Andrew J. Church

TL;DR: Investigation found no evidence of viral encephalitis or other recognized causes of rapid-onset parkinsonism, and investigated the possibility that this phenotype could be a postinfectious autoimmune CNS disorder, and therefore similar to Sydenham's chorea.

TL;DR: Assessment of dopamine-2 receptor antibodies can help define autoimmune movement and psychiatric disorders, and is found to be helpful in patients with movement disorders characterized by parkinsonism, dystonia and chorea.

TL;DR: Findings support a new subgroup of postinfectious autoimmune inflammatory disorders associated with Group A β hemolytic streptococcus, abnormal basal ganglia imaging, and elevated ABGA.

TL;DR: In vitro experiments using cultured neurons showed that commercial anti-NGE antibodies induced apoptosis compared to blank incubation and control anti-HuD antibody, suggesting molecular mimicry and autoimmune cross-reactivity may be the pathogenic mechanism in post-streptococcal CNS disease.

TL;DR: Findings support an autoantibody pathogenesis of Sydenham's chorea by measuring Th1 (IFN-gamma, IL-12) and Th2 (IL-4,IL-10) cytokines, oligoclonal bands and anti-basal ganglia antibodies (ABGA).