Working memory deficits are central to the cognitive impairment of schizophrenia and other psychiatric disorders. The D1 receptor (D1R) is probably the best established mediator of working memory in neuroscience studies for over three decades and represents a highly promising therapeutic target for enhancing working memory in these disorders, yet this mechanism has never been tested in humans. Schizotypal personality disorder (SPD) patients who evidence moderate, focal impairments in working memory represent a unique population to test the effect of a D1 agonist on working memory impairment in humans. Cognitive impairment is the most salient predictor of functional outcome in schizophrenia (SCZ) and is essentially refractory to conventional treatments. Identifying pharmacologic agents that target the cognitive deficits of SCZ is thus the top priority in SCZ research, but so far, clinical trials of a number of drugs with preclinical promise have yielded disappointing results. Currently, no study to date has directly tested a selective D1R agonist in relation to the cognitive impairment of SCZ without the confound of neuroleptics. The investigators propose to examine the efficacy of DAR-0100A, a highly selective, full D1R agonist supported by pre-clinical and preliminary pilot clinical data, in ameliorating the cognitive deficits in SPD subjects receiving no medications including antipsychotics. SPD will be classified as a schizophrenic disorder in DSM-5 and ICD-10. The investigators have characterized the cognitive deficits of SPD and demonstrated that, as with chronic SCZ, a core component consists of impairments in working memory. Studies of SPD obviate confounds associated with SCZ, such as the effects of overt psychotic episodes, medication history, severe, persistent functional impairment and multiple treatments. Furthermore, the cognitive deficits of SPD are less global and more readily reversible than those of chronic SCZ, providing a unique opportunity to test the D1 mechanism of cognitive enhancement. DAR-0100A, which is the active enantiomer of dihydrexidine (DHX), is a full D1R agonist with a10-60 fold selectivity over the D2R. DHX administration improves cognition in single doses in young adult and aged monkeys and rodents. A single treatment with DAR-0100A in adult humans with SCZ was demonstrated to enhance prefrontal perfusion. Pilot data from our group and Columbia suggest DAR-0100A improves cognitive performance, particularly working memory, in the schizophrenia spectrum.