according to my experience the influence on cognitive functions by atypical neuroleptics is mild and in most cases positive. For example, olanzapine (ZYPREXA), risperidone (RISPERDAL), amisulpride (SOLIAN) and quetiapine (SEROQUEL) have a generally positive impact on neurocognitive functions in patients with paranoid hallucinatoric schizophrenia. The psychosis itself has devastating influence on neurocognitive functions, also in form of negative symptomes (depression, social dysfunction, memory impairment, etc.) accompanying and/or following the acute psychosis. Any negative impact of atypical neuroleptics may be self-limiting and not pronounced, and is by far not so severe as mediated by classical neuroleptics like haloperidol and other butyrophenones (and diphenylbutylpiperidines), and, especially, phenothiazines and thioxanthenes. These latter "classical" neuroleptics generally suppress neurocognitive functions.
according to my experience the influence on cognitive functions by atypical neuroleptics is mild and in most cases positive. For example, olanzapine (ZYPREXA), risperidone (RISPERDAL), amisulpride (SOLIAN) and quetiapine (SEROQUEL) have a generally positive impact on neurocognitive functions in patients with paranoid hallucinatoric schizophrenia. The psychosis itself has devastating influence on neurocognitive functions, also in form of negative symptomes (depression, social dysfunction, memory impairment, etc.) accompanying and/or following the acute psychosis. Any negative impact of atypical neuroleptics may be self-limiting and not pronounced, and is by far not so severe as mediated by classical neuroleptics like haloperidol and other butyrophenones (and diphenylbutylpiperidines), and, especially, phenothiazines and thioxanthenes. These latter "classical" neuroleptics generally suppress neurocognitive functions.
Pro-cognitive receptors are: prefrontal serotoninergic 5HT1A and 5HT2A agonism, 5HT2C (antagonism), prefrontal dopaminergic D1, prefrontal GABA-ergic and glutamatergic (AMPA) as well as prefrontal noradrenergic (alpha1) and histaminergic H1 agonism which all are inplicated in working memory - they increase signal-to-noise ratio (not sure "enough" for H1), they are required for attention and vigilance maintenance; mesolimbic dopaminergic D2 receptor antagonism lowers the threshold of a representation of gaining permission to enter into the prefrontal working memory circuits. Any substance or any antipsychotic posessing any, some or all of these will have a pro-cogntive effect(s). Note that all receptors function on the principle of the "golden middle" with the famous U-inverted curve of functional efficiency.