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Biomedical subjects

B J Mitterauer

Publications and source records attributed to B J Mitterauer.

5 recordsLinked to original sources

Where and how could intentional programs be generated in the brain? A hypothetical model based on glial-neuronal interactions.

Based on glial-neuronal interaction a formalism (negative language) for the generation of intentional programs is proposed. An intentional program generates a specific multirelational structure in an inner or outer appropriate environment according to the principle of feasibility. After description of the glial spatio-temporal boundary-setting function in its interaction with the neuronal system, it is hypothesized that intentional programs may be generated in glial networks (syncytia) in line with the formalism of negative language. Gap junctions are interpreted as multirelational negation operators, generating cycles in a permutation system. These cycles could represent intentional programs that can either be realized or not in neuronal networks embodying a permutation system. The feasibility of these intentional programs is essentially dependent on appropriate environmental information. Since the realization of intentional programs in neuronal networks allows high degrees of freedom, the problem of free will is tackled, as well. Free will is defined as the subjective freedom to choose between the inner determination of intentional programs and the overdetermination of their feasibility in an appropriate environment. Finally, the possible implementation of the proposed brain model in robot brains is briefly discussed.

Cell Communication↗

The loss of self-boundaries: towards a neuromolecular theory of schizophrenia.

I start out with the hypothesis that the basic symptoms of schizophrenia are caused by a loss of self-boundaries. Phenomenologically, schizophrenic symptoms are based on the inability of the brain to delimit conceptual boundaries. At the cellular level in the brain, I have in previous work attributed a spatio-temporal boundary setting function to the glial cells such that glial cells determine the grouping of neurons into functional units. Mutations in genes that result in non-splicing of introns can produce aberrant versions of neurotransmitter receptors that lack protein domains encoded by entire exons and can also have protein sequence encoded by introns that have not been properly spliced out. I propose that such "chimeric" receptors are generated in glial cells and that they cannot interact properly with their cognate neurotransmitters. The glia will then lose their inhibitory function with respect to the information processing within neuronal networks. The loss of glial boundary-setting may result in a 'borderless' generalization of information processing such that the structuring of the brain in functional domains is almost completely lost. This loss of glial boundary setting could be an explanation of the loss of self-boundaries in schizophrenia.

Alternative Splicing↗

Bipolar mood disorders: an affected sibling study. II. Symptom correlations.

Part II of the affected sibling study raises questions of symptom correlation (incidence of delusions, states of confusion, suicide tendencies and attempts, hallucinatory episodes, hypochondriac attitudes, angry manias, and depressive stupor) in mood disorders. The investigated sample (307 sibling groups, 701 hospitalized patients; selection principle: at least 1 sibling showing a bipolar or manic axial syndrome) directs our attention to the possibility that the multiplicity of specific manic and depressive syndromes derives not only from the genetic complexity of the mood-producing system but mirrors the full range of human behavior. Moods must be conceptualized as interpretative metalanguages with respect to the entire wealth of behavioral object languages.

Anger↗

Bipolar mood disorders: an affected sibling study. I. Genetic background and course of illness.

The study uses the 'affected (and hospitalized) siblings method' to investigate aspects of correlation in the psychopathology of bipolar mood disorders. In part one, age of onset, duration of phases, and course of illness are the points of interest. The sample includes 307 sibling groups (701 hospitalized individuals). The incidence of pure or schizoaffective type mania in at least 1 sibling has been the criterion for selection. The genetic background is also presented and the question is raised whether double tainting is the rule rather than the exception. The hypothesis that schizophrenic syndromes and mood disorders develop from separate genetic pools is supported. Strong evidence against the unipolar/bipolar dichotomy is presented. The investigation brings the breadth of the cyclothymic spectrum and inhomogeneity with respect to the course of bipolar disorders into perspective.

Adolescent↗