Abstract
The incidence of obesity in middle age is increasing markedly, and in parallel the prevalence of metabolic disorders including cardiovascular disease and type II diabetes is also rising. Numerous studies have demonstrated that both obesity and metabolic disorders are associated with poorer cognitive performance, cognitive decline, and dementia. In this review we discuss the effects of obesity on cognitive performance, including both clinical and preclinical observations, and discuss some of the potential mechanisms involved, namely inflammation and vascular and metabolic alterations.
Highlights
The incidence of obesity, classified by a body mass index (BMI, body mass divided by the square of one’s height) >30 kg/m2, is rising steadily throughout the world’s population
A crosssectional longitudinal study of over 2000 middle aged workers supported the linear association between BMI and cognitive function determined by the word-list learning test, which evaluates verbal learning and memory, and Digit-symbol Substitution test (DSST), which assesses attention, response speed, and visuomotor coordination
Obesity and cognitive decline it difficult to draw absolute comparisons, but impairment of specific cognitive domains such as executive function and shortterm memory have been consistently identified in obese individuals when compared to normal weight counterparts (Cournot et al, 2006; Mond et al, 2007; Lokken et al, 2009; Sabia et al, 2009)
Summary
MILD COGNITIVE IMPAIRMENT A growing body of research indicates that obesity in mid-life is a predictor of mild cognitive impairment at old age. Both hypertrophied adipocytes and adipose tissue-resident immune cells (primarily lymphocytes and macrophages) contribute to increased circulating levels of proinflammatory cytokines where there is an increase of tumor necrosis factor (TNF)-α, important feeding-related peptides such as leptin and resistin, plasminogen activator inhibitor 1, C-reactive protein and interleukins (IL)-1β and IL-6 (Visser et al, 1999; Yudkin et al, 1999; Ouchi et al, 2011) in obese individuals Those with a higher waist circumference and waist-hip ratio showed higher C-reactive protein and IL-6 concentrations, with IL-6 positively associated with total body fat (Hermsdorff et al, 2011). Further preclinical data have demonstrated that after a lipopolysaccharide (LPS) challenge in diet-induced obese rats, an exacerbated and prolonged fever was observed as well as an increase in plasma TNF-α, IL-6, and IL-1ra levels compared to lean controls (Pohl et al, 2009) Cytokines, such as IL-1β and IL-6 have been shown to disrupt neural circuits involved in cognition and memory (Jankowsky and Patterson, 1999; Gemma and Bickford, 2007). An imaging study conducted by Harrison and colleagues showed that after inducing systemic inflammation by injection of Salmonella typhi vaccine an acute decline in spatial memory (but not medial temporal lobe independent procedural memory) was observed in humans (Harrison et al, 2014), suggesting that the medial temporal lobe is acutely sensitive to systemic inflammation
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