Late-life body mass index, rapid weight loss, apolipoprotein E ε4 and the risk of cognitive decline and incident dementia

Abstract

Purpose of the study To examine the effect of late-life body mass index (BMI) and rapid weight loss on incident mild cognitive impairment (MCI) and Alzheimer’s disease (AD) Design Prospective longitudinal cohort study Setting National Alzheimer’s Coordinating Center (NACC) Uniform Data Set, including 34 past and current National Institute on Aging-funded AD Centers across the United States Participants 6940 older adults (n=5061 normal cognition (NC); n=1879 MCI) Measurements BMI (kg/m2) and modified Framingham Stroke Risk Profile (FSRP) score (sex, age, systolic blood pressure, anti-hypertension medication, diabetes mellitus, cigarette smoking, prevalent cardiovascular disease, atrial fibrillation) were assessed at baseline. Cognition and weight were assessed annually. Results Multivariable binary logistic regression, adjusting for age, sex, race, education, length of follow-up, and modified FSRP related late-life BMI to risk of diagnostic conversion from NC to MCI or AD and from MCI to AD. Secondary analyses related late-life BMI to diagnostic conversion in the presence of rapid weight loss (>5% decrease in 12 months) and apolipoprotein E (APOE) ε4. During a mean 3.8-year follow-up period, 12% of NC participants converted to MCI or AD and 49% of MCI participants converted to AD. Higher baseline BMI was associated with a reduced probability of diagnostic conversion, such that for each one-unit increase in baseline BMI there was a reduction in diagnostic conversion for both NC (OR=0.977, 95%CI 0.958–0.996, p=0.015) and MCI participants (OR=0.962, 95%CI 0.942–0.983, p<0.001). The protective effect of higher baseline BMI did not persist in the setting of rapid weight loss but did persist when adjusting for APOE. Conclusions Higher late-life BMI is associated with a lower risk of incident MCI and AD but is not protective in the presence of rapid weight loss.

Social network types and cognitive decline among older Korean adults: A longitudinal population‐based study

“…The association between BMI in late life and CD has been controversial . While some studies observed that higher BMI is linked with increased risk of dementia, others found an inverse association in elders, consistent with our findings. More research examining the association BMI between CD is needed.…”

“…The association between BMI in late life and CD has been controversial. 48 While some studies observed that higher BMI is linked with increased risk of dementia, 49 others found an inverse association in elders, 50 relationships between specific domains of cognitive function and SN types. Forth, we did not include persons who died or dropped out of the survey.…”

High levels of plasma fibrinogen are related to post‐stroke cognitive impairment

“…It has been shown that long-term intake of high-fat diets, even in the absence of obesity, leads to cognitive deficits (Cifre, Palou, & Oliver, 2018). One study indicates that obesity may increase the risk for AD by twofold (Salas et al, 2018), whereas other studies report that a higher BMI is associated with a lower risk of cognitive deficits (Bell et al, 2017;Cova et al, 2016) and that a lower BMI contributes to cognitive impairment (Mathys, Gholamrezaee, Henry, von Gunten, & Popp, 2017;Pilleron et al, 2015). Another study showed that participants with a baseline BMI ≥ 25 kg/m 2 had significantly higher MMSE scores compared with participants with BMI < 25 kg/m 2 (Coin et al, 2012).…”

Should weight loss in elderly people be recommended?

“…This mechanism is not fully understood because fat tissue simultaneously produces soluble receptors for TNFα (srTNFα), which can neutralise the secreted TNFα. This phenomenon is the subject of numerous discussions which try to explain the better prognosis of obese elderly people with cardiovascular diseases [28,29].…”

“…Mechanizm ten nie został do końca poznany, ponieważ tkanka tłuszczowa produkuje równocześnie rozpuszczalne receptory dla TNF-α (srTNFα), które mogą neutralizować wydzielany TNF-α. Zjawisko to jest przedmiotem licznych dyskusji, które próbują wyjaśnić lepsze rokowanie otyłych osób starszych z chorobami układu krążenia [28,29].…”