND, and 576 as dementia. The three diagnostic groups were compared on each of the 12 NPI items. Within each diagnostic group, comparisons were also made between symptomatic (NPS+; total score > 1) and asymptomatic (NPS-; total score = 0) subjects on measures of general cognitive status and functional disability. A subset of the NCI and CIND individuals were also compared on a comprehensive neuropsychological test battery.
There was at least one NPI item reported in 60% of subjects with NCI, 74% with CIND, and 89% with dementia. The item scores for delusions, hallucinations, agitation, apathy, disinhibition, aberrant motor behavior, and problems with appetite were greater in dementia subjects than in NCI or CIND. There were no significant differences between subjects with NCI and CIND on any NPI item. For each diagnostic group, NPS+ subjects were more impaired on functional but not neuropsychological measures.
Across all levels of cognition, neuropsychiatric symptoms (NPS) are an important feature in individuals referred to dementia clinics. The current data suggest that NPS may precede cognitive deficits in individuals classified as not cognitively impaired and cognitively impaired-not demented.
PubMed ID
16505306 View in PubMed
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Conjugal multiple sclerosis: population-based prevalence and recurrence risks in offspring. Canadian Collaborative Study Group.

https://arctichealth.org/en/permalink/ahliterature196335
Source
Ann Neurol. 2000 Dec;48(6):927-31
Publication Type
Article
Date
Dec-2000
Author
G C Ebers
I M Yee
A D Sadovnick
P. Duquette
Author Affiliation
Department of Clinical Neurology, University of Oxford, UK.
Source
Ann Neurol. 2000 Dec;48(6):927-31
Date
Dec-2000
Language
English
Publication Type
Article
Keywords
Adult
Canada - epidemiology
Female
Humans
Male
Multiple Sclerosis - epidemiology - genetics - physiopathology
Prevalence
Recurrence
Risk
Abstract
From a population-based sample of 15,504 patients attending Canadian multiple sclerosis (MS) clinics, we have determined the frequency of conjugal MS and have estimated the recurrence risk in offspring of such matings. Twenty-three MS cases were found among 13,550 spouses of study probands for a crude conjugal rate of 0.17% (95% CI of 0.10%-0.24%). Despite ascertainment bias that expectedly inflates this number, this is a frequency intermediate between the point prevalence (0.1%) and lifetime risk (0.2%) for the general population and close to an order of magnitude less than reported for half siblings reared apart (1.06%) from the same population. Six of the 49 offspring of conjugal pairs also had MS, and age conversion gives a rate similar to the concordance rate for Canadian monozygotic twins. However, this correction may not be appropriate in this special case. Despite an ascertainment bias in favor of recognizing affected spouses and a large population sample, the common environment in adulthood shared by spousal pairs could not be shown to increase the risk of conjugal MS. Although the high recurrence rate in offspring is similarly subject to an upward bias, the low risk for MS spouses and the high risk for offspring support other data indicating that familial risk is genetically determined. Furthermore, these results imply that susceptibility alleles are shared by unrelated individuals with the disease.
Notes
Comment In: Ann Neurol. 2001 Oct;50(4):552-311601510
PubMed ID
11117550 View in PubMed
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Evidence for genetic basis of multiple sclerosis. The Canadian Collaborative Study Group.

https://arctichealth.org/en/permalink/ahliterature211670
Source
Lancet. 1996 Jun 22;347(9017):1728-30
Publication Type
Article
Date
Jun-22-1996
Author
A D Sadovnick
G C Ebers
D A Dyment
N J Risch
Author Affiliation
Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada.
Source
Lancet. 1996 Jun 22;347(9017):1728-30
Date
Jun-22-1996
Language
English
Publication Type
Article
Keywords
Canada - epidemiology
Family
Female
Humans
Male
Multiple Sclerosis - epidemiology - genetics
Risk factors
Abstract
BACKGROUND Increased familial risks in multiple sclerosis (MS) range from 300-fold for monozygotic twins to 20-40-fold for biological first-degree relatives, suggesting a genetic influence. Yet if one identical twin has MS the other usually will not. One way of sorting out the contributions of genes and environment is to study half-sibs. METHODS In a Canadian population-based sample of 16 000 MS cases seen at 14 regional MS clinics one half-sib (or more) was reported by 939 index cases. By interview we elicited information on family structure and an illness in half-sibs and any full brothers or sisters. FINDINGS The age-adjusted MS rate in the 1839 half-sibs of these index cases was 1.32 percent compared with 3.46 percent for the 1395 full sibs of the same cases (p
PubMed ID
8656905 View in PubMed
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Familial risks for Alzheimer disease from a population-based series.

https://arctichealth.org/en/permalink/ahliterature219490
Source
Genet Epidemiol. 1994;11(4):365-74
Publication Type
Article
Date
1994
Author
C. Hirst
I M Yee
A D Sadovnick
Author Affiliation
Department of Medical Genetics, University Hospital-UBC Site, University of British Columbia, Vancouver, Canada.
Source
Genet Epidemiol. 1994;11(4):365-74
Date
1994
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alzheimer Disease - diagnosis - epidemiology - genetics
Bias (epidemiology)
British Columbia - epidemiology
Cross-Sectional Studies
Female
Genes, Dominant - genetics
Genetics, Population
Humans
Incidence
Longitudinal Studies
Male
Models, Genetic
Molecular Epidemiology
Morbidity
Pedigree
Population Surveillance
Proportional Hazards Models
Risk factors
Abstract
Kaplan-Meier risks estimates are calculated and compared for two consecutive series (N1 = 840, N2 = 819) of first-degree relatives of Alzheimer disease (AD) patients diagnosed as either "probable" or "autopsy-confirmed" AD. The consistency of results increases confidence in estimates and suggests consistent case ascertainment over 8 years. Lifetime risk estimates to age 88 for the combined sample (23.4% +/- 3.0%) do not approach the 50% risk compatible with an autosomal dominant model of transmission. These results support our previous finding and suggest that an autosomal dominant gene(s) is not responsible for all cases of AD.
PubMed ID
7813898 View in PubMed
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A genetic basis for familial aggregation in multiple sclerosis. Canadian Collaborative Study Group.

https://arctichealth.org/en/permalink/ahliterature214317
Source
Nature. 1995 Sep 14;377(6545):150-1
Publication Type
Article
Date
Sep-14-1995
Author
G C Ebers
A D Sadovnick
N J Risch
Author Affiliation
Department of Clinical Neurological Sciences, University of Western Ontario, London, Canada.
Source
Nature. 1995 Sep 14;377(6545):150-1
Date
Sep-14-1995
Language
English
Publication Type
Article
Keywords
Adoption
Adult
Canada - epidemiology
Child
Environment
Female
Genetic Testing
Humans
Longitudinal Studies
Male
Multiple Sclerosis - epidemiology - etiology - genetics
Prevalence
Abstract
Genetic-environmental interactions probably underlie spontaneous human autoimmune disorders, a category of complex traits thought to include multiple sclerosis (MS). The geographical distribution and familial aggregation of this disease have often been ascribed to the role of infectious agents, but there is no consensus. Increased family risks range from 300-fold for monozygotic twins to 20-40-fold for biological first-degree relatives over the general population prevalence of 0.1% (ref. 6). We screened a population-based sample of 15,000 individuals with MS by using standardized, personally administered questionnaires to identify adopted index cases and/or those who had adopted relatives. The frequency of MS among first-degree non-biological relatives living with the index case was no greater than expected from Canadian population prevalence data and significantly less than for biological relatives. These findings indicate that familial aggregation of MS is genetically determined: no effect of shared environment was detectable.
Notes
Comment In: Nature. 1995 Sep 14;377(6545):105-67675076
PubMed ID
7675080 View in PubMed
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Genetics of multiple sclerosis in British Columbia and throughout Canada.

https://arctichealth.org/en/permalink/ahliterature219323
Source
Ann Neurol. 1994;36 Suppl:S18-21
Publication Type
Article
Date
1994
Author
A D Sadovnick
Author Affiliation
Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
Source
Ann Neurol. 1994;36 Suppl:S18-21
Date
1994
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
British Columbia - epidemiology
Canada - epidemiology
Environment
Family
Female
Humans
Male
Middle Aged
Models, Genetic
Molecular Biology - trends
Multiple Sclerosis - epidemiology - etiology - genetics
Pedigree
Research Design
Abstract
Since the inception of the MS Clinic, Vancouver Hospital and Health Sciences Centre, all consecutive, unrelated patients with multiple sclerosis (MS) have had their family histories documented by the Clinic's geneticist as part of the overall assessment. The family histories are updated annually. These data, along with the longitudinal clinical information on each patient, have resulted in a unique resource for clinical genetic/genetic epidemiological/molecular genetic research on MS. Analyses of these data have included the calculation of age-adjusted familial risks for MS; genetic modeling, necessary for molecular genetic research; and family studies involving affected relative pairs, studies of the nontransmitted parental haplotypes, and multiplex families. The results of the work to date are discussed. In addition, the impact of these data on the development of the Canadian Collaborative Project on Genetic Susceptibility to Multiple Sclerosis is reviewed. This project involves all 14 MS "sites" across Canada, and the study's overall objective is to elucidate the roles of genetic and environmental factors in the causation of MS.
PubMed ID
8017882 View in PubMed
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Genetic susceptibility to MS: a second stage analysis in Canadian MS families.

https://arctichealth.org/en/permalink/ahliterature193481
Source
Neurogenetics. 2001 Jul;3(3):145-51
Publication Type
Article
Date
Jul-2001
Author
D A Dyment
C J Willer
B. Scott
H. Armstrong
A. Ligers
J. Hillert
D W Paty
S. Hashimoto
V. Devonshire
J. Hooge
L. Kastrukoff
J. Oger
L. Metz
S. Warren
W. Hader
C. Power
A. Auty
A. Nath
R. Nelson
M. Freedman
D. Brunet
J E Paulseth
G. Rice
P. O'Connor
P. Duquette
Y. Lapierre
G. Francis
J P Bouchard
T J Murray
V. Bhan
C. Maxner
W. Pryse-Phillips
M. Stefanelli
A D Sadovnick
N. Risch
G C Ebers
Author Affiliation
The Wellcome Trust Center for Human Genetics, Oxford, UK.
Source
Neurogenetics. 2001 Jul;3(3):145-51
Date
Jul-2001
Language
English
Publication Type
Article
Keywords
Canada
Family
Female
Genetic Linkage
Genetic markers
Genetic Predisposition to Disease
Genome, Human
HLA-DR Antigens - genetics
HLA-DRB1 Chains
Humans
Linkage Disequilibrium
Male
Multiple Sclerosis - genetics
Nuclear Family
Software
Abstract
Four published genome screens have identified a number of markers with increased sharing in multiple sclerosis (MS) families, although none has reached statistical significance. One hundred and five markers previously identified as showing increased sharing in Canadian, British, Finnish, and American genome screens were genotyped in 219 sibling pairs ascertained from the database of the Canadian Collaborative Project on Genetic Susceptibility to MS (CCPGSMS). No markers examined met criteria for significant linkage. Markers located at 5p14 and 17q22 were analyzed in a total of 333 sibling pairs and attained mlod scores of 2.27 and 1.14, respectively. The known HLA Class II DRB1 association with MS was confirmed (P
PubMed ID
11523565 View in PubMed
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A genome survey indicates a possible susceptibility locus for bipolar disorder on chromosome 22.

https://arctichealth.org/en/permalink/ahliterature196145
Source
Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):585-90
Publication Type
Article
Date
Jan-16-2001
Author
J R Kelsoe
M A Spence
E. Loetscher
M. Foguet
A D Sadovnick
R A Remick
P. Flodman
J. Khristich
Z. Mroczkowski-Parker
J L Brown
D. Masser
S. Ungerleider
M H Rapaport
W L Wishart
H. Luebbert
Author Affiliation
Department of Psychiatry, University of California at San Diego, La Jolla, CA 92093, USA,
Source
Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):585-90
Date
Jan-16-2001
Language
English
Publication Type
Article
Keywords
Bipolar Disorder - classification - epidemiology - genetics
British Columbia - epidemiology
California - epidemiology
Chromosome Mapping
Chromosomes, Human, Pair 10 - genetics
Chromosomes, Human, Pair 13 - genetics
Chromosomes, Human, Pair 21 - genetics
Chromosomes, Human, Pair 22 - genetics
Chromosomes, Human, Pair 3 - genetics
Chromosomes, Human, Pair 5 - genetics
Female
Genetic Predisposition to Disease
Genome, Human
Genotype
Humans
Lod Score
Male
Microsatellite Repeats
Polymerase Chain Reaction
Schizophrenia - epidemiology - genetics
Abstract
Bipolar disorder or manic depressive illness is a major psychiatric disorder that is characterized by fluctuation between two abnormal mood states. Mania is accompanied by symptoms of euphoria, irritability, or excitation, whereas depression is associated with low mood and decreased motivation and energy. The etiology is currently unknown; however, numerous family, twin, and adoption studies have argued for a substantial genetic contribution. We have conducted a genome survey of bipolar disorder using 443 microsatellite markers in a set of 20 families from the general North American population to identify possible susceptibility loci. A maximum logarithm of odds score of 3.8 was obtained at D22S278 on 22q. Positive scores were found spanning a region of nearly 32 centimorgans (cM) on 22q, with a possible secondary peak at D22S419. Six other chromosomal regions yielded suggestive evidence for linkage: 3p21, 3q27, 5p15, 10q, 13q31-q34, and 21q22. The regions on 22q, 13q, and 10q have been implicated in studies of schizophrenia, suggesting the possible presence of susceptibility genes common to both disorders.
Notes
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PubMed ID
11149935 View in PubMed
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28 records – page 1 of 3.