Data/hora: 11/06/2024 18:51:01

Provedor de dados: | 17
País: | United Kingdom
Título: | Evidence for gliadin antibodies as causative agents in schizophrenia.
Autores: | Chris J. Carter.
Data: | 2010-12-02
Ano: | 2010
Palavras-chave: | Genetics &amp; Genomics; Immunology; Neuroscience; Bioinformatics.
Resumo: | Antibodies to gliadin, a component of gluten, have frequently been reported in schizophrenia. Highly immunogenic B cell epitopes along its length are homologous to numerous proteins relevant to schizophrenia, including members of the DISC1 interactome, glutamate, dopamine and neuregulin signaling networks, and plasticity or myelination pathways. Antibodies to gliadin may cross react with these key proteins, as has already been observed with synapsin 1 and calreticulin. Gliadin may thus be a causative agent in schizophrenia, under certain genetic and immunological conditions, producing its effects via antibody mediated knockdown of multiple proteins relevant to the disease process. Because of such homology, an autoimmune response may be sustained by the human antigens that resemble gliadin itself, a scenario supported by many reports of immune activation both in the brain and in lymphocytes in schizophrenia. Gluten free diets and removal of such antibodies may be of therapeutic benefit in certain cases of schizophrenia.
Tipo: | Manuscript

Identificador:

http://precedings.nature.com/documents/5351/version/1

oai:nature.com:10.1038/npre.2010.5351.1

http://dx.doi.org/10.1038/npre.2010.5351.1

Fonte: | Nature Precedings
Fonte: | Creative Commons Attribution 3.0 License