Ther Adv Neurol Disord 2021 30;14:17562864211003486. Epub 2021 Mar 30.
Department of Neurology, Thomas Jefferson University, 900 Walnut Street, Philadelphia, PA 19107, USA; Neuroimmunology Unit, National and Kapodistrian University of Athens, Athens, Greece.
Antibodies against glutamic acid decarboxylase (GAD), originally linked to stiff person syndrome (SPS), now denote the "" () that also include autoimmune epilepsy, limbic encephalitis, cerebellar ataxia and nystagmus with overlapping symptomatology highlighting autoimmune neuronal excitability disorders. The reasons for the clinical heterogeneity among GAD-antibody associated syndromes remain still unsettled, implicating variable susceptibility of GABAergic neurons to anti-GAD or other still unidentified autoantibodies. Although anti-GAD antibody titers do not correlate with clinical severity, very high serum titers, often associated with intrathecal synthesis of anti-GAD-specific IgG, point to effects of GAD or related autoantibodies within the central nervous system. Read More