Ciência Diária » Por que os sintomas da esquizofrenia surgem após a adolescência?

Por que os sintomas da esquizofrenia surgem após a adolescência?

Submitted by Ciência Diária on Wednesday, 3 March 201087 Comentários

Há tempos médicos se perguntam por que a esquizofrenia, um transtorno psíquico grave que afeta mais de 50 milhões de pessoas no mundo, geralmente começa a manifestar os sintomas na passagem entre a adolescência e a fase adulta. Dois novos estudos conduzidos por pesquisadores do Johns Hopkins, nos EUA, parecem ter descoberto a resposta, identificando o mecanismo de duas anormalidades cerebrais.

Anormalidades no cérebro relacionadas à esquizofrenia são influenciadas por um gene conhecido como DISC1.

As anormalidades no cérebro relacionadas à doença são influenciadas por um gene conhecido como DISC1. Em um experimento com ratos, os pesquisadores examinaram como ele atua na formação de conexões de células nervosas do cérebro, já que uma das explicações para o distúrbio é a anormalidade destes processos (na adolescência, há reorganização deste sistema, o que implica em partes o aparecimento dos sintomas). A maior atividade do gene foi, como se supunha, nas células nervosas. Ao desativar parcialmente a atividade do DISC1, observaram a redução em número e tamanho das espinhas dendríticas, extensões para a entrada de outras células nervosas.

Para determinar como o DISC1 regula a formação da espinha dendrítica, os pesquisadores estudaram proteínas cerebrais que interagem com a proteína expressa pelo gene. Eles identificaram a Kal-7 que, em estudos anteriores, mostrou-se fundamental para a correta formação das espinhas. Outros experimentos sugerem que a proteína DISC1 atua como local de armazenamento temporário para a Kal-7, até que possa ser liberada para desencadear uma série molecular que resulte na formação da espinha dendrítica.

A presença de um gene defeituoso DISC1 pode, assim, resultar em ligações fracas entre as células nervosas e neurônios vizinhos. Esta anormalidade já foi identifica em autópsias de cérebros de pacientes com esquizofrenia. Embora a ligação e quebra de ligações ocorram no decorrer de uma vida, esta “poda” pode ocorrer na adolescência. Uma grande quantidade de desligamentos nesta fase pode ser uma das razões para o surgimento dos sintomas da esquizofrenia.

Um estudo anterior usou um modelo animal para a esquizofrenia, desligando temporariamente o gene DISC1 no córtex pré-frontal de camundongos, uma região que é distinta em pessoas com esquizofrenia. O experimento permitiu observar outras funções do gene no cérebro.

Os pesquisadores então injetaram peças curtas de ácidos nucleicos, projetados para desligar o gene DISC1 em cavidades dos cérebros em desenvolvimento de ratos concebidos duas semanas antes. Os testes mostraram que aqueles trechos de RNA migraram para as células do córtex pré-frontal, parte do cérebro próximo à testa.

A desativação foi temporária, com a função do gene totalmente restaurada após três semanas. O gene foi reativado diversas vezes, mostrando aos cientistas diferenças entre atividades cerebrais de animais “normais” e “doentes”.

A equipe constatou que no grupo cujo gene DISC1 havia sido desativado as células nervosas do córtex pré-frontal – que produzem dopamina, um dos sinais químicos que as células nervosas usam para se comunicar – estavam muito imaturas durante a adolescência. Além disso, os animais apresentaram sinais de um déficit de interneurônios, as células nervosas que conectam os neurônios em outras vias neurais.

Eles também identificaram várias diferenças no comportamento dos ratos, em comparação com os animais saudáveis que entravam na adolescência. Por exemplo: o grupo com gene desativado reagiu mais a estimulantes, movimentando-se mais do que o resto. Curiosamente, os efeitos foram ligeiramente atenuados quando os pesquisadores deram clozapina aos animais, uma droga usada para tratar a esquizofrenia.

Tomadas em conjunto, ambas as pesquisas sugerem que as diferenças anatômicas, aparentemente influenciadas pelo gene DISC1, causam problemas que começam antes do nascimento – mas que só apresentam sintomas na fase adulta. Compreender melhor o mecanismo pode eventualmente levar os pesquisadores ao desenvolvimento de terapias que interfiram ou atenuem os sintomas.

Veja também:

- Pesquisa quer encontrar relação genética entre autismo e esquizofrenia
- Tratamento de grupo de risco pode prevenir avanço da esquizofrenia
- Teste de sangue promete diagnóstico rápido e preciso da esquizofrenia

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