Biochemical studies in schizophrenia

Abstract

The reviews that follow deal with many of the major currents of biological research in schizophrenia. As is frequently pointed out in the reviews, there are possible areas of congruence in this research. Decreased MAO activity may contribute to increased dopaminergic activity, the biosynthesis of methylated indoleamines, and skeletal muscle pathology. Increased turnover of brain amines can be produced by some viral diseases. Decreased MAO activity, increased dopaminergic activity, or slow viruses affecting the nervous system can produce neuromuscular dysfunction. The hemolysins described by Durell and Archer may be part of a tissue destruction acute phase reaction that could also account for increased serum creatine phosphokinase activity. Whether any or all of these lines of inquiry will survive further study and prove to have a definite place in the pathogenesis or pathophysiology of at least some types of schizophrenia is unknown. Because of fundamental discoveries in the neural sciences and the increasing sophistication of clinical investigations, however, it is not unreasonable to expect further major advances in determining the pathogenesis of schizophrenia. As the biological factors that contribute to the pathogenesis of schizophrenia are identified, it will be necessary to relate them both to the experiential world of the schizophrenic, which also clearly participates in the pathogenesis of the symptomatic expression of the biochemical diathesis, and to psychopathology. It is in the latter area that our understanding is weakest. A major effort to further unravel the intricacies of the neural underpinnings of the higher mental functions will be required to correct that deficit.