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. Author manuscript; available in PMC: 2018 Feb 14.
Published in final edited form as: Acta Physiol (Oxf). 2015 Nov 5;216(1):90–100. doi: 10.1111/apha.12614

Figure 3.

Figure 3

Summary of evidence for the role of streptococcal infections in the induction of antibodies that may lead to movement or neuropsychiatric disorders. The pathogenesis of Sydenham chorea and PANDAS begins with an infection with group A streptococci in the throat or soft tissues or skin. The susceptible host may produce antibodies which react with brain tissues and in particular the dopamine receptors or neural antigens such as tubulin or lysoganglioside (Kirvan et al. 2003, 2006a,b, 2007, Ben-Pazi et al. 2013, Cox et al. 2013). Antibodies target primarily the basal ganglia, in particular the ventral tegumental area or the substantia nigra which project to the striatum. The mechanism of the antibodies as shown would signal the neuronal cell through activation of CaMKII and lead to excess dopamine release. Binding of high-avidity cross-reactive antistreptococcal/antineuronal antibodies to lysoganglioside or dopamine receptors on the surface of neurons may lead to alterations in dopamine transmission.