Background Age-related dementia, most commonly caused by Alzheimer disease or cerebrovascular factors (vascular dementia), is a major public health threat. Chronic arterial hypertension is a well-established risk factor for both types of dementia, but the link between hypertension and its treatment and cognition remains poorly understood. In this scientific statement, a multidisciplinary team of experts examines the impact of hypertension on cognition to assess the state of the knowledge, to identify gaps, and to provide future directions. Methods Authors with relevant expertise were selected to contribute to this statement in accordance with the American Heart Association conflict-of-interest management policy. Panel members were assigned topics relevant to their areas of expertise, reviewed the literature, and summarized the available data. Results Hypertension disrupts the structure and function of cerebral blood vessels, leads to ischemic damage of white matter regions critical for cognitive function, and may promote Alzheimer pathology. There is strong evidence of a deleterious influence of midlife hypertension on late-life cognitive function, but the cognitive impact of late-life hypertension is less clear. Observational studies demonstrated a cumulative effect of hypertension on cerebrovascular damage, but evidence from clinical trials that antihypertensive treatment improves cognition is not conclusive. Conclusions After carefully reviewing the literature, the group concluded that there were insufficient data to make evidence-based recommendations. However, judicious treatment of hypertension, taking into account goals of care and individual characteristics (eg, age and comorbidities), seems justified to safeguard vascular health and, as a consequence, brain health.

Objectives The purpose of this narrative review was to synthesize current research findings related to self-management, in order to better understand the processes of priority setting and decision-making in among adults with multimorbidity. Design A narrative literature review was undertaken, synthesizing findings from published, peer-reviewed empirical studies that addressed priority setting and/or decision-making in self-management of multimorbidity. Data sources A search of PubMed, PsychINFO, CINAHL and SocIndex databases was conducted from database inception through December 2013. References lists from selected empirical studies and systematic reviews were evaluated to identify any additional relevant articles. Review methods Full text of potentially eligible articles were reviewed and selected for inclusion if they described empirical studies that addressed priority setting or decision-making in self-management of multimorbidity among adults. Two independent reviewers read each selected article and extracted relevant data to an evidence table. Processes and factors and processes of multimorbidity self-management were identified and sorted into categories of priority setting, decision-making, and facilitators/barriers. Results Thirteen articles were selected for inclusion; most were qualitative studies describing processes, facilitators, and barriers of multimorbidity self-management. The findings revealed that patients prioritize a dominant chronic illness and re-prioritize over time as conditions and treatments change; that multiple facilitators (e.g. support programs) and barriers (e.g. lack of financial resources) impact individuals’ self-management priority setting and decision-making ability; as do individual beliefs, preferences, and attitudes (e.g., perceived personal control, preferences regarding treatment). Conclusions Health care providers need to be cognizant that individuals with multimorbidity engage in day-to-day priority setting and decision-making among their multiple chronic illnesses and respective treatments. Researchers need to develop and test interventions that support day-to-day priority setting and decision-making and improve health outcomes for individuals with multimorbidity.

ObjectiveTo identify existing prognostic delirium prediction models and evaluate their validity and statistical methodology in the older adult (≥60 years) acute hospital population.DesignSystematic review.Data sources and methodsPubMed, CINAHL, PsychINFO, SocINFO, Cochrane, Web of Science and Embase were searched from 1 January 1990 to 31 December 2016. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses and CHARMS Statement guided protocol development. Inclusion criteria: age >60 years, inpatient, developed/validated a prognostic delirium prediction model. Exclusion criteria: alcohol-related delirium, sample size ≤50. The primary performance measures were calibration and discrimination statistics. Two authors independently conducted search and extracted data. The synthesis of data was done by the first author. Disagreement was resolved by the mentoring author.ResultsThe initial search resulted in 7,502 studies. Following full-text review of 192 studies, 33 were excluded based on age criteria (<60 years) and 27 met the defined criteria. Twenty-three delirium prediction models were identified, 14 were externally validated and 3 were internally validated. The following populations were represented: 11 medical, 3 medical/surgical and 13 surgical. The assessment of delirium was often non-systematic, resulting in varied incidence. Fourteen models were externally validated with an area under the receiver operating curve range from 0.52 to 0.94. Limitations in design, data collection methods and model metric reporting statistics were identified.ConclusionsDelirium prediction models for older adults show variable and typically inadequate predictive capabilities. Our review highlights the need for development of robust models to predict delirium in older inpatients. We provide recommendations for the development of such models.

Background The immune response in Alzheimer’s disease (AD) involves activation of microglia which may remove β-amyloid. However, overproduction of inflammatory compounds may exacerbate neural damage in Alzheimer’s disease. AD pathology accumulates years before diagnosis, yet the extent to which neuroinflammation is involved in the earliest disease stages is unknown. Objective To determine whether neuroinflammation exacerbates neural damage in preclinical AD. Methods We utilized cerebrospinal fluid (CSF) and magnetic resonance imaging collected in 192 asymptomatic late-middle-aged adults (mean age=60.98 years). Neuroinflammatory markers chitinase-3-like protein 1 (YKL-40) and monocyte chemoattractant protein-1 (MCP-1) in CSF were utilized as markers of neuroinflammation. Neural cell damage was assessed using CSF neurofilament light chain protein (NFL), CSF total tau (T-Tau), and neural microstructure assessed with diffusion tensor imaging (DTI). With regard to AD pathology, CSF Aβ42 and tau phosphorylated at threonine 181 (P-Tau181) were used as markers of amyloid and tau pathology, respectively. We hypothesized that higher YKL-40 and MCP-1 in the presence of AD pathology would be associated with higher NFL, T-Tau, and altered microstructure on DTI. Results Neuroinflammation was associated with markers of neural damage. Higher CSF YKL-40 was associated with both higher CSF NFL and T-Tau. Inflammation interacted with AD pathology, such that greater MCP-1 and lower Aβ42 was associated with altered microstructure in bilateral frontal and right temporal lobe and that greater MCP-1 and greater P-Tau181 was associated with altered microstructure in precuneus. Conclusion Inflammation may play a role in neural damage in preclinical AD.

Results suggest that identifying early clinically relevant cognitive decline in late middle-age is feasible using robust norms and multi-test criteria.