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Objective: To determine the relationship between alterations in resting state functional connectivity and social cognition dysfunction among patients with frontotemporal dementia (FTD), Alzheimer's disease (AD), Parkinson's disease (PD), and healthy controls (HC). Methods: Fifty-seven participants (FTD = 10, AD = 18, PD = 19, and HC = 10) underwent structural and functional imaging and completed the Awareness of Social Inference Test-Emotion Evaluation Test (TASIT-EET), Behavioral Inhibition System/Behavioral Activation System (BIS/BAS) scale, Revised Self-Monitoring Scale (RSMS), Interpersonal Reactivity Index (IRI), and Social Norms Questionnaire (SNQ). A multi-variate pattern analysis (MVPA) was carried out to determine activation differences between the groups. The clusters from the MVPA were used as seeds for the ROI-to-voxel analysis. Relationship between social cognition deficits and uncinate integrity was also investigated. Results: BOLD signal activation differed among the four groups of AD, PD, FTD, and HC in the left inferior temporal gyrus-anterior division [L-ITG (ant)], right central opercular cortex (R-COp), right supramarginal gyrus, posterior division (R-SMG, post), right angular gyrus (R-AG), and R-ITG. The BOLD co-activation of the L-ITG (ant) with bilateral frontal pole (FP) and paracingulate gyrus was positively associated with IRI-perspective taking (PT) (r = 0.38, p = 0.007), SNQ total (r = 0.37, p = 0.009), and TASIT-EET (r = 0.47, p < 0.001). Conclusion: Patients with neurodegenerative diseases showed alterations in connectivity in brain regions important for social cognition compared with HCs. Functional connectivity correlated with performance on social cognition tasks and alterations could be responsible for some of the social cognition deficits observed in all neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Background: Changes in social cognition occur in patients with Alzheimer's disease (AD) and Parkinson's disease (PD) and can be caused by several factors, including emotion recognition deficits and neuropsychiatric symptoms (NPS). The aims of this study were to investigate: (1) group differences on emotion detection between patients diagnosed with AD or PD and their respective caregivers; (2) the association of emotion detection with empathetic ability and NPS in individuals with AD or PD; (3) caregivers' depression and perceived burden in relation to patients' ability to detect emotions, empathize with others, presence of NPS; and (4) caregiver's awareness of emotion detection deficits in patients with AD or Parkinson. Methods: In this study, patients with probable AD (N = 25) or PD (N = 17), and their caregivers (N = 42), performed an emotion detection task (The Awareness of Social Inference Test--Emotion Evaluation Test, TASIT-EET). Patients underwent cognitive assessment, using the Behavioral Neurology Assessment (BNA). In addition, caregivers completed questionnaires to measure empathy (Interpersonal Reactivity Index, IRI) and NPS (Neuropsychiatric Inventory, NPI) in patients and self-reported on depression (Geriatric Depression Scale, GDS) and burden (Zarit Burden Interview, ZBI). Caregivers were also interviewed to measure dementia severity (Clinical Dementia Rating (CDR) Scale) in patients. Results: The results suggest that individuals with AD and PD are significantly worse at recognizing emotions than their caregivers. Moreover, caregivers failed to recognize patients' emotion recognition deficits and this was associated with increased caregiver burden and depression. Patients' emotion recognition deficits, decreased empathy and NPS were also related to caregiver burden and depression. Conclusions: Changes in emotion detection and empathy in individuals with AD and PD has implications for caregiver burden and depression and may be amenable to interventions with both patients and caregivers. [ABSTRACT FROM AUTHOR]

Background/Aims: Neuropsychiatric symptoms (NPS) are common in Alzheimer disease (AD) and vascular dementia (VaD), and are distressful to patients and caregivers. NPS are likely related to the underlying pathology. Previous studies suggest that frontal lobe lesions and vascular changes such as white matter hyperintensities (WMH) have a significant association with specific NPS. The current study aimed to compare NPS in patients with AD, VaD, and mixed AD/VaD, and to evaluate the differences in the prevalence of NPS in relation to frontal WMH volume. Methods: In total, 180 patients with NPS and MRI data (92 probable AD, 51%; 34 probable VaD, 19%; and 54 probable mixed AD/VaD, 30%) were included in the study. Regression analyses were performed to determine the relationships between NPS prevalence and diagnosis, and between NPS and frontal WMH. Results: VaD patients had significantly more agitation (p < 0.05; 40 vs. 14%) and sleep disturbances (p < 0.05; 57 vs. 32%) than AD patients, and significantly more depression (p < 0.05; 48 vs. 20%) and aberrant motor behaviors (p < 0.05; 31 vs. 13%) than mixed AD/VaD patients. AD patients with delusions had significantly greater right frontal WMH volumes than those without (p < 0.05; delusions 1/0 = 314.8/112.6 mm 3). Conclusion: Differences in NPS prevalence are likely related to the underlying pathology and warrant further study as they have implications for treatment. [ABSTRACT FROM AUTHOR]

Background and Objectives: There is no disease-modifying treatment of corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP), 2 disorders characterized by their striking phenotypic, and, in CBS, pathologic heterogeneity. Seed amplification assays (SAAs) could enable the detection of neuropathologic processes, such as α-synuclein (αSyn) copathology, that affect the success of future disease-modifying treatment strategies. The primary objective was to assess possible αSyn copathology in CBS and PSP, as detected in CSF using an αSyn SAA (αSyn-SAA). Secondary objectives were to evaluate the association of αSyn-SAA positivity with other biomarkers including of Alzheimer disease (AD), and with clinical presentation. We hypothesized that αSyn-SAA positivity would be detectable in CBS and PSP and that it would be associated with AD biomarker positivity and β-amyloid (Aβ) 42 levels, neurodegeneration as assessed by neurofilament light chain (NfL) levels, and symptoms associated with synucleinopathies., Methods: This cross-sectional observational study included patients clinically diagnosed with CBS and PSP who underwent a lumbar puncture between 2012 and 2021 (Toronto Western Hospital, Canada). CSF was tested for αSyn-SAA positivity, AD biomarkers, and NfL levels. Clinical data were derived from medical records., Results: We tested the CSF of 40 patients with CBS (19 female patients, 65.9 ± 8.6 years) and 28 with PSP (13 female patients, 72.5 ± 8.7 years old), mostly White (n = 50) or Asian (n = 14). αSyn-SAA positivity was observed in 35.9% patients with CBS and 28.6% with PSP. In young-onset, but not late-onset patients, αSyn-SAA positivity and AD positivity were associated (odds ratio [OR] 8.8, 95% CI 1.2-82.6, p < 0.05). A multivariable linear regression analysis showed a significant interaction of αSyn-SAA status by age at onset on CSF Aβ42 levels (β = 0.3 ± 0.1, p < 0.05). Indeed, age at onset was positively related to Aβ42 levels only in αSyn-SAA-positive patients, as shown by slope comparison. A logistic regression analysis also suggested that REM sleep behavior disorder was associated with αSyn-SAA positivity (OR 60.2, 95% CI 5.2-1,965.8; p < 0.01)., Discussion: We detected a frequency of αSyn-SAA positivity in CBS and PSP in line with pathologic studies, highlighting the usefulness of SAAs for in vivo detection of otherwise undetectable neuropathologic processes. Our results also suggest that AD status (specifically low Aβ42) and older age at onset may contribute to αSyn-SAA positivity. This opens new perspectives for the stratification of patients in clinical trials.