High-fat diets, insulin resistance and declining cognitive function

Greenwood, Carol E.; Winocur, Gordon

doi:10.1016/j.neurobiolaging.2005.08.017

Cited by 291 publications

(175 citation statements)

References 46 publications

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“…There are several pathways through which body mass might influence changes in cognitive functioning over time. For example, greater adipose tissue and body mass, for example, increases the production of proinflammatory cytokines tied to metabolic syndrome (Wisse, 2004) and greater body mass predicts greater leptin and insulin resistance, insulin dysregulation, and inflammation, all of which are associated with cognitive decline (Consondine et al, 1996;Al Hazzouri, Stone, Haan, & Yaffe, 2013;Greenwood & Winocur, 2005;Visser et al, 1999;Wisse, 2004). One potential biologically-mediated pathway that could explain the association between higher body mass and cognitive decline is inflammation.…”

Section: Body Mass Inflammation and Cognitionmentioning

confidence: 99%

Body mass and cognitive decline are indirectly associated via inflammation among aging adults

Bourassa

Sbarra

2017

Brain, Behavior, and Immunity

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Inflammatory models of neurodegeneration suggest that higher circulating levels of inflammation can lead to cognitive decline. Despite established independent associations between greater body mass, increased inflammation, and cognitive decline, no prior research has explored whether markers of systemic inflammation might mediate the association between body mass and changes in cognitive functioning. To test such a model, we used two longitudinal subsamples (ns = 9066; 12,561) of aging adults from the English Longitudinal Study of Ageing (ELSA) study, which included two cognitive measures components of memory and executive functioning, as well as measurements of body mass and systemic inflammation, assessed via Creactive protein (CRP). Greater body mass was indirectly associated with declines in memory and executive functioning over 6 years via relatively higher levels of CRP. Our results suggest that systemic inflammation is one biologically plausible mechanism through which differences in body mass might influence changes in cognitive functioning among aging adults.

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Section: Body Mass Inflammation and Cognitionmentioning

confidence: 99%

Body mass and cognitive decline are indirectly associated via inflammation among aging adults

Bourassa

Sbarra

2017

Brain, Behavior, and Immunity

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“…In addition to its well-known adverse effects on the cardiovascular and peripheral nervous systems, diabetes also appears to negatively impact the brain, increasing the risk of depression and dementia2 , 3 . Human subjects with either type 1 (caused by insulin deficiency) or type 2 (mediated by insulin resistance) diabetes typically exhibit impaired cognitive function compared to age-matched non-diabetic subjects 3,4 . Cognitive deficits have also been documented in studies of rodent models of diabetes.…”

Section: Introductionmentioning

confidence: 99%

“…Keywords glucocorticoid; dentate gyrus; streptozotocin; water maze; object recognition As a result of high calorie diets and sedentary lifestyles, diabetes is rapidly becoming more prevalent in Western societies 1 . In addition to its well-known adverse effects on the cardiovascular and peripheral nervous systems, diabetes also appears to negatively impact the brain, increasing the risk of depression and dementia2 , 3 . Human subjects with either type 1 (caused by insulin deficiency) or type 2 (mediated by insulin resistance) diabetes typically exhibit impaired cognitive function compared to age-matched non-diabetic subjects 3,4 .…”

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confidence: 99%

Diabetes impairs hippocampal function through glucocorticoid-mediated effects on new and mature neurons

et al. 2008

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Multiple organ systems are adversely affected by diabetes, including the brain, which undergoes changes that may increase the risk of cognitive decline. Although diabetes influences the hypothalamic-pituitary-adrenal axis, the role of this neuroendocrine system in diabetes-induced cognitive dysfunction remains unexplored. Here we demonstrate that, in both insulin-deficient rats and insulin-resistant mice, diabetes impairs hippocampus-dependent memory, perforant path synaptic plasticity and adult neurogenesis, and the adrenal steroid corticosterone contributes to these adverse effects. Rats treated with streptozocin have reduced levels of insulin, and exhibit hyperglycemia, increased levels of corticosterone, and impairments in hippocampal neurogenesis, synaptic plasticity and learning. Similar deficits are observed in db/db mice, which are characterized by insulin resistance, elevated corticosterone levels and obesity. Changes in hippocampal plasticity and function in both models are reversed when normal physiological levels of corticosterone are maintained, suggesting that cognitive impairment in diabetes may result from glucocorticoidmediated deficits in neurogenesis and synaptic plasticity. Keywords glucocorticoid; dentate gyrus; streptozotocin; water maze; object recognition As a result of high calorie diets and sedentary lifestyles, diabetes is rapidly becoming more prevalent in Western societies 1 . In addition to its well-known adverse effects on the cardiovascular and peripheral nervous systems, diabetes also appears to negatively impact the brain, increasing the risk of depression and dementia2 , 3 . Human subjects with either type 1 (caused by insulin deficiency) or type 2 (mediated by insulin resistance) diabetes typically exhibit impaired cognitive function compared to age-matched non-diabetic subjects 3,4 . Cognitive deficits have also been documented in studies of rodent models of diabetes. For Supplementary Information accompanies this paper.Competing interests statement. The authors declare that they have no competing financial interests. Conflict of Interest:The authors declare no conflict of interest. NIH Public Access Author ManuscriptNat Neurosci. Author manuscript; available in PMC 2010 August 25. Published in final edited form as:Nat Neurosci. 2008 March ; 11(3): 309-317. doi:10.1038/nn2055. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript example, rats rendered diabetic by treatment with the pancreatic β-cell toxin streptozocin (STZ; a model of type 1 diabetes) exhibit impaired performance in tests of spatial learning ability 5, 6. Similar deficits have been reported in the db/db mouse7, a model of Type 2 diabetes in which obesity, hyperglycemia, and elevations in circulating corticosterone levels arise from a mutation that inactivates the leptin receptor 8 . However, the mechanism(s) responsible for cognitive dysfunction in diabetes has not been established.Within the hippocampus, changes in the strength of synapses between groups of neurons play a critic...

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“…Hence the possibility of weak learning with high-fat food merits further attention. Such effects could reflect the strong influence of high-fat food on metabolism in the body and the brain (e.g., Gerozissis, 2004;Greenwood & Winocur, 2005). The effects of a high-fat diet on the brain have been connected to poor learning in other paradigms, as well as to increased obesity (Woods, D'Alessio, Tso et al, 2004).…”

Section: Postingestional Sources Of Reward Over Long Delaymentioning

confidence: 99%