Objective: To assess the impact of a multi‐strategic, interdisciplinary intervention on antipsychotic and benzodiazepine prescribing in residential aged care facilities (RACFs). Design, setting: Prospective, longitudinal intervention in Australian RACFs, April 2014 – March 2016. Participants: 150 RACFs (with 12 157 residents) comprised the main participant group; two further groups were consultant pharmacists (staff education) and community pharmacies (prescribing data). Data for all RACF residents, excluding residents receiving respite or end‐stage palliative care, were included. Intervention: A multi‐strategic program comprising psychotropic medication audit and feedback, staff education, and interdisciplinary case review at baseline and 3 months; final audit at 6 months. Main outcome measure: Mean prevalence of regular antipsychotic and benzodiazepine prescribing at baseline, and at 3 and 6 months. Secondary measures: chlorpromazine and diazepam equivalent doses/day/resident; proportions of residents for whom drug was ceased or the dose reduced; prevalence of antidepressant and prn (as required) psychotropic prescribing (to detect any substitution practice). Results: During the 6‐month intervention, the proportion of residents prescribed antipsychotics declined by 13% (from 21.6% [95% CI, 20.4–22.9%] to 18.9% [95% CI, 17.7–20.1%]), and that of residents regularly prescribed benzodiazepines by 21% (from 22.2% [95% CI, 21.0–23.5%] to 17.6% [95% CI, 16.5–18.7]; each, P < 0.001). Mean chlorpromazine equivalent dose declined from 22.9 mg/resident/day (95% CI, 19.8–26.0) to 20.2 mg/resident/day (95% CI, 17.5–22.9; P < 0.001); mean diazepam equivalent dose declined from 1.4 mg/resident/day (95% CI, 1.3–1.5) to 1.1 mg/resident/day (95% CI, 0.9–1.2; P < 0.001). For 39% of residents prescribed antipsychotics and benzodiazepines at baseline, these agents had been ceased or their doses reduced by 6 months. There was no substitution by sedating antidepressants or prn prescribing of other psychotropic agents. Conclusions: The RedUSe program achieved significant reductions in the proportions of RACF residents prescribed antipsychotics and benzodiazepines. Trial registration: Australian New Zealand Clinical Trials, ACTRN12617001257358.

Background: Although many studies have investigated the association between stress and risk of dementia, findings are inconsistent due to the variation in the measures used to assess stress. Objective: We conducted a systematic review and meta-analysis to investigate the association between psychological stress (including neuroticism, stressful life events, and perceived stress) and the risk of incident dementia and mild cognitive impairment in adults. Methods: PsycINFO, Embase, and MEDLINE were searched to October 2020 for eligible observational, prospective studies. Of the 1,607 studies screened, 26 (24 unique cohorts) were included in the qualitative analysis and 16 (15 unique cohorts) were included in the quantitative analysis. Results: Across studies, higher perceived stress was significantly associated with an increased risk of mild cognitive impairment (Cases/Total N = 207/860: hazard ratio [HR] = 1.19, 95% confidence interval [CI] = 1.03–1.38) and all-cause dementia (Cases/Total N = 203/1,882: HR = 1.44, 95% CI = 1.07–1.95). Exposure to two or more stressful life events (versus none) was significantly associated with an increased risk of all-cause dementia (Cases/Total N = 3,354/11,597: HR = 1.72, 95% CI = 1.14–2.60), while one or more stressful life events was not. Higher neuroticism was significantly associated with an increased risk of Alzheimer’s disease dementia (Cases/Total N = 497/4,771: HR = 1.07, 95% CI = 1.01–1.12), but not all-cause dementia. Conclusion: This review suggests that psychological stress in adulthood is associated with an increased risk of dementia. Further research is needed to clarify the mechanisms underlying these associations.

The pathogenesis of Alzheimer’s disease (AD) has been postulated to preferentially impact specific neural networks in the brain. The olfactory system is a well-defined network that has been implicated in early stages of the disease, marked by impairment in olfaction and the presence of pathological hallmarks of the disease, even before clinical presentation. Discovering the cellular mechanisms involved in the connectivity of pathology will provide insight into potential targets for treatment. We review evidence from animal studies on sensory alteration through denervation or enrichment, which supports the notion of using the olfactory system to investigate the implications of connectivity and activity in the spread of pathology in AD.

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