The choroid plexus and system disease in mental illness. I. A new brain attack mechanism via the second blood--brain barrier.

Schizophrenia and certain idiopathic neuroses and retardations may be caused by polygenic sensitization to exogeneous peptide antigens or viruses causing a covert immune complex basal lamina disease of the choroid plexus. This organ has the general structure and disease susceptibility of many other transport organs but acts as a second blood--brain barrier putting at risk to contamination and dysfunction the periventricular primary personality (limbic) brain now thought to be centrally involved in schizophrenia. Genetic variability selects different antigens and different target organs so that a complex statistical structure of disease expression can result over the transport organ group as well as between this group and the endocrines and exocrines. This leads to the concept of intra- and intercombined system diseases all of which may have a covert biphasic (hyper-hypo) time course. To this extrinsic combinatorial complexity may be added an intrinsic or neural combinatorial complexity resulting from the fact that the choroid plexus is threaded throughout the limbic system and subject to spotty disease characteristic of many immunopathies. In this way a wide range of behavioral disorders may arise as well as mental retardations if the process occurs during development. In this paper we discuss basic mechanisms. In the next paper of the series we examine systemic lupus erythematosus, the prototypical "combined transport dysfunction," as a model for schizophrenia. In the last paper we search for specific exogeneous peptide triggers for schizophrenia viewed as one expression of combined transport organ dysfunction. We conclude that immunofluorescent and virological surveys should be conducted in all mental illnesses as well as clinical trials of interferon therapy and elemental diets.