BackgroundEstablishing the cognitive phenotype of psychotic symptoms in Alzheimer's disease (AD) could localise discrete pathology and target symptomatic treatment. This study aimed to establish whether psychotic symptoms would be associated with poorer performance on neuropsychological tests known to correlate with striatal dopaminergic function and to investigate whether these differences would be attributed to the paranoid (persecutory delusions) or misidentification (misidentification phenomena +/− hallucinations) subtype.MethodsSeventy patients with probable AD (34 psychotic and 36 nonpsychotic) were recruited to the study. Analysis of covariance was used to compare motor speed and the rapid visual processing test of sustained visual attention, after adjusting for potential confounding factors. Multivariate analyses were used to compare performance across other cognitive domains. Significant findings were explored by separating patients on the basis of subtype.ResultsRapid visual processing performance accuracy was reduced in patients with psychotic symptoms (F 1,58 = 5.94, p = 0.02) and differed significantly across subtypes (F 2,51 = 3.94, p = 0.03), largely because of poorer performance in the misidentification compared with nonpsychotic group. Multivariate analyses (corrected for multiple comparisons) showed poorer performance on the incomplete letters task in psychotic patients (F 1,63 = 8.77, p = 0.004) and across subtypes (F 2,55 = 10.90, p < 0.001), similarly attributed to the misidentification subtype.ConclusionsThese findings provide further support of the involvement of dopaminergic networks in the psychosis endophenotype in AD and, in addition, implicate the ventral (temporo‐occipital) pathway in the misidentification subtype. Future studies should investigate the early trajectory of neuropathological change in vivo across psychosis subtypes.© 2015 The Authors. International Journal of Geriatric Psychiatry published by John Wiley & Sons, Ltd.

[(18)F]fallypride is a high-affinity dopamine D2/3 receptor tracer with the ability to reliably quantify D2/3 receptor sites in both striatal and corticolimbic regions. The translational potential of [(18)F]fallypride imaging is, however, limited by the lengthy scanning sessions (60-80 minutes duration over a total of 3-4 hours) required by current protocols. The aims of our study were to adapt [(18)F]fallypride imaging for use in clinical populations with neurological and neuropsychiatric disorders, by reducing the duration of individual scanning sessions; and to establish the reproducibility and reliability of our adapted protocol in healthy older people. Eight participants (five male and three female; mean age=75.87±4.39 years) were scanned twice, 4-6 weeks apart. [(18)F]fallypride binding potential was determined from image data collected during three sampling times: 0-30; 60-90; and 210-240 minutes post injection. High reproducibility and reliability (test-retest variability <8%; intraclass correlation coefficient >0.8) were observed in all but the prefrontal regions, and remained so when sampling times were reduced to 20 minutes (0-20; 70-90; 220-240 minutes). The adapted protocol is feasible for use across neuropsychiatric disorders in which dopamine has been implicated and is sufficiently sensitive to detect within-subject changes between 2.7% and 5.5% in striatal and limbic regions.

The protocol is feasible for use in AD and represents the first step towards establishing dose-occupancy relationships across older clinical populations.

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