Apolipoproteína E e Doença de Alzheimer

Autores

  • Denise Prado formação acadêmica, Mestre em Ciências Farmacêuticas, Faculdade de Ciências da Saúde, Universidade Fernando Pessoa, Porto, Portugal.
  • Inês Lopes Cardoso Bioquímico, Professor Associado, Faculdade de Ciências da Saúde, Universidade Fernando Pessoa, Porto, Portugal.

DOI:

https://doi.org/10.34024/rnc.2013.v21.8211

Palavras-chave:

Apolipoproteína E,, Doença de Alzheimer, Demência, Fatores de Risco, Alelos da APOE

Resumo

Contexto. A doença de Alzheimer (DA) é uma demência que afe­ta indivíduos tanto em idades avançadas como em idades precoces. Trata-se de uma doença resultante de perdas das funções neuronais cognitivas que envolve principalmente a memória. Objetivo. Neste artigo pretende-se fazer uma breve revisão bibliográfica sobre o pa­pel da apolipoproteína E (apoE) como fator de risco genético para o desenvolvimento de DA. Método. Para tal foi realizada uma revisão sistemática da literatura existente sobre o tema, tendo sido revistos 72 artigos científicos entre 1972 e 2007. Foram efetuadas pesquisas nos motores de busca da PubMed, B-on, Google Acadêmico, Me­dline e Science Direct, utilizando os unitermos: “apolipoprotein E” e “Alzheimer’s disease”. Resultados. Como resultados desta pesqui­sa verificou-se existir influência da apoE na acumulação do péptido β-amilóide e consequentemente na patogénese da DA. Foi ainda possível relacionar a presença dos diversos alelos codificantes da apoE (com localização 19q13.2) e suas combinações com um melhor ou pior prognóstico para o desenvolvimento de DA, sendo o alelo ε4 o responsável pelo aumento do risco de desenvolvimento precoce de DA. Conclusão. No entanto, esta apolipoproteína não é em si sufi­ciente para causar DA, mas promove o aumento do risco do indivíduo vir a desenvolver a doença.

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2013-03-31

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Prado, D., & Cardoso, I. L. (2013). Apolipoproteína E e Doença de Alzheimer. Revista Neurociências, 21(1), 118–125. https://doi.org/10.34024/rnc.2013.v21.8211

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Revisão de Literatura
Recebido: 2019-02-23
Publicado: 2013-03-31