Objectives: Adiposity may have a role in the risk of dementia. Fewer studies have focused on the relationship between change in adiposity and cognitive decline. Our study aimed to explore the association between the change in adiposity and cognitive function in Black and White older adults.
Methods: The participants were 12,204 older adults without cognitive impairment (62.8 ± 8.0 years) in the United States. The percent body mass index change (%BMI change) and percent waist circumference change (%WC change) were measured at 2 in-home visits (first: 2003-2007, second: 2013-2016). Cognitive status was assessed by the Six-Item Screener annually. Memory and executive function were measured by word list learning, MOCA recall and orientation, and letter and animal fluency every 2 years. Logistic regression or linear regression models were used to estimate the relationship between percent change in adiposity and cognitive function.
Results: After 12.7 ± 1.7 years, a greater decrease in %BMI change or %WC change was significantly associated with a higher risk of cognitive impairment. Compared to older adults with -5% ≤ change ≤ 5% from baseline, a significantly higher risk of cognitive impairment and greater loss in memory and executive function were found among those who experienced more than a 10% decline in %BMI change or %WC change. Older adults who experienced a 5%-10% decrease in %BMI change had a higher risk of cognitive impairment and greater loss of memory compared to those with -5% ≤ change ≤ 5%.
Discussion: A greater decrease in %BMI (>5%) and %WC (>10%) change was associated with greater cognitive loss observed over time.
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http://dx.doi.org/10.1093/geronb/gbad184 | DOI Listing |
Immun Ageing
January 2025
Institute for Behavioral Medicine Research, Ohio State University, 460 Medical Center Drive, Columbus, OH, 43210, USA.
Background: Obesity and metabolic syndrome are major public health concerns linked to cognitive decline with aging. Prior work from our lab has demonstrated that short-term high fat diet (HFD) rapidly impairs memory function via a neuroinflammatory mechanism. However, the degree to which these rapid inflammatory changes are unique to the brain is unknown.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Consuming prebiotics demonstrated therapeutic potential against obesity, as illustrated by our previous study on xylooligosaccharide (XOS), revealing that XOS reduced adiposity, diminished systemic inflammation, and restored cognitive function in obese insulin-resistant rats through the gut-brain axis. Fresh bananas at various ripening stages are being transformed into snacks, indicating potential as prebiotic-based treats enriched with fructooligosaccharide and inulin. Despite those findings, there remains a notable gap in the literature concerning the impact of these prebiotic-based snacks on brain inflammation, reactive oxygen species (ROS) production, and cognitive function in high-fat diet (HFD)-induced obese rats.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Universidade de Brasília, Brasília, Brazil.
Background: Recent research has demonstrated that the consumption of high fat diet (HFD) can lead to metabolic dysfunctions and cognitive impairments in both mice models and humans. Given the potential negative effects of HFD, it is crucial to explore non-pharmacological alternatives that can serve as a potential treatment for both metabolic dysfunctions and behavioral effects induced by HFD. Therefore, the aim of this study is to assess the impact of chronic and intermittent exposure to cold temperature on the metabolic and cognitive changes associated with HFD consumption.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Linkoping University, Linkoping, Sweden.
Background: Excessive dietary fat is not only a risk factor for metabolic disorders but also for premature cognitive decline and Alzheimer's disease. Recent findings from our study revealed that even a few days of a high-fat diet (HFD) are sufficient to disrupt hippocampal bioenergetics, activate microglia, and induce cognitive decline in mice. We hypothesize that microglia, rather than merely responding to diet-induced damage, play a critical role in disrupting synaptic homeostasis.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Nova Southeastern University, Fort Lauderdale, FL, USA.
Background: Cerebral amyloid angiopathy (CAA), characterized by the accumulation of amyloid protein in the cerebral vasculature, is highly prevalent in Alzheimer's disease (AD) patients and, on its own, increases the risk of hemorrhagic stroke, cognitive impairment, and dementia. Currently, there are no effective ways to treat or prevent CAA. Ketogenic diet (KD), characterized by high-fat, low-carbohydrate, and moderate amounts of protein consumption, has gained considerable attention in recent years for its potential therapeutic use in patients with neurodegenerative diseases, including Alzheimer's disease.
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