AI Article Synopsis

  • The study focuses on understanding how psychotic symptoms in Alzheimer's disease (AD) relate to cognitive function, particularly in relation to dopaminergic pathways.
  • It involved 70 AD patients (34 with psychotic symptoms and 36 without) and found that those with psychotic symptoms performed worse on visual processing tasks, especially the misidentification subtype.
  • Results suggest that dopaminergic networks are involved in these psychotic symptoms, highlighting a need for further research into the early changes in the brain associated with different types of psychosis in AD.

Article Abstract

Background: Establishing 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.

Methods: Seventy 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.

Results: Rapid visual processing performance accuracy was reduced in patients with psychotic symptoms (F1,58  = 5.94, p = 0.02) and differed significantly across subtypes (F2,51  = 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 (F1,63  = 8.77, p = 0.004) and across subtypes (F2,55  = 10.90, p < 0.001), similarly attributed to the misidentification subtype.

Conclusions: These 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988507PMC
http://dx.doi.org/10.1002/gps.4265DOI Listing

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