Abstract
The maldevelopmental model of schizophrenia postulates pathological alterations in embryonal neurogenesis as the etiopathogenetic basis of schizophrenic psychosis; the neurotrophic factor hypothesis explains these changes as the result of disturbances of processes involving the trophic factors. Neurotransmitter deficits are thereby interpreted as epiphenomena of underlying neurotrophic factor deficacy. The functional systems of the various neurotrophic factors are characterized by complex interaction mechanisms. Both primary genetic alterations, and secondary impairments, induced by exogene noxae, of the receptors and signal transducers associated with neurotrophic factors, as well as of the neurotrophic factors themselves are possible. Preliminary clinical studies indicate that schizophrenic psychoses may be associated with changes in the genetic code of certain neurotrophic factors. Various phenomena typical of the schizophrenic psychoses can be interpreted according to the neurotrophic factor hypothesis.