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Background and purpose: Behavioral variant frontotemporal dementia (bvFTD) and primary psychiatric disorders (PPD), such as mood, psychotic, and autism spectrum disorders, share similar clinical characteristics of behavior and social cognition. Better understanding of clinical progression in bvFTD and PPD is essential for adequate disease monitoring and trial design. Methods: In this longitudinal study (N = 89), patients with bvFTD and PPD with at least one follow‐up assessment were included from the Social Brain Project of the Alzheimer Center Amsterdam. Behavioral change and social cognitive decline were assessed via informant‐rated questionnaires (Cambridge Behavioral Inventory–Revised, Frontal Behavioral Inventory [FBI], Stereotypy Rating Inventory, Frontotemporal Dementia Rating Scale, Revised Self‐Monitoring Scale [RSMS]‐caregiver) and patient assessment (Ekman 60‐Faces Test, RSMS‐patient, Emotional Contagion Scale). Clinical trajectories (median = 1.4 years, interquartile range = 1.0–2.2) were examined using linear mixed models. In a subsample, associations with baseline serum neurofilament light (sNfL) were examined. Results: At baseline, behavioral and social cognitive symptoms were similar between diagnosis groups, except for poorer emotion recognition in bvFTD. Over time, behavioral symptoms worsened in bvFTD, whereas most measures remained stable and the FBI improved in PPD. Regarding social cognition, emotion recognition and caregiver‐reported socioemotional sensitivity worsened in bvFTD and remained stable in PPD. Patient‐reported social cognitive measures did not change over time. Higher sNfL was associated with faster behavioral change. Conclusions: Trajectories of behavior and social cognition differentiate bvFTD from PPD, provided that social cognition is not patient‐reported. Therefore, we stress the need to optimize longitudinal social cognitive assessment in bvFTD. sNfL may be a useful prognostic marker of behavioral progression in neuropsychiatric populations. [ABSTRACT FROM AUTHOR]

Background: Age related hearing loss has been associated with increased prevalence and incidence of dementia. Underlying mechanisms that connect hearing loss with dementia remain largely unclear. Methods: We studied the association of hearing loss and other risk markers for dementia in two cohorts with normal cognition and different age: 65 participants from the EMIF‐AD 90+ study (mean age 92.7 years, 56.9% female) and 60 participants from the EMIF‐AD PreclinAD study (mean age 74.4, 43.3% female). Individuals were selected when they had hearing function ('digits‐in‐noise test') and neuropsychological testing available. Amyloid binding potential (BPND) was derived from dynamic PET scans. We used linear regression analysis and generalized estimating equations to test the association of hearing loss and BPND. We used linear mixed models to test the association of hearing function and cognition over time. In the oldest‐to‐old individuals, magnetic resonance imaging was available at the time of hearing function testing, and we performed mediation analyses to study whether cognitive decline is mediated through regional brain regions. All models included age, sex, and amyloid status as covariates, and longitudinal analyses were corrected for education years. Results: Oldest‐to‐old individuals showed worse hearing functioning than the younger cohort (p<.001). In oldest‐to‐old hearing loss was not associated with BPND (p =.70), whereas younger individuals showed an association of hearing loss with higher BPND (p =.003, figure 1). Oldest‐to‐old individuals showed associations of worse hearing with a steeper decline in memory (β ± SE = ‐0.018 ± 0.007), global cognition (β ± SE = ‐0.017 ± 0.007) and language (β ± SE = ‐0.014 ± 0.007), while in the younger cohort worse hearing was associated with steeper decline in language only (β ± SE = ‐0.086 ± 0.02, figure 2). Mediation analyses demonstrated that the hippocampus and nucleus accumbens fully mediate the effects of hearing loss on memory and global cognition in the older individuals (figure 3‐4). Conclusions: Hearing loss was associated with amyloid burden in younger individuals only, and with cognitive decline in both age groups. These results suggest that mechanisms linking hearing loss with risk for dementia depends on age. [ABSTRACT FROM AUTHOR]

Human musicality might have co-evolved with social cognition abilities, but common neuroanatomical substrates remain largely unclear. In behavioural variant frontotemporal dementia, social cognitive abilities are profoundly impaired, whereas these are typically spared in Alzheimer's disease. If musicality indeed shares a neuroanatomical basis with social cognition, it could be hypothesized that clinical and neuroanatomical associations of musicality and social cognition should differ between these causes of dementia. We recruited 73 participants from the Amsterdam Dementia Cohort ( n = 30 female; aged 50-78), of whom 23 had behavioural variant frontotemporal dementia, 22 Alzheimer's disease and 28 were healthy controls. Musicality was assessed using a music-emotion recognition test, melody, tempo, accent and tuning subscores, a musicality summed score, the identification of auditory hedonic phenotypes and music emotion induction using skin conductance responses. Social cognition was assessed across multiple levels, including emotion recognition, theory of mind, socio-emotional sensitivity and understanding of social norms. We used ANCOVA to investigate subgroup differences in musicality and social cognition and linear regressions to investigate associations between musicality and social cognition. All analyses were adjusted for age, sex, musical training and mini mental state examination. Finally, we performed voxel-based morphometry analyses on T 1 -weighted MRI to study whether regions for musicality and social cognition overlapped anatomically. We found that patients with behavioural variant frontotemporal dementia performed worse on music-emotion recognition (all P < 0.001) and tempo recognition (all P < 0.05) compared with Alzheimer's disease and on musicality summed score (all P = 0.02) compared to controls only. Furthermore, patients with behavioural variant frontotemporal dementia had lower mean skin conductance responses during emotion-inducing music, compared to Alzheimer's disease (all P < 0.045). Worse music emotion recognition scores were associated with worse facial emotion recognition ( P < 0.0001), worse theory of mind ( P = 0.0005) and worse understanding of social norms ( P = 0.01). Melody and tempo recognition were associated with facial emotion recognition and theory of mind, and accent recognition was associated with the theory of mind. Music emotion recognition and tempo recognition were also associated with executive functions. Worse music emotion recognition, melody recognition, tempo recognition, facial emotion recognition and theory of mind scores were all related to atrophy in the anterior temporal regions and the fusiform gyri, which play a role in multisensory integration, and worse tempo recognition was associated with atrophy of the anterior cingulate cortex. These results support the idea that musicality and social cognition may share a neurobiological basis, which may be vulnerable in behavioural variant frontotemporal dementia., Competing Interests: The authors report no competing interests., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Guarantors of Brain.)

The behavioural variant of Alzheimer's disease (bvAD) is characterized by early predominant behavioural changes, mimicking the behavioural variant of frontotemporal dementia (bvFTD), which is characterized by social cognition deficits and altered biometric responses to socioemotional cues. These functions remain understudied in bvAD. We investigated multiple social cognition components (i.e. emotion recognition, empathy, social norms and moral reasoning), using the Ekman 60 faces test, Interpersonal Reactivity Index, empathy eliciting videos, Social Norms Questionnaire and moral dilemmas, while measuring eye movements and galvanic skin response. We compared 12 patients with bvAD with patients with bvFTD (n = 14), typical Alzheimer's disease (tAD, n = 13) and individuals with subjective cognitive decline (SCD, n = 13), using ANCOVAs and age- and sex-adjusted post hoc testing. Patients with bvAD (40.1 ± 8.6) showed lower scores on the Ekman 60 faces test compared to individuals with SCD (49.7 ± 5.0, P < 0.001), and patients with tAD (46.2 ± 5.3, P = 0.05) and higher scores compared to patients with bvFTD (32.4 ± 7.3, P = 0.002). Eye-tracking during the Ekman 60 faces test revealed no differences in dwell time on the eyes (all P > 0.05), but patients with bvAD (18.7 ± 9.5%) and bvFTD (19.4 ± 14.3%) spent significantly less dwell time on the mouth than individuals with SCD (30.7 ± 11.6%, P < 0.01) and patients with tAD (32.7 ± 12.1%, P < 0.01). Patients with bvAD (11.3 ± 4.6) exhibited lower scores on the Interpersonal Reactivity Index compared with individuals with SCD (15.6 ± 3.1, P = 0.05) and similar scores to patients with bvFTD (8.7 ± 5.6, P = 0.19) and tAD (13.0 ± 3.2, P = 0.43). The galvanic skin response to empathy eliciting videos did not differ between groups (all P > 0.05). Patients with bvAD (16.0 ± 1.6) and bvFTD (15.2 ± 2.2) showed lower scores on the Social Norms Questionnaire than patients with tAD (17.8 ± 2.1, P < 0.05) and individuals with SCD (18.3 ± 1.4, P < 0.05). No group differences were observed in scores on moral dilemmas (all P > 0.05), while only patients with bvFTD (0.9 ± 1.1) showed a lower galvanic skin response during personal dilemmas compared with SCD (3.4 ± 3.3 peaks per min, P = 0.01). Concluding, patients with bvAD showed a similar although milder social cognition profile and a similar eye-tracking signature to patients with bvFTD and greater social cognition impairments and divergent eye movement patterns compared with patients with tAD. Our results suggest reduced attention to salient facial features in these phenotypes, potentially contributing to their emotion recognition deficits., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain.)