Neurocysticercosis (NC) presents a spectrum of clinical symptoms, with two broad clinical entities based on the CNS location of the parasite: parenchymal (P-NC) or extraparenchymal (EP-NC). In view of the importance of inflammation in the pathogenesis of NC, it is surprising that the possible occurrence of anti-brain autoantibodies in NC has not been explored until recently. In this study the presence of autoantibodies to nine ubiquitous intracellular proteins from extraparenchymal (EP-NC) was reported. Levels of these autoantibodies were greatly reduced or absent in P-NC, an observation consistent with our understanding of the immunological potential of these two distinct anatomical areas of the brain. In more recent work, we similarly observed autoantibodies to tubulin and MOG in the CSF of EP-NC, but not P-NC patients. In addition to the evident importance of the early inflammatory response, the identification of autoantibodies to the neuronal surface protein MOG (and perhaps other anti-neuronal autoantibodies) provides a potentially critical role in the pathogenesis of NC through their predicted potential for antibody mediated cytotoxicity and the subsequent release of intracellular proteins which, in turn, would stimulate a cascade of more autoantibodies to the liberated intracellular proteins. These, together with antibodies to metacestode proteins may be expected to play an important role in the continuously evolving and variable pathogenesis of NC, as is summarized in the hypothetical model presented.
Neurocysticercosis; Anti-brain autoantibodies; Tubulin; MOG; Extraparenchymal; Parenchymal