We conclude that PiB-positron emission tomography can detect cerebrovascular beta-amyloid and may serve as a method for identifying the extent of CAA in living subjects.

Background Extrapyramidal motor symptoms precede dementia in Parkinson disease (PDD) by many years, whereas dementia occurs early in dementia with Lewy bodies (DLB). Despite this clinical distinction, the neuropsychological and neuropathologic features of these conditions overlap. In addition to widespread distribution of Lewy bodies, both diseases have variable burdens of neuritic plaques and neurofibrillary tangles characteristic of Alzheimer disease (AD). Objectives To determine whether amyloid deposition, as assessed by PET imaging with the β-amyloid–binding compound Pittsburgh Compound B (PiB), can distinguish DLB from PDD, and to assess whether regional patterns of amyloid deposition correlate with specific motor or cognitive features. Methods Eight DLB, 7 PDD, 11 Parkinson disease (PD), 15 AD, and 37 normal control (NC) subjects underwent PiB-PET imaging and neuropsychological assessment. Amyloid burden was quantified using the PiB distribution volume ratio. Results Cortical amyloid burden was higher in the DLB group than in the PDD group, comparable to the AD group. Amyloid deposition in the PDD group was low, comparable to the PD and NC groups. Relative to global cortical retention, occipital PiB retention was lower in the AD group than in the other groups. For the DLB, PDD, and PD groups, amyloid deposition in the parietal (lateral and precuneus)/posterior cingulate region was related to visuospatial impairment. Striatal PiB retention in the DLB and PDD groups was associated with less impaired motor function. Conclusions Global cortical amyloid burden is high in dementia with Lewy bodies (DLB) but low in Parkinson disease dementia. These data suggest that β-amyloid may contribute selectively to the cognitive impairment of DLB and may contribute to the timing of dementia relative to the motor signs of parkinsonism.

Our understanding of the emotional features of schizophrenia has benefited greatly from the adoption of methods and theory from the field of affective science. This article covers basic concepts and methods from affective science on the psychological and neural mechanisms contributing to emotions and reviews the ways in which this research has advanced our understanding of emotional response deficits in schizophrenia. We review naturalistic studies and elicitation studies that evoke emotion responses among participants, including emotion expression, experience, and autonomic physiology. We also consider how these emotion response measures correspond to schizophrenia symptoms, and we focus particular attention on the issue of sex differences in emotional responding and how this may influence our understanding emotional functioning among individuals with schizophrenia.

The present study was designed to investigate the relationship among physiologic concordance, patient-perceived therapist empathy, and social-emotional process during psychotherapy. Simultaneous measures of skin conductance (SC) were obtained from 20 unique and established patient-therapist dyads during a live therapy session followed by patient ratings of therapist empathy. Paired SC data of hypothetical dyads were used to test the reliability of the proposed measure of SC concordance. Observer microanalyses of social-emotional process were used to compare short segments of high versus low physiologic concordance. Results show a significant positive correlation (r=0.47, p=0.03) between SC concordance and patient ratings of perceived therapist empathy. Microanalyses suggest that during moments of high versus low SC concordance, there were significantly more positive social-emotional interactions for both patients and therapists (p=0.01). The results support a biological model of perceived patient empathy and patient-therapist social-emotional process during psychotherapy.

ObjectiveTo determine whether amyloid deposition is associated with impaired neuropsychological (NP) performance and whether cognitive reserve (CR) modifies this association.MethodsIn 66 normal elderly controls and 17 patients with Alzheimer disease (AD), we related brain retention of Pittsburgh Compound B (PiB) to NP performance and evaluated the impact of CR using education and American National Adult Reading Test intelligence quotient as proposed proxies.ResultsWe found in the combined sample of subjects that PiB retention in the precuneus was inversely related to NP performance, especially in tests of memory function, but also in tests of working memory, semantic processing, language, and visuospatial perception. CR significantly modified the relationship, such that at progressively higher levels of CR, increased amyloid deposition was less or not at all associated with poorer neuropsychological performance. In a subsample of normal controls, both the main effect of amyloid deposition of worse memory performance and the interaction with CR were replicated using a particularly challenging memory test.InterpretationAmyloid deposition is associated with lower cognitive performance both in AD patients and in the normal elderly, but the association is modified by CR, suggesting that CR may be protective against amyloid-related cognitive impairment. ANN NEUROL 2010;67:353–364

Motivational impairment is a common feature of both depression and psychosis; however, the psychological and neural mechanisms that give rise to motivational impairment in these disorders are poorly understood. Recent research has suggested that aberrant effort-cost decision-making (ECDM) may be a potential contributor to motivational impairment in both psychosis and depression. ECDM refers to choices that individuals make regarding the amount of 'work' they are willing to expend to obtain a certain outcome or reward. Recent experimental work has suggested that those with psychosis and depression may be less willing to expend effort to obtain rewards compared with controls, and that this effort deficit is related to motivational impairment in both disorders. In the current review, we aim to summarize the current literature on ECDM in psychosis and depression, providing evidence for transdiagnostic impairment. Next, we discuss evidence for the hypothesis that a seemingly similar behavioral ECDM deficit might arise from disparate psychological and neural mechanisms. Specifically, we argue that effort deficits in psychosis might be largely driven by deficits in cognitive control and the neural correlates of cognitive control processes, while effort deficits in depression might be largely driven by reduced reward responsivity and the associated neural correlates of reward responsivity. Finally, we will provide some discussion regarding future directions, as well as interpretative challenges to consider when examining ECDM transdiagnostically.

Negative symptoms are a core clinical feature of schizophrenia, but conceptual and methodological problems with current instruments can make their assessment challenging. One hypothesis is that current symptom assessments may be influenced by impairments in memory and may not be fully reflective of actual functioning outside of the laboratory. The present study sought to investigate the validity of assessing negative symptoms using ecological momentary assessment (EMA). Participants with schizophrenia (N=31) completed electronic questionnaires on smartphones four times a day for one week. Participants also completed Effort-Based Decision Making and Reinforcement Learning (RL) tasks to assess the relationship between EMA and laboratory measures, which tap into negative symptom relevant domains. Hierarchical linear modeling analyses revealed that clinician-rated and self-report measures of negative symptoms were significantly related to negative symptoms assessed via EMA. However, working memory moderated the relationship between EMA and retrospective measures of negative symptoms, such that there was a stronger relationship between EMA and retrospective negative symptom measures among individuals with better working memory. We also found that negative symptoms assessed via EMA were related to poor performance on the Effort task, while clinician-rated symptoms and self-reports were not. Further, we found that negative symptoms were related to poorer performance on learning reward contingencies. Our findings suggest that negative symptoms can be assessed through EMA and that working memory impairments frequently seen in schizophrenia may affect recall of symptoms. Moreover, these findings suggest the importance of examining the relationship between laboratory tasks and symptoms assessed during daily life.

These results suggest that clinical heterogeneity in MCI is reflected in SPECT perfusion differences, and that the pattern of perfusion abnormalities evolves with increasing clinical severity.