This paper presents a new explanatory model for
schizophrenia based upon philosophical, molecular and neurobiological
hypotheses as well as on years of experience in observing and treating these
patients. To start with, a novel interpretation of the Hegelian concept of
mediation is presented. Mediation is defined as the rejection of non-realizable
programs, such as thoughts and ideas, at a certain point in time in the
evolution of a living system. Whenever a system treats non-realizable programs
as if they were realizable, its ability to “test the reality” is lost, and
consequently a loss of ego-boundaries may occur. On the molecular level, I will
try to show how “non-splicing” of introns during the mRNA splicing process is
equivalent to a loss of the rejection function corresponding to mediation. At
the cellular level in the brain, mediation can be explained in terms of glial-neuronal interactions. Glia exert a
spatio-temporal boundary setting
function determining the grouping of neurons into functional units. Mutations
in genes that result in non-splicing of introns can produce truncated (“chimeric”)
neurotransmitter receptors. I propose that such dysfunctional receptors are
generated in glial cells and that they cannot interact properly with their
cognate neurotransmitters. The glia will then lose their inhibitory-rejecting
function with respect to the information processing within neuronal networks.
This loss of glial boundary setting could be an explanation for the loss of ego
or body boundaries in schizophrenia. Pertinent examples of case studies are
given attempting to deduce the main symptoms of schizophrenia from the proposed
hypothesis. Some implications for the design of delusional robots are also
discussed. Finally, the evolutionary potency of non-coding introns is
philosophically interpreted that schizophrenics may be “too soon on earth”.
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