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Through various manifestations, social inappropriateness is frequently the first clinical sign of a neurodegenerative process, especially in AD and bvFTD, years before noticeable impairment on classical neuropsychological assessment and brain atrophy on imaging.

Background A widely held dictum in aging research is that heterogeneity in health increases with age, but the basis for this claim has not been fully investigated. We examined heterogeneity at different ages across health characteristics to describe variation and trends; we investigated the comparative importance of between‐age versus within‐age heterogeneity. Design This was a cohort study. Setting Community‐dwelling older adults. Participants A total of 30,097 adults aged 45 to 86 years, from the Canadian Longitudinal Study on Aging, were included. Measurements Thirty‐four health characteristics in eight domains (physical measures, vital signs, physiological measures, physical performance, function/disability, chronic conditions, frailty, laboratory values) were assessed cross‐sectionally. We used regression models to examine heterogeneity in health characteristics (using absolute deviation) and domains (using effective variance) in relation to age. Comparison between between‐age and within‐age heterogeneity was quantified by estimating the age threshold at which the former exceeds the latter. Results Of the 34 health characteristics, 17 showed increased heterogeneity, 8 decreased, and 9 no association with age. The associations between heterogeneity and age increased generally but were nonlinear for most domains and nonmonotonic for some. We observed peak heterogeneity at approximately 70 years. Between‐age heterogeneity, compared with within‐age heterogeneity, was most important for forced expiratory volume in 1 second and grip strength but varied across characteristics. Conclusion Overall health heterogeneity increases with age but does not uniformly increase across all variables and domains. Heterogeneity in aging reinforces the need for geriatric assessment and personalized care, depending on which health characteristics are assessed, their measurement properties, and their referent group. Our findings suggest further research to develop improved single‐dimension and multidimensional instruments, as well as specific vital and laboratory reference ranges for older adults.

In late life, traumas may act cumulatively to exacerbate vulnerability to post-traumatic stress disorder (PTSD). PTSD is also a risk factor for cognitive decline. Major neurocognitive disorder (MND) can be associated with worsening of already controlled PTSD symptoms, late-life resurgence or de novo emergence. Misidentifying PTSD symptoms in MND can have negative consequences for the patient and families. We review the literature pertaining to PTSD and dementia and describe five cases referred for consultation in geriatric psychiatry initially for behavioural and psychological symptoms of dementia (BPSD), which were eventually diagnosed and treated as PTSD in MND subjects. We propose that certain PTSD symptoms in patients with MND are misinterpreted as BPSD and therefore, not properly addressed. For example, flashbacks could be interpreted as hallucinations, hypervigilance as paranoia, nightmares as sleep disturbances, and hyperreactivity as agitation/aggression. We suggest that better identification of PTSD symptoms in MND is needed. We propose specific recommendations for care, namely: clarifying diagnosis by distinguishing PTSD symptoms coexisting with different types of dementia from a specific dementia symptom (BPSD), gathering a detailed history of the trauma in order to personalise non-pharmacological interventions, adapting psychotherapeutic strategies to patients with dementia, using selective serotonin reuptake inhibitors as first-line treatment and avoiding antipsychotics and benzodiazepines. Proper identification of PTSD symptoms in patients with MND is essential and allows a more tailored and efficient treatment, with decrease in inappropriate use of physical and chemical restraints.

Tobacco addiction is the most important preventable cause of morbidity and mortality in Canada. Family physicians, nurse practitioners and other front-line health care professionals are well positioned to influence and assist their patients in quitting, thereby reducing the burden on both personal health and the public health care system.

Background We aimed to systematically describe the burden and distribution of white matter hyperintensities (WMH) and investigate correlations with neuropsychiatric symptoms in pathologically proven Alzheimer’s disease (AD) and frontotemporal lobar degeneration (FTLD). Methods Autopsy-confirmed cases were identified from the Sunnybrook Dementia Study, including 15 cases of AD and 58 cases of FTLD (22 FTLD-TDP cases; 10 FTLD-Tau [Pick’s] cases; 11 FTLD-Tau Corticobasal Degeneration cases; and 15 FTLD-Tau Progressive Supranuclear Palsy cases). Healthy matched controls (n = 35) were included for comparison purposes. Data analyses included ANCOVA to compare the burden of WMH on antemortem brain MRI between groups, adjusted linear regression models to identify associations between WMH burden and neuropsychiatric symptoms, and image-guided pathology review of selected areas of WMH from each pathologic group. Results Burden and regional distribution of WMH differed significantly between neuropathological groups (F5,77 = 2.67, P’ = 0.029), with the FTLD-TDP group having the highest mean volume globally (8032 ± 8889 mm3) and in frontal regions (4897 ± 6163 mm3). The AD group had the highest mean volume in occipital regions (468 ± 420 mm3). Total score on the Neuropsychiatric Inventory correlated with bilateral frontal WMH volume (β = 0.330, P = 0.006), depression correlated with bilateral occipital WMH volume (β = 0.401, P < 0.001), and apathy correlated with bilateral frontal WMH volume (β = 0.311, P = 0.009), all corrected for the false discovery rate. Image-guided neuropathological assessment of selected cases with the highest burden of WMH in each pathologic group revealed presence of severe gliosis, myelin pallor, and axonal loss, but with no distinguishing features indicative of the underlying proteinopathy. Conclusions These findings suggest that WMH are associated with neuropsychiatric manifestations in AD and FTLD and that WMH burden and regional distribution in neurodegenerative disorders differ according to the underlying neuropathological processes.

Although age and female representation increased over time, the modest trends are unlikely to resolve the persistently wide gaps with actual populational prevalence, especially for coronary artery disease and HF. Representation is modulated by the cardiovascular condition studied and some modifiable protocol elements.