Psychological aspects of pre-symptomatic testing for Machado–Joseph disease and familial amyloid polyneuropathy type I

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Miniatura
Data
2006
Autores
Rolim, Luísa
Leite, Ângela
Lêdo, S.
Paneque, M.
Sequeiros, J.
Fleming, Manuela
Título da revista
ISSN da revista
Título do Volume
Editora
Clin Genet
Resumo
Machado–Joseph disease [MJD, also spinocerebellar ataxia type 3 (SCA3)] and familial amyloid polyneuropathy type I (FAP-I or ATTR V30M) are neurodegenerative disorders, inherited in an autosomal dominant fashion, which have a high prevalence in Portugal, probably due to a founder effect. MJD and FAP-I are late-onset diseases, with symptoms emerging usually during adulthood. CGPP, which is the national reference centre for these disorders, has a genetic lab that offers diagnostic, pre-symptomatic and prenatal testing and an outpatient clinic to counsel and follow relatives at risk for hereditary ataxias, FAP- I and Huntington disease (HD). The present work is a review of our 10- year experience with psychological counselling of individuals at risk for MJD and FAP-I. Persons at risk for FAP-I may show a better response to pre-symptomatic testing than those who are at risk for MJD and HD because of the availability of liver transplantation, which may improve their health and life expectancy. Psychological well-being and specific distress of MJD and FAP-I test applicants, before undergoing genetic testing (baseline level) and 3 to 6 months after disclosure of test results, have shown a low level of change, both in identified carriers and non-carriers. A major goal of psychological characterization of at-risk individuals for MJD and FAP-I is to determine the factors that influence the uptake of genetic testing.
Descrição
Palavras-chave
familial amyloidosis, genetic counselling, genetic testing, hereditary ataxias, psychosocial genetics
Citação
Rolim L, Leite Aˆ , Leˆ do S, Paneque M, Sequeiros J, Fleming M. Psychological aspects of pre-symptomatic testing for Machado–Joseph disease and familial amyloid polyneuropathy type I. Clin Genet 2006: 69: 297–305. # Blackwell Munksgaard, 2006