New concepts in the development of schizophrenia, autism spectrum disorders, and degenerative brain diseases based on chronic inflammation: A working hypothesis from continued advances in neuroscience research.

Abstract

This paper was written prompted by a poignant film about adolescent girl with schizophrenia who babysits for a younger girl in an isolated cabin. Schizophrenia is an illness that both authors are fascinated with and that they continue to study and investigate. There is now compelling evidence that schizophrenia is a very complex syndrome that involves numerous neural pathways in the brain, far more than just dopaminergic and serotonergic systems. One of the more popular theories in recent literature is that it represents a hypo glutaminergic deficiency of certain pathways, including thalamic ones. After much review of research and study in this area, we have concluded that most such theories contain a number of shortcomings. Most are based on clinical responses to certain drugs, particularly antipsychotic drugs affecting the dopaminergic neurotransmitters; thus, assuming dopamine release was the central cause of the psychotic symptoms of schizophrenia. The theory was limited in that dopamine excess could only explain the positive symptoms of the disorder. Antipsychotic medications have minimal effectiveness for the negative and cognitive symptoms associated with schizophrenia. It has been estimated that 20–30% of patients show either a partial or no response to antipsychotic medications. In addition, the dopamine hypothesis does not explain the neuroanatomic findings in schizophrenia.