This paper presents the hypothesis that NMDA receptor delayed maturation (NRDM) may lead to the pathogenesis of schizophrenic psychotic symptoms. This hypothesis is further analyzed in the language of a neural modeling formulation. This formulation points to a possible chain of pathological events, leading from molecular-level NRDM to over-increased synaptic plasticity, and to the formation of pathological attractors, a putative macroscopic-level correlate of schizophrenic positive symptoms. The relations of the NRDM hypothesis to other alterations which are assumed to take place in schizophrenia are discussed, together with possible ways to test this hypothesis. 1 The NRDM Hypothesis NMDA receptor antagonist drugs exacerbate schizophrenic symptoms and, in animals, produce neurodegenerative effects in brain areas thought be to involved in the pathogenesis of this disorder. Consequently, it has been proposed that spontaneously occurring NMDA receptor hypofunction causes schizophrenia...

Therapeutic suggestions resulting from computational models of Alzheimer disease are made. Although several computational models of this disease have been published in the last decade few conclusions were drawn. Two such models are introduced here and directions for their further extensions are outlined. Assuming that computational models reflect real neural mechanisms leads to some therapeutic suggestions that should slow down the degeneration of synaptic connections and thus the development of the disease, at least in its early stages.