Abstract
AbstractBackgroundWeight loss has been shown to be detectable more than ten years prior to Alzheimer disease (AD) diagnosis and is associated with higher morbidity, mortality and progression of cognitive decline. We aimed to investigate associations between nutritional status, including weight loss and body composition, and MRI measures of cerebral atrophy and cerebrovascular pathology in patients with mild cognitive impairment (MCI), AD dementia and controls.MethodsWe included 412 patients from the NUDAD project, comprising 129 patients with AD dementia (68±8 years, 48%F, MMSE 24[21‐26]), 107 patients with MCI (67±8 years, 63%F, MMSE 27[25‐28]), and 176 controls (61±8 years, 62;54%F, MMSE 29[27‐29]). Body mass index (BMI), fat mass (FM), fat free mass index (FFMI), waist circumference and mini nutritional assessment (MNA) scores were measured as indicators of nutritional status and transformed to Z‐scores. On MRI, we performed visual ratings (medial temporal atrophy (MTA, 0‐4), global cortical atrophy (GCA, 0‐3), white matter hyperintensities (WMH, 0‐4), microbleeds (0; 1‐2; 3‐5; >5)). Associations between nutritional status and MRI measures were analyzed using linear regression, adjusted for age, sex, syndrome diagnosis and cardiovascular risk factors.ResultsMCI and AD patients had lower BMI, FM and total MNA scores than controls. Lower BMI (ß ‐0.09 (‐0.16; ‐0.01), p<0.05) and lower FFMI (ß ‐0.11 (‐0.22; 0.00), p<0.05) were associated with higher MTA scores, but not with GCA, WMH or microbleeds. Lower FM (ß ‐0.13 (‐0.24;‐0.02), p<0.05) and lower waist circumference (ß ‐0.14 (‐0.25;‐0.02), p<0.05) were associated with more microbleeds, but not with MTA, GCA or WMH scores. Stratification by syndrome diagnosis showed that the observed associations of FM and waist with microbleeds were only significant in MCI patients.ConclusionIn our memory clinic cohort, lower indicators of nutritional status were associated with more MTA and microbleeds, two MRI markers indicative of underlying AD pathology; with strongest associations in MCI and amyloid‐positive controls. Our findings indicate that nutritional status has a role in the development of AD, either as early consequence of the underlying pathology or as an aggravating factor.
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