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Gluten Ataxia
Author(s) -
BOSCOLO SABRINA,
SARICH ALESSANDRA,
LORENZON ANDREA,
PASSONI MONICA,
RUI VERONICA,
STEBEL MARCO,
SBLATTERO DANIELE,
MARZARI ROBERTO,
HADJIVASSILIOU MARIOS,
TONGIORGI ENRICO
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1381.034
Subject(s) - tissue transglutaminase , dermatitis herpetiformis , gluten , medicine , autoantibody , gliadin , antibody , immunology , ataxia , disease , pathology , chemistry , enzyme , biochemistry , psychiatry
Gluten sensitivity is an autoimmune disease that usually causes intestinal atrophy resulting in a malabsorption syndrome known as celiac disease. However, gluten sensitivity may involve several organs and is often associated with extraintestinal manifestations. Typically, patients with celiac disease have circulating anti‐tissue transglutaminase and anti‐gliadin antibodies. When patients with gluten sensitivity are affected by other autoimmune diseases, other autoantibodies may arise like anti‐epidermal transglutaminase in dermatitis herpetiformis, anti‐thyroid peroxidase antibodies in thyroiditis, and anti‐islet cells antibodies in type 1 diabetes. The most common neurological manifestation of gluten sensitivity is ataxia, the so‐called gluten ataxia (GA). In patients with GA we have demonstrated that anti‐gliadin and anti‐tissue transglutaminase antibodies cross‐react with neurons but that additional anti‐neural antibodies are present. The aim of the present article is to review the knowledge on animal models of gluten sensitivity, as well as reviewing the role of anti‐neural antibodies in GA.