Glycemia but not the Metabolic Syndrome is Associated with Cognitive Decline: Findings from the European Male Ageing Study

Sarrazin, Verena; Pendleton, Neil; O'Neill, Terence W; Bártfai, György; Casanueva, Felipe F.; Forti, Gianni; Rastrelli, Giulia; Giwercman, Aleksander; Han, Thang S.; Huhtaniemi, Ilpo; Kula, Krzysztof; Lean, Michael E. J.; Punab, Margus; Lee, David M.; Correa, Elon; Ahern, Tomás; Laurent, Michaël; Verschueren, Sabine; LʼAbbate, Antonio; Gielen, Evelien; Rutter, Martin K.; Vanderschueren, Dirk; Wu, Frederick C. W.; Tournoy, Jos

doi:10.1016/j.jagp.2017.02.004

Cited by 18 publications

(24 citation statements)

References 44 publications

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“…The present finding confirmed those from the European Male Ageing Study that found no evidence for a relationship between MetS or inflammation and CD in a sample of ageing men, while glycemia was negatively associated with visuo-constructional abilities and processing speed in a mean follow-up of 4.4 years [52].…”

Section: Discussionsupporting

confidence: 91%

Midlife Metabolic Profile and the Risk of Late-Life Cognitive Decline

Tortelli

Lozupone

Guerra

et al. 2017

JAD

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Abstract. Among metabolic syndrome components, the effects of higher plasma glucose levels on cognitive decline (CD) have been considered in few studies. We evaluated the associations among midlife glycemia, total cholesterol, high-density lipoprotein cholesterol, triglycerides, midlife insulin resistance [homeostasis model assessment for insulin resistance (HOMAindex)], and CD in the older subjects of the population-based MICOL Study (Castellana Grotte, Italy) at baseline (M1) and at follow-ups seven (M2) and twenty years later (M3). At M1, a dementia risk score and a composite cardiovascular risk score for dementia were calculated. For 797 subjects out of 833, we obtained a Mini-Mental State Examination (MMSE) score at M3, subdividing these subjects in three cognitive functioning subgroups: normal cognition, mild CD, and moderate-severe CD. Mean fasting glycemia at baseline was significantly higher in moderate-severe CD subgroup (114.6 ± 71.4 mg/dl) than in the normal cognition subgroup (101.2 ± 20.6). Adjusting for gender, age, and other metabolic components, higher fasting glycemia values both at M1 [odds ratio (OR) = 1.31; 95% confidence interval (CI): 1.08-1.59] and M2 (OR = 1.26; 95% CI: 1.01-1.57) were associated with an increased risk of moderate-severe CD. Mean HOMA index value was significantly higher in the moderate-severe CD subgroup (5.7 ± 9.4) compared to the normal cognition subgroup (2.9 ± 1.4) at M1. The dementia risk probability (MMSE < 24) increased moving through higher categories of the dementia risk score and decreased as long as the cardiovascular score increased. The present findings highlighted the indication to control blood glucose levels, regardless of a diagnosis of diabetes mellitus, as early as midlife for prevention of late-life dementia.

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Section: Discussionsupporting

confidence: 91%

Midlife Metabolic Profile and the Risk of Late-Life Cognitive Decline

Tortelli

Lozupone

Guerra

et al. 2017

JAD

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“…MetS is strongly related to the risk of developing type 2 diabetes and cardiovascular disease [96] and has also been shown to have a deleterious influence on cognition [102,103]. However, some research also suggests that certain components of MetS have a larger effect than others [104,105]. It is yet unclear what the relative contribution of each of the components of MetS on cognition is.…”

Section: Comorbiditiesmentioning

confidence: 99%

Cognitive impairment in chronic obstructive pulmonary disease: disease burden, determinants and possible future interventions

Beers

Janssen

Gosker

et al. 2018

Expert Review of Respiratory Medicine

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Introduction: Cognitive impairment (CI) is an important but an under-recognized extra-pulmonary feature of chronic obstructive pulmonary disease (COPD). It is related to the burden of disability, worse health outcomes, and impaired self-management. Areas covered: CI includes deterioration of a wide range of cognitive functions, such as memory and various executive functions. Risk of hospitalization might be higher in patients with COPD compared to those without, with CI negatively impacting the wellbeing of patients with COPD. Disease-specific factors such as hypoxemia and inflammation, lifestyle factors such as dietary insufficiencies and lack of physical activity, and comorbidities such as obstructive sleep apnea and depression are likely to synergistically contribute to the development of CI in COPD. Tailored interventions can possibly improve CI in COPD, but this needs further investigation. Expert commentary: Further research is warranted involving the optimization of neuropsychological testing for screening and outcome assessment, longitudinal studies to investigate the development of CI in COPD over time, and randomized clinical trials to test the feasibility and efficacy of promising interventions.

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“…Glucotoxicity induces cell injury of hepatocytes and pancreatic cells through molecular mechanisms of endoplasmic reticulum stress, oxidative stress, and mitochondrial impairment [ 6 7 ]. Moreover, chronic exposure to hyperglycemia can deteriorate cognitive function [ 8 ]. Hyperglycemia-induced impairment of cognitive function is considered a brain complication of diabetes [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Diabetes and Alzheimer's Disease: Mechanisms and Nutritional Aspects

et al. 2018

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Blood glucose homeostasis is well maintained by coordinated control of various hormones including insulin and glucagon as well as cytokines under normal conditions. However, chronic exposure to diabetic environment with high fat/high sugar diets and physical/mental stress can cause hyperglycemia, one of main characteristics of insulin resistance, metabolic syndrome, and diabetes. Hyperglycemia impairs organogenesis and induces organ abnormalities such as cardiac defect in utero. It is a risk factor for the development of metabolic diseases in adults. Resulting glucotoxicity affects peripheral tissues and vessels, causing pathological complications including diabetic neuropathy, nephropathy, vessel damage, and cardiovascular diseases. Moreover, chronic exposure to hyperglycemia can deteriorate cognitive function and other aspects of mental health. Recent reports have demonstrated that hyperglycemia is closely related to the development of cognitive impairment and dementia, suggesting that there may be a cause-effect relationship between hyperglycemia and dementia. With increasing interests in aging-related diseases and mental health, diabetes-related cognitive impairment is attracting great attention. It has been speculated that glucotoxicity can result in structural damage and functional impairment of brain cells and nerves, hemorrhage of cerebral blood vessel, and increased accumulation of amyloid beta. These are potential mechanisms underlying diabetes-related dementia. Nutrients and natural food components have been investigated as preventive and/or intervention strategy. Among candidate components, resveratrol, curcumin, and their analogues might be beneficial for the prevention of diabetes-related cognitive impairment. The purposes of this review are to discuss recent experimental evidence regarding diabetes and cognitive impairment and to suggest potential nutritional intervention strategies for the prevention and/or treatment of diabetes-related dementia.

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Glycemia but not the Metabolic Syndrome is Associated with Cognitive Decline: Findings from the European Male Ageing Study

Cited by 18 publications

References 44 publications

Midlife Metabolic Profile and the Risk of Late-Life Cognitive Decline

Midlife Metabolic Profile and the Risk of Late-Life Cognitive Decline

Cognitive impairment in chronic obstructive pulmonary disease: disease burden, determinants and possible future interventions

Diabetes and Alzheimer's Disease: Mechanisms and Nutritional Aspects

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