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Although declines in cognitive capacity are assumed to be a characteristic of aging, increasing evidence shows that it is age-related disease, rather than age itself, that causes cognitive impairment. Even so, older age is a primary risk factor for cognitive decline, and with individuals living longer as a result of medical advances, cognitive impairment and dementia are increasing in prevalence. On March 26 to 27, 2018, the American Geriatrics Society convened a conference in Bethesda, MD, to explore cognitive impairment across the subspecialties. Bringing together representatives from several subspecialties, this was the third of three conferences, supported by a U13 grant from the National Institute on Aging, to aid recipients of Grants for Early Medical/Surgical Specialists' Transition to Aging Research (GEMSSTAR) in integrating geriatrics into their subspecialties. Scientific sessions focused on the impact of cognitive impairment, sensory contributors, comorbidities, links between delirium and dementia, and issues of informed consent in cognitively impaired populations. Discussions highlighted the complexity not only of cognitive health itself, but also of the bidirectional relationship between cognitive health and the health of other organ systems. Thus, conference participants noted the importance of multidisciplinary team science in future aging research. This article summarizes the full conference report, "The Impact of Cognitive Impairment Across Specialties," and notes areas where GEMSSTAR scholars can contribute to progress as they embark on their careers in aging research. J Am Geriatr Soc 67:2011-2017, 2019.

Background: The neurocognitive effect of statins in older adults remain uncertain.Objectives: The aim of this study was to investigate the associations of statin use with cognitive decline and incident dementia among older adults.Methods: This analysis included 18,846 participants ≥65 years of age in a randomized trial of aspirin, who had no prior cardiovascular events, major physical disability, or dementia initially and were followed for 4.7 years. Outcome measures included incident dementia and its subclassifications (probable Alzheimer's disease, mixed presentations); mild cognitive impairment (MCI) and its subclassifications (MCI consistent with Alzheimer's disease, other MCI); and changes in domain-specific cognition, including global cognition, memory, language and executive function, psychomotor speed, and the composite of these domains. Associations of baseline statin use versus nonuse with dementia and MCI outcomes were examined using Cox proportional hazards models and with cognitive change using linear mixed-effects models, adjusting for potential confounders. The impact of statin lipophilicity on these associations was further examined, and effect modifiers were identified.Results: Statin use versus nonuse was not associated with dementia, MCI, or their subclassifications or with changes in cognitive function scores over time (p > 0.05 for all). No differences were found in any outcomes between hydrophilic and lipophilic statin users. Baseline neurocognitive ability was an effect modifier for the associations of statins with dementia (p for interaction < 0.001) and memory change (p for interaction = 0.02).Conclusions: In adults ≥65 years of age, statin therapy was not associated with incident dementia, MCI, or declines in individual cognition domains. These findings await confirmation from ongoing randomized trials. [ABSTRACT FROM AUTHOR]

Keywords: aging; aspirin; body weight EN aging aspirin body weight 1110 1112 3 04/20/20 20200331 NES 200331 A recent meta-analysis[1] of individual patient data from several randomized, controlled trials evaluating aspirin for the prevention of primary or secondary cardiovascular events found that the protective effect of low-dose aspirin (<=100 mg) was limited to individuals weighing <70 kg, driven by lean body mass (LBM) but not body mass index (BMI).[1] Given the limited number of people >=70 years of age who were included in the meta-analysis[1] and calls for validation of these findings,[2],[3] we investigated whether body habitus modulated the efficacy of aspirin in a post hoc analysis of the ASPREE trial (Aspirin in Reducing Events in the Elderly).[4] ASPREE randomized 19 114 older participants to daily 100-mg enteric-coated aspirin (9525) or matched placebo (9589) and followed them up for a median of 4.7 years for disability-free survival and other clinical outcomes.[4] Trial participants were community-dwelling Australian (16 703) and US (2411) men and women who were >=70 years of age at enrollment or >=65 years of age for US blacks and Hispanics. At baseline, anthropometric indexes (mean±SD) of body weight, BMI, waist circumference, and LBM in the aspirin versus placebo groups were 77.0±15.1 kg versus 77.0±14.8 kg, 28.1±4.8 kg/m SP 2 sp versus 28.1±4.7 kg/m SP 2 sp , 97±13 cm versus 97±13 cm, and 49.8±8.3 kg versus 49.9±8.2 kg, respectively. Larger BMI or waist circumference or LBM also did not alter the effect of aspirin on the risk of cardiovascular disease or major hemorrhage (Figure). [Extracted from the article]