{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T01:48:16Z","timestamp":1786672096234,"version":"build-2736575974"},"reference-count":23,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,1,9]],"date-time":"2006-01-09T00:00:00Z","timestamp":1136764800000},"content-version":"vor","delay-in-days":283,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2005,4]]},"abstract":"<jats:p><jats:bold>A<jats:sc>bstract<\/jats:sc>: <\/jats:bold> Glutamic acid decarboxylase (GAD) catalyzes the conversion of glutamic acid to \u03b3\u2010aminobutyric acid (GABA). Autoantibodies directed against GAD (antiGAD\u2010Ab) have been described in patients with insulin\u2010dependent diabetes mellitus, stiff\u2010man syndrome, and in a few patients with progressive cerebellar ataxia. The presence of these autoantibodies suggests an autoimmune pathophysiological mechanism for the neurological manifestations in these disorders. However, the exact role of antiGAD\u2010Ab and GABAergic neurotransmission in the pathogenesis of the neurological manifestations, particularly in progressive cerebellar ataxia, is not fully understood. The cases of two patients with subacute cerebellar ataxia associated with antiGAD\u2010Ab presenting with abnormal eye movements are reported. One patient presented a periodic alternating nystagmus (PAN), whereas the other presented a downbeat nystagmus (DBN) and slow vertical saccades. The potential role of antiGAD\u2010Ab and the resultant GABAergic neurotransmission deficit in oculomotor manifestations is discussed.<\/jats:p>","DOI":"10.1196\/annals.1325.042","type":"journal-article","created":{"date-parts":[[2005,4,12]],"date-time":"2005-04-12T11:02:19Z","timestamp":1113303739000},"page":"446-454","source":"Crossref","is-referenced-by-count":38,"title":["Potential Role of Anti\u2010GAD Antibodies in Abnormal Eye Movements"],"prefix":"10.1111","volume":"1039","author":[{"given":"CAROLINE","family":"TILIKETE","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ALAIN","family":"VIGHETTO","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PAUL","family":"TROUILLAS","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00c9ROME","family":"HONNORAT","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,7,8]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198804213181602"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199005313222202"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00868343"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp.71.1.100"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.52.4.857"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1995.00540290050017"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.58.2.225"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.49.4.1026"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1007\/s100720200055"},{"key":"e_1_2_6_11_2","first-page":"11","article-title":"Clinical presentation of immune mediated cerebellar ataxia","volume":"159","author":"Honnorat J.","year":"2003","journal-title":"Rev. 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