No abstract

The locus of the largest dopaminergic abnormality in schizophrenia is presynaptic, which affects dopamine synthesis capacity, baseline synaptic dopamine levels, and dopamine release. Current drug treatments, which primarily act at D(2/3) receptors, fail to target these abnormalities. Future drug development should focus on the control of presynaptic dopamine synthesis and release capacity.

Problems in set shifting as measured by a variety of neuropsychological tasks are present in people with eating disorders.

Although some statistically significant effects on negative symptoms were evident, none reached the threshold for clinically significant improvement.

No abstract