[FTS5–01–01]: PREVENTION: THE FIRST LINE OF CARE

19551 A New Model of Potentially Modifiable Risk Factors for Dementia Gill Livingston, MBChB, MD, University College London, London, United Kingdom One way of considering risk in dementia is to calculate the Population Attributable Fraction (PAF), which is the percentage reduction in new cases over a given time if a particular risk factor were completely eliminated. The work to-date focuses on cardiovascular risk factors for dementia; and depression and low educational attainment. Which modifiable risk factors? We calculated a combined PAF for known modifiable risk factors for all-cause incident dementia listed in the UK National Institute of Health and Care Excellence and US National Institute of Health guidelines. We used data from meta-analyses. PAF for modifiable risk factors The attributable risk in a population depends on the prevalence of the risk factor and the strength of its association (relative risk) with the disease. While systematic reviews adjusted for many confounders, they could not adjust for all the risk factors in our total PAF calculation. We therefore calculated overall PAF by using a formula to adjust for communality when confounding has not been fully accounted for (PAF = 1-[(1-PAF1)(1-PAF2)(1-PAF3)...] ) allow calculation of each factor’s unique risk. We found three principal component using this method, which explained 53% of the total variance between the nine risk factors, suggesting substantial overlap. We then calculated overall PAF from nine risk factors; education to age 11 or 12, midlife hypertension, midlife obesity, hearing loss, later-life depression, diabetes, physical inactivity, smoking and social isolation. We will present the new model of life course risk factors in the conference. There are additional factors which we do not have data to include in our calculations but may be important. These encompass, dietary factors, alcohol use, visual impairment, bilingualism, living near major roads and sleep disorders which have received some attention for their role in the development of cognitive impairment. We will discuss other limitations of the data at the conference. The general principle is that there is an important proportion of modifiable risk factors in dementia, which could translate into a large impact on the global burden of dementia which would then have huge implications for social and healthcare costs. EMBARGOED FOR RELEASE UNTIL THURSDAY JULY 20, 2017, 5:01 AM BST/12:01 AM EDT Page 5 of 6 Abstract 19552 Treatment of Cognition Robert J Howard, MD, University College London, London, United Kingdom19552 Treatment of Cognition Robert J Howard, MD, University College London, London, United Kingdom Treatment with cholinesterase inhibitors modestly improves cognition, activities of daily living and global clinician rating of patients with mild, moderate and severe Alzheimer’s disease (AD). Improvements are close to minimal clinically important values such that clinicians should not expect to be able to make decisions about response in an individual treated patient. Treatment decisions will often be influenced by experience of side-effects, in particular nausea, vomiting, diarrhea, vivid dreams and cramps. These drugs do not improve non-cognitive AD symptoms and there is no convincing evidence for additional cognitive or functional benefit with higher than standard (>10mg donepezil) dosing. Although most trials have been of short duration, treatment benefits appear to be sustained, even in severely affected individuals, and this should be considered in discontinuation decisions. Meta-analyses report cognitive benefits in patients with dementia with Lewy bodies and Parkinson’s disease dementia. Although not recommended for patients with frontotemporal or vascular dementia, patients with mixed vascular and AD pathology may benefit from treatment. Memantine improves cognition, activities of daily living and global rating, but benefits are smaller than those seen with cholinesterase inhibitors, often not reaching clinically important levels and is often used for patients who cannot tolerate a cholinesterase inhibitor. Combination treatment with a cholinesterase inhibitor is associated with very small additional benefit compared to cholinesterase inhibitor alone. Cognitive stimulation therapy has better evidence to support claims for improving cognition in AD than cognitive training and cognitive rehabilitation. It is important to bear in mind that most cognitive intervention studies have not included active control interventions or strategies to blind outcome assessors that would allow meaningful comparison with the results of pharmaceutical trials. Finally, physical exercise may improve activities of daily living in AD, but reported effects on cognition have not been consistent. Together with the difficulties in interpretation of efficacy associated again with failure to include adequate control interventions or to blind outcome assessors, it is still unclear whether the intensity of prescribed exercise needs to exceed a threshold above which cognitive benefits can be demonstrated. Abstract 19553 Approach to Agitation and Other Psychiatric Syndromes/ Behaviors19553 Approach to Agitation and Other Psychiatric Syndromes/ Behaviors Lon S Schneider, MD, MS, Keck School of Medicine of USC, Los Angeles, CA, USA We will highlight the commission’s approach to agitation and other psychiatric syndromes, behaviors. The goals are to recognize psychiatric symptoms, manage, protect, and individualize care over the long-term. Psychiatric symptoms in dementia are common, generally increasing with stage of dementia and affecting nearly everyone with dementia at some point. Many different symptoms co-occur and may cluster into affective, psychosis, apathy, and hyperactivity, highlighting the need for careful assessment and a management strategy, for example, the DICE approach. We will outline interventions with the best evidence for the assessment and management of agitation, including pleasant events and maximizing communication as prevention strategies, and providing good quality care. We will discuss management principles for agitation and their overlap with other symptoms (such as hallucinations, delusions, depression and apathy) which may co-occur. Indications for drug interventions including antipsychotics and antidepressants, harmful effects, and withdrawal will be outlined. Assessing and managing agitation might start with asking the person what is wrong and involve improving communication and person-centered care, consideration and management of physical causes (pain, infection, discomfort etc.) pleasant activities, social engagement, occupational interventions, caregiver interventions; before considering pharmacological treatments. For management of depressive symptoms it is important to consider risk for self-harm, self-neglect, underlying delirium, pain, and the need for tailored treatment to patient’s needs and wishes. Substantial improvement in quality of life can be gained with considerate and personalized interventions for psychiatric symptoms including agitation. EMBARGOED FOR RELEASE UNTIL THURSDAY JULY 20, 2017, 5:01 AM BST/12:01 AM EDT Page 6 of 6 Proposal ID FTS5-02-01 Public Health & Psychosocial: Advancing Health Disparities Research with the National Institute on Aging Focused Topic Session, July 20, 2017: 11:45 AM-1:15 PM The session will focus on the inaugural grantees of PAR15-349: Health Disparities and Alzheimer’s Disease (R01) and PAR15-350: Emerging Directions for Addressing Health Disparities in Alzheimer’s Disease (R03). This session will highlight the oncoming new information that will result because of the awards. Chair Carl Hill, Ph.D., M.P.H. (hillcv@mail.nih.gov), National Institutes of Health (NIH), Bethesda MD Chair Rachel Whitmer, PhD, Kaiser Permanente Division of Research, Oakland CA 94530 Abstract 19570: Racial Disparities in the Health of Caregivers for Persons with Alzheimer’s Disease Julie M Zissimopoulos, Ph.D, University of Southern California, Los Angeles, CA19570: Racial Disparities in the Health of Caregivers for Persons with Alzheimer’s Disease Julie M Zissimopoulos, Ph.D, University of Southern California, Los Angeles, CA Abstract 19571: Alzheimer’s Disease & Related Dementias: Geography, Environments, and Mechanisms (ADRD-GEM) Jiu-Chiuan Chen, MD, ScD, University of Southern California, Los Angeles, CA19571: Alzheimer’s Disease & Related Dementias: Geography, Environments, and Mechanisms (ADRD-GEM) Jiu-Chiuan Chen, MD, ScD, University of Southern California, Los Angeles, CA Abstract 19572: Lifecourse Health, Cerebral Pathology and Ethnic Disparities in Dementia Rachel A. Whitmer, PhD, University of California, San Francisco, San Francisco, CA, Kaiser Permanente Division of Research, Oakland, CA19572: Lifecourse Health, Cerebral Pathology and Ethnic Disparities in Dementia Rachel A. Whitmer, PhD, University of California, San Francisco, San Francisco, CA, Kaiser Permanente Division of Research, Oakland, CA Abstract 19573: Discussant Elizabeth Rose Mayeda, PhD, MPH, University of California, San Francisco, San Francisco, CA19573: Discussant Elizabeth Rose Mayeda, PhD, MPH, University of California, San Francisco, San Francisco, CA Abstract 19574: Offspring Study of Mechanisms for Racial in Alzheimer's Disease Jennifer J Manly, PhD, Columbia University, New York, NY19574: Offspring Study of Mechanisms for Racial in Alzheimer's Disease Jennifer J Manly, PhD, Columbia University, New York, NY Abstract 19575: Imaging and Health Disparities Charles S DeCarli, MD, Department of Neurology, University of California at Davis, Davis, CA19575: Imaging and Health Disparities Charles S DeCarli, MD, Department of Neurology, University of California at Davis, Davis, CA Abstract 19576: Health Disparities in Alzheimer's Disease Among Mexican Americans Sid O'Bryant, PhD, University of North