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- W2898090625 abstract "Dopamine D2/3 receptor occupancy by antipsychotic drugs is central to clinical response and many of their side effects. Yet the locus of dopaminergic alterations in the majority of patients with schizophrenia is not the D2/3 receptor but, instead, presynaptic, comprising elevated striatal dopamine synthesis and release capacity. However, whilst this explains why dopamine D2/3 receptor blockade is effective in many patients, a proportion of patients does not respond. In some this is because of inadequate antipsychotic blockade of dopamine receptors, but there are others who do not respond to antipsychotic treatment despite substantial dopamine D2/3 receptor blockade. The neurobiology of treatment resistance does not seem to involve the presynaptic dopamine dysfunction typically seen in patients, suggesting that it needs different treatments. Disruptions to the glutamatergic system, and to dopamine D1 and D2/3 receptors and serotonin 2A receptors have all been proposed as potential mechanisms underlying treatment resistance and as targets for novel treatments." @default.
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- W2898090625 date "2018-10-01" @default.
- W2898090625 modified "2023-10-16" @default.
- W2898090625 title "The neurobiology of antipsychotic treatment response and resistance" @default.
- W2898090625 doi "https://doi.org/10.1093/med/9780198828761.003.0005" @default.
- W2898090625 hasPublicationYear "2018" @default.
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