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Age at onset of multiple sclerosis may be influenced by place of residence during childhood rather than ancestry.

https://arctichealth.org/en/permalink/ahliterature170585
Source
Neuroepidemiology. 2006;26(3):162-7
Publication Type
Article
Date
2006
Author
J. Kennedy
P. O'Connor
A D Sadovnick
M. Perara
I. Yee
B. Banwell
Author Affiliation
The Hospital for Sick Children, University of Toronto, Toronto, Ont. L5M 4A7, Canada.
Source
Neuroepidemiology. 2006;26(3):162-7
Date
2006
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age of Onset
Aged
Asia - ethnology
Caribbean Region - ethnology
Child
Child, Preschool
Cohort Studies
Emigration and Immigration
Europe - ethnology
Humans
Middle Aged
Multiple Sclerosis - epidemiology
Ontario - epidemiology
Residence Characteristics
Risk factors
Abstract
Multiple sclerosis (MS) most commonly affects individuals of Northern European descent who live in countries at high latitude. The relative contributions of ancestry, country of birth and residence as determinants of MS risk have been studied in adult MS, but have not been explored in the pediatric MS population. In this study, we compare the demographics of pediatric- and adult-onset MS patients cared for in Toronto, Ontario, Canada, a multicultural region. The country of birth, residence during childhood, and ancestry were compared for 44 children and 573 adults. Our results demonstrate that although both the pediatric and adult cohorts were essentially born and raised in the same region of Ontario, Canada, children with MS were more likely to report Caribbean, Asian or Middle Eastern ancestry, and were less likely to have European heritage compared with individuals with adult-onset MS. The difference in ancestry between the pediatric and adult MS cohorts can be explained by two hypotheses: (1) individuals raised in a region of high MS prevalence, but whose ancestors originate from regions in which MS is rare, have an earlier age of MS onset, and (2) the place of residence during childhood, irrespective of ancestry, determines lifetime MS risk -- a fact that will be reflected in a change in the demographics of the adult MS cohort in our region as Canadian-raised children of recent immigrants reach the typical age of adult-onset MS.
PubMed ID
16493204 View in PubMed
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Incidence of acquired demyelination of the CNS in Canadian children.

https://arctichealth.org/en/permalink/ahliterature153073
Source
Neurology. 2009 Jan 20;72(3):232-9
Publication Type
Article
Date
Jan-20-2009
Author
B. Banwell
J. Kennedy
D. Sadovnick
D L Arnold
S. Magalhaes
K. Wambera
M B Connolly
J. Yager
J K Mah
N. Shah
G. Sebire
B. Meaney
M-E Dilenge
A. Lortie
S. Whiting
A. Doja
S. Levin
E A MacDonald
D. Meek
E. Wood
N. Lowry
D. Buckley
C. Yim
M. Awuku
C. Guimond
P. Cooper
F. Grand'Maison
J B Baird
V. Bhan
A. Bar-Or
Author Affiliation
Research Institute, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, M5G 1X8 Canada. brenda.banwell@sickkids.ca
Source
Neurology. 2009 Jan 20;72(3):232-9
Date
Jan-20-2009
Language
English
Publication Type
Article
Keywords
Adolescent
Age Distribution
Canada - epidemiology
Central Nervous System Diseases - diagnosis - drug therapy - epidemiology
Child
Child, Preschool
Demography
Demyelinating Diseases - diagnosis - drug therapy - epidemiology
Encephalomyelitis, Acute Disseminated - epidemiology
Female
Glucocorticoids - administration & dosage
Humans
Immunoglobulins, Intravenous - therapeutic use
Incidence
Infant
Injections, Intravenous
Magnetic Resonance Imaging
Male
Methylprednisolone - administration & dosage
Myelitis, Transverse - epidemiology
Optic Neuritis - epidemiology
Sex Distribution
Abstract
The incidence of acquired demyelination of the CNS (acquired demyelinating syndromes [ADS]) in children is unknown. It is important that physicians recognize the features of ADS to facilitate care and to appreciate the future risk of multiple sclerosis (MS).
To determine the incidence, clinical features, familial autoimmune history, and acute management of Canadian children with ADS.
Incidence and case-specific data were obtained through the Canadian Pediatric Surveillance Program from April 1, 2004, to March 31, 2007. Before study initiation, a survey was sent to all pediatric health care providers to determine awareness of MS as a potential outcome of ADS in children.
Two hundred nineteen children with ADS (mean age 10.5 years, range 0.66-18.0 years; female to male ratio 1.09:1) were reported. The most common presentations were optic neuritis (ON; n = 51, 23%), acute disseminated encephalomyelitis (ADEM; n = 49, 22%), and transverse myelitis (TM; n = 48, 22%). Children with ADEM were more likely to be younger than 10 years, whereas children with monolesional ADS (ON, TM, other) were more likely to be older than 10 years (p
PubMed ID
19153370 View in PubMed
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Narrowing in on the causative defect of an intriguing X-linked myopathy with excessive autophagy.

https://arctichealth.org/en/permalink/ahliterature188829
Source
Neurology. 2002 Aug 27;59(4):596-601
Publication Type
Article
Date
Aug-27-2002
Author
B A Minassian
R. Aiyar
S. Alic
B. Banwell
M. Villanova
M. Fardeau
J W Mandell
V C Juel
M. Rafii
M. Auranen
H. Kalimo
Author Affiliation
Division of Neurology, Department of Paediatrics, Hospital for Sick Children and University of Toronto, Ontario, Canada. bminass@sickkids.ca
Source
Neurology. 2002 Aug 27;59(4):596-601
Date
Aug-27-2002
Language
English
Publication Type
Article
Keywords
Adolescent
Autophagy - genetics
Calcium - metabolism
Child
Complement Membrane Attack Complex - biosynthesis
DNA Mutational Analysis
Finland - epidemiology
France - epidemiology
Genetic Linkage
Genetic markers
Humans
Male
Microsatellite Repeats
Muscle, Skeletal - metabolism - pathology
Muscular Diseases - diagnosis - epidemiology - genetics - pathology
Physical Chromosome Mapping
United States - epidemiology
X Chromosome - genetics
Abstract
X-Linked myopathy with excessive autophagy (XMEA) is a childhood-onset slowly progressive disease of skeletal muscle with no cardiac, nervous system, or other organ involvement. Pathology is distinctive: membrane-bound autophagic vacuoles, multifold reduplication of the basement membrane, and intense deposition of membrane attack complex and calcium at the myofiber surface. XMEA has been linked to the most telomeric 10.5 cM of Xq28. The authors now report identification of new families, refinement of the locus, mapping of genes to the region, and screening of candidate genes for mutations.
Seven new families were ascertained, including an American family with XMEA. Using 11 new microsatellite genetic markers, the authors fine-mapped a recombination in this family and a common ancestral haplotype in two French families, which localized the gene in a 4.37-Mb region. Sequence data were assembled from public and private databases and a near-continuous sequence derived for the entire region. With this sequence, a gene map of 82 genes and 28 expressed sequence tag clusters was constructed; to date, 12 candidate genes have been screened for mutations.
This study doubles the number of reported families with XMEA and more firmly establishes its distinctive clinicopathologic features. It also advances the search for the XMEA causative defect by reducing the disease locus to approximately half its previous size, assembling an almost complete sequence of the refined region, identifying all known genes in this sequence, and excluding the presence of mutations in 10% of these genes.
PubMed ID
12196656 View in PubMed
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