Founder Effects of Spinocerebellar Ataxias in the American Continents and the Caribbean.

Founder effects Latin America and the Caribbean MJD Machado-Joseph disease Prevalence SCA10 SCA2 SCA3 SCA7 Spinocerebellar ataxia Spinocerebellar ataxia type 10 Spinocerebellar ataxia type 2 Spinocerebellar ataxia type 3 Spinocerebellar ataxia type 7

Journal

Cerebellum (London, England)
ISSN: 1473-4230
Titre abrégé: Cerebellum
Pays: United States
ID NLM: 101089443

Informations de publication

Date de publication:
Jun 2020
Historique:
pubmed: 23 2 2020
medline: 16 3 2021
entrez: 23 2 2020
Statut: ppublish

Résumé

Spinocerebellar ataxias (SCAs) comprise a heterogeneous group of autosomal dominant disorders. The relative frequency of the different SCA subtypes varies broadly among different geographical and ethnic groups as result of genetic drifts. This review aims to provide an update regarding SCA founders in the American continents and the Caribbean as well as to discuss characteristics of these populations. Clusters of SCAs were detected in Eastern regions of Cuba for SCA2, in South Brazil for SCA3/MJD, and in Southeast regions of Mexico for SCA7. Prevalence rates were obtained and reached 154 (municipality of Báguano, Cuba), 166 (General Câmara, Brazil), and 423 (Tlaltetela, Mexico) patients/100,000 for SCA2, SCA3/MJD, and SCA7, respectively. In contrast, the scattered families with spinocerebellar ataxia type 10 (SCA10) reported all over North and South Americas have been associated to a common Native American ancestry that may have risen in East Asia and migrated to Americas 10,000 to 20,000 years ago. The comprehensive review showed that for each of these SCAs corresponded at least the development of one study group with a large production of scientific evidence often generalizable to all carriers of these conditions. Clusters of SCA populations in the American continents and the Caribbean provide unusual opportunity to gain insights into clinical and genetic characteristics of these disorders. Furthermore, the presence of large populations of patients living close to study centers can favor the development of meaningful clinical trials, which will impact on therapies and on quality of life of SCA carriers worldwide.

Identifiants

pubmed: 32086717
doi: 10.1007/s12311-020-01109-7
pii: 10.1007/s12311-020-01109-7
doi:

Substances chimiques

ATXN10 protein, human 0
ATXN2 protein, human 0
Ataxin-10 0
Ataxin-2 0
Repressor Proteins 0
ATXN3 protein, human EC 3.4.19.12
Ataxin-3 EC 3.4.19.12

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

446-458

Subventions

Organisme : CONACyT
ID : 258043
Organisme : CONACyT
ID : A1-S-10669

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Auteurs

Roberto Rodríguez-Labrada (R)

Centre for the Research and Rehabilitation of Hereditary Ataxias, 80100, Holguín, Cuba.

Ana Carolina Martins (AC)

Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, 91540-070, Brazil.

Jonathan J Magaña (JJ)

Department of Genetics, Laboratory of Genomic Medicine, National Rehabilitation Institute (INR-LGII), 14389, Mexico City, Mexico.

Yaimeé Vazquez-Mojena (Y)

Centre for the Research and Rehabilitation of Hereditary Ataxias, 80100, Holguín, Cuba.

Jacqueline Medrano-Montero (J)

Centre for the Research and Rehabilitation of Hereditary Ataxias, 80100, Holguín, Cuba.

Juan Fernandez-Ruíz (J)

Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autonoma de Mexico, 04510, Mexico City, Mexico.

Bulmaro Cisneros (B)

Department of Genetics and Molecular Biology, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360, Mexico City, Mexico.

Helio Teive (H)

Movement Disorders Unit, Neurology Service, Internal Medicine Department, Hospital de Clínicas Federal University of Paraná, Curitiba, PR, 80240-440, Brazil.

Karen N McFarland (KN)

University of Florida, Gainesville, Florida, 32610, USA.

Maria Luiza Saraiva-Pereira (ML)

Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, 91540-070, Brazil.
Hospital de Clínicas de Porto Alegre (HCPA), Porto Alegre, RS, 90035-903, Brazil.
Departamento de Bioquímica, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, 90035-903, Brazil.

César M Cerecedo-Zapata (CM)

Department of Genetics, Laboratory of Genomic Medicine, National Rehabilitation Institute (INR-LGII), 14389, Mexico City, Mexico.
Rehabilitation and Social Inclusion Center of Veracruz (CRIS-DIF), Xalapa, 91070, Veracruz, Mexico.

Christopher M Gomez (CM)

Department of Neurology, The University of Chicago, Chicago, 60637, USA.

Tetsuo Ashizawa (T)

Program of Neuroscience, Houston Methodist Research Institute, Houston, TX, 77030, USA.

Luis Velázquez-Pérez (L)

Centre for the Research and Rehabilitation of Hereditary Ataxias, 80100, Holguín, Cuba. velazq63@gmail.com.
Cuban Academy of Sciences, 10100, La Havana, Cuba. velazq63@gmail.com.

Laura Bannach Jardim (LB)

Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, 91540-070, Brazil.
Hospital de Clínicas de Porto Alegre (HCPA), Porto Alegre, RS, 90035-903, Brazil.
Departamento de Medicina Interna, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, 90035-903, Brazil.

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