Nutritional care and support should be an integral part of dementia management. In all stages of the disease, the decision for or against nutritional interventions should be made on an individual basis after carefully balancing expected benefit and potential burden, taking the (assumed) patient will and general prognosis into account.

Abstract. The use of supplements with omega-3 (ω3) fatty acids (FAs) such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) is widespread due to proposed beneficial effects on the nervous and cardiovascular systems. Many effects of ω3 FAs are believed to be caused by down-regulation and resolution of inflammation. Alzheimer's disease (AD) is associated with inflammation mediated by microglia and astrocytes, and ω3 FAs have been proposed as potential treatments for AD. The focus of the present study is on the effects of DHA and EPA on microglial phagocytosis of the AD pathogen amyloid-␤ (A␤), on secreted and cellular markers of immune activity, and on production of brain-derived neurotrophic factor (BDNF). Human CHME3 microglial cells were exposed to DHA or EPA, with or without the presence of A␤ 42 . Phagocytosis of A␤ 42 was analyzed by flow cytometry in conjunction with immunocytochemistry using antibodies to cellular proteins. Secreted proteins were analyzed by ELISA. Both DHA and EPA were found to stimulate microglial phagocytosis of A␤ 42 . Phagocytosis of A␤ 42 was performed by microglia with a predominance of M2 markers. EPA increased the levels of BDNF in the culture medium. The levels of TNF-␣ were decreased by DHA. Both DHA and EPA decreased the pro-inflammatory M1 markers CD40 and CD86, and DHA had a stimulatory effect on the anti-inflammatory M2 marker CD206. DHA and EPA can be beneficial in AD by enhancing removal of A␤ 42 , increasing neurotrophin production, decreasing pro-inflammatory cytokine production, and by inducing a shift in phenotype away from pro-inflammatory M1 activation.

High adherence to prudent diet may diminish the adverse effects of high adherence to Western diet on cognitive decline.

Objectives: We studied the nutritional status and the effects of nutritional intervention on body weight, cognition and activities of daily life (ADL)-function in demented individuals. Design: Controlled non-randomised study. Setting: Group-living for demented elderly (GLD), ie community assisted housing. Subjects and interventions: Twenty-two residents living in one of two units (GLD-I), received oral liquid supplements (1720 kJ=410 kcal=day) and the personnel of the GLD-I were given nutritional education. Fourteen residents in the other unit (GLD-C) served as controls. After 6 months 21 (83 (4) y, 81% women) and 12 (85 (4) y, 100% women) of the participants, respectively, were re-examined according to body mass index (BMI, kg=m 2 ), cognitive function (Mini Mental State Examination (MMSE, 0 -30 p) and Clinical Dementia Rating Scale (CDR) and the Katz' ADL index. Results: Body mass index (BMI) 20 was found in 19% of the participants and 44% had BMI 23. BMI correlated with MMSE (r ¼ 0.43, P < 0.01). The weight of the residents in the intervention group increased by 3.4 (3) kg (P ¼ 0.001) at follow-up, whereas the weight remained unchanged in the control group. The cognitive function was low at the start in both groups, ie MMSE 9 and no apparent positive effect of the nutritional intervention was seen. In addition, the ADL functions appeared to deteriorate in both groups. Conclusions: Being underweight was common among demented elderly in group-living and was related to low cognitive capacity. Five months of oral supplementation, along with education of personnel, was followed by a weight gain. In this study the nutritional treatment did not affect the rate of decline in cognitive function or Katz' ADL index. Sponsorship: Supported by grants from the Swedish National Board of Health and Social Welfare. Semper Foods AB provided the liquid supplements.

Appropriate dietary pattern for preserving cognitive function in northern Europe remains unknown. We aimed to identify a Nordic dietary pattern index associated with slower cognitive decline compared to the Mediterranean-DASH Intervention for Neurodegenerative Delay, Mediterranean Diet, Dietary Approaches to Stop Hypertension, and Baltic Sea Diet indices. A total of 2223 dementia-free adults aged ≥60 were followed for 6 years. Mini-Mental State Examination was administrated at baseline and follow-ups. Dietary intake was assessed by 98-item food frequency questionnaire, and the Nordic Prudent Dietary Pattern (NPDP) was identified. Data were analysed using mixed-effects and parametric survival models and receiver operating characteristic curves with adjustment for potential confounders. Moderate (β = 0.139, 95% CI 0.077−0.201) and high adherence (β = 0.238, 95% CI 0.175−0.300) to NPDP were associated with less cognitive decline compared to other four indices. High adherence to NPDP was also associated with the lowest risk of MMSE decline to ≤24 (HR = 0.176, 95% CI 0.080−0.386) and had the greatest ability to predict such decline (area under the curve = 0.70). Moderate-to-high adherence to the NPDP may predict a better-preserved cognitive function among older adults in Nordic countries. Regional dietary habits should be considered in developing dietary guidelines for the prevention of cognitive impairment and dementia.