As malnutrition is common in patients with Alzheimer’s disease (AD), we evaluated nutritional status and body composition of patients with AD, mild cognitive impairment (MCI) and controls, and studied associations of AD biomarkers and cognitive performance with nutritional status and body composition. We included 552 participants, of which 198 patients had AD, 135 patients had MCI and 219 controls. We assessed nutritional status (mini nutritional assessment (MNA)) and body composition (body mass index (BMI), fat-free mass (FFM) and waist circumference). Linear regression analyses (adjusted for age, gender and education where appropriate) were applied to test associations of AD biomarkers and cognitive performance on five domains with nutritional parameters (dependent). Patients with MCI and AD had a lower BMI and MNA score than controls. Worse performance in all cognitive domains was associated with lower MNA score, but not with body composition. AD biomarkers were associated with MNA score, BMI and waist circumference, and associations with MNA score remained after adjustment for cognitive performance. Both AD biomarkers and cognitive performance were associated with nutritional status, associations with AD biomarkers remained after adjustment for cognition. Our data suggest that malnutrition is not only related to impaired cognition but also to AD pathology.

Background: Malnutrition is common in patients with Alzheimer’s disease (AD) dementia and mild cognitive impairment (MCI) and is associated with institutionalization and increased mortality. Malnutrition is the result of a negative energy balance, which could be due to reduced dietary intake and/or higher energy expenditure. To study underlying mechanisms for malnutrition, we investigated dietary intake and resting energy expenditure (REE) of patients with AD dementia, MCI, and controls. In addition, we studied associations of global cognition (Mini-Mental State Examination (MMSE)) and AD biomarkers with dietary intake and REE. Methods: We included 219 participants from the NUDAD project, 71 patients with AD dementia (age 68 ± 8 years, 58% female, MMSE 24 ± 3), 52 with MCI (67 ± 8 years, 42% female, MMSE 26 ± 2), and 96 controls (62 ± 7 years, 52% female, MMSE 28 ± 2). We used a 238-item food frequency questionnaire to assess dietary intake (energy, protein, carbohydrate, and fat). In a subgroup of 92 participants (30 patients with AD dementia, 22 with MCI, and 40 controls) we measured REE with indirect calorimetry. Between-group differences in dietary intake and REE were tested with ANOVAs. In the total sample, linear regression analyses were used to explore potential associations of MMSE score and AD biomarkers with dietary intake and REE. All analyses were adjusted for age, sex, education, and body mass index or fat-free mass. Results: Patients with AD dementia and MCI did not differ from controls in total energy intake (1991 ± 71 and 2172 ± 80 vs 2022 ± 61 kcal/day, p > 0.05) nor in protein, carbohydrate, or fat intake. Patients with AD dementia and MCI had a higher REE than controls (1704 ± 41 and 1754 ± 47 vs 1569 ± 34 kcal/day, p < 0.05). We did not find any association of MMSE score or AD biomarkers with dietary intake or REE. Conclusions: We found a higher REE, despite similar energy intake in patients with AD and MCI compared to controls. These findings suggest that elevated metabolism rather than reduced energy intake explains malnutrition in AD. These results could be useful to optimize dietary advice for patients with AD dementia and MCI.

Our aim is to compare olfactory and gustatory function and food preferences of patients with Mild Cognitive Impairment (MCI) and Alzheimer’s disease (AD) with controls. We included 22 patients with MCI, 30 patients with AD and 40 controls and assessed olfactory threshold, odor discrimination and odor identification (Sniffin’ Sticks), gustatory functioning (Taste Strips), and food preferences (Macronutrient and Taste Preference Ranking Task). Linear regression analyses were used to study associations of five cognitive domains or AD biomarkers with olfactory functioning. Groups did not differ in olfactory threshold, gustatory function and food preferences. Patients with MCI and AD scored lower on odor discrimination and identification than controls. Poorer memory, but no other cognitive domain, was associated with poorer odor discrimination and odor identification, but not with odor threshold. No associations with AD biomarkers were found. In conclusion, patients with MCI and AD have poorer odor discrimination and identification ability than controls, but similar detection thresholds. This is likely a consequence of poorer memory rather than directly caused by AD pathology.

Nutrition is one of the modifiable risk factors for cognitive decline and Alzheimer’s disease (AD) dementia, and is therefore highly relevant in the context of prevention. However, knowledge of dietary quality in clinical populations on the spectrum of AD dementia is lacking, therefore we studied the association between dietary quality and cognitive impairment in Alzheimer’s disease (AD) dementia, mild cognitive impairment (MCI) and controls. We included 357 participants from the NUDAD project (134 AD dementia, 90 MCI, 133 controls). We assessed adherence to dietary guidelines (components: vegetables, fruit, fibers, fish, saturated fat, trans-fat, salt, and alcohol), and cognitive performance (domains: memory, language, visuospatial functioning, attention, and executive functioning). In the total population, linear regression analyses showed a lower vegetable intake is associated with poorer global cognition, visuospatial functioning, attention and executive functioning. In AD dementia, lower total adherence to dietary guidelines and higher alcohol intake were associated with poorer memory, a lower vegetable intake with poorer global cognition and executive functioning, and a higher trans-fat intake with poorer executive functioning. In conclusion, a suboptimal diet is associated with more severely impaired cognition—this association is mostly attributable to a lower vegetable intake and is most pronounced in AD dementia.

In cognitively normal adults, nutritional parameters are related to cognitive decline and incidence of dementia. Studies on the role of nutrition in predementia stages subjective cognitive decline and mild cognitive impairment, and mild stages of Alzheimer's disease (AD) dementia in a clinical setting are lacking. In the absence of a curative treatment, this evidence is important for targeting nutritional factors to potentially prevent or delay further cognitive decline. Our aim is to investigate associations of nutritional parameters with clinical progression in patients ranging from those who are cognitively normal to those who have AD dementia. Longitudinal. Memory clinic, 551 patients (219 with subjective cognitive decline, 135 with mild cognitive impairment, and 197 with AD dementia), mean age 64 ± 8 years. We assessed body mass index, fat-free mass, Mini-Nutritional Assessment, and dietary intake with the Dutch Healthy Diet food frequency questionnaire and the 238-item healthy life in an urban setting (HELIUS) food frequency questionnaire at baseline. Cox proportional hazard models were used to evaluate associations of nutritional parameters with clinical progression. Additional analyses were restricted to patients who were amyloid positive. We observed clinical progression in 170 patients (31%) over 2.2 ± 0.9 years. Poorer Mini-Nutritional Assessment score [hazard ratio (95% confidence interval) 1.39 (1.18-1.64)], lower body mass index [1.15 (0.96-1.38)], lower fat-free mass [1.40 (0.93-2.10)], and a less healthy dietary pattern [1.22 (1.01-1.48)] were associated with a higher risk of clinical progression. Similar effect sizes were found in patients who were amyloid positive. Poorer nutritional status and a less healthy dietary pattern are associated with a higher risk of clinical progression. This study provides support for investigating whether improving nutritional status can alter the clinical trajectory of AD.