Effect of age and glucoregulation on cognitive performance

Messier, Claude; Tsiakas, Maria; Gagnon, Marc‐André; Desrochers, Alain; Awad, Nesrine

doi:10.1016/s0197-4580(03)00004-6

Cited by 84 publications

(30 citation statements)

References 67 publications

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“…Future research should consider the possible impact of these findings in terms of glucoregulation in the ‘higher-normal’ range and its relationship with memory performance, as increased metabolic demand during regional activation (i.e. memory testing) may be associated with regional low-grade hypoglycaemia and ultimately an inability to compensate for drops in glucose levels during the activation of these circuits during memory testing [10].…”

Section: Discussionmentioning

confidence: 99%

“…A review by Awad et al [9] of the relationship between impaired glucose tolerance, type 2 diabetes and cognitive function highlighted research linking sub-clinical levels of glucose in the high-normal range for glucose tolerance or impaired glucose tolerance (fasting glucose levels <7 mmol/L) with cognitive function, smaller hippocampal volumes and poor glucose regulation [10]. Notably, research has shown a decrement in cognitive function associated with impaired glucose tolerance in men, while women appear to demonstrate virtually identical scores to normoglycaemic women [11].…”

Section: Introductionmentioning

confidence: 99%

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High “Normal” Blood Glucose Is Associated with Decreased Brain Volume and Cognitive Performance in the 60s: The PATH through Life Study

et al. 2013

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ContextType 2 diabetes is associated with cerebral atrophy, cognitive impairment and dementia. We recently showed higher glucose levels in the normal range not to be free of adverse effects and to be associated with greater hippocampal and amygdalar atrophy in older community-dwelling individuals free of diabetes.ObjectiveThis study aimed to determine whether blood glucose levels in the normal range (<6.1 mmol/L) were associated with cerebral volumes in structures other than the hippocampus and amygdale, and whether these glucose-related regional volumes were associated with cognitive performance.Design, Setting and Participants210 cognitively healthy individuals (68–73 years) without diabetes, glucose intolerance or metabolic syndrome were assessed in the large, community-based Personality and Total Health Through Life (PATH) study.Main Outcome MeasureBaseline blood glucose levels in the normal range (3.2–6.1 mmol/l) were used to determine regional brain volumes and associated cognitive function at wave 3.ResultsHigher blood glucose levels in the normal range were associated with lower grey/white matter regional volumes in the frontal cortices (middle frontal gyrus, inferior frontal gyrus precentral gyrus). Moreover, identified cerebral regions were associated with poorer cognitive performance and the structure-function associations were gender specific to men.ConclusionThese findings stress the need to re-evaluate what is considered as healthy blood glucose levels, and consider the role of higher normal blood glucose as a risk factor for cerebral health, cognitive function and dementia. A better lifetime management of blood glucose levels may contribute to improved cerebral and cognitive health in later life and possibly protect against dementia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

High “Normal” Blood Glucose Is Associated with Decreased Brain Volume and Cognitive Performance in the 60s: The PATH through Life Study

et al. 2013

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“…Multiple mechanisms have been proposed to mediate the association of age-related cognitive decline and diabetes, including decreased ATP production, poor Aβ clearance or degradation, weak synaptic communication, hyperphosphorylation of microtubule-associated proteins (Tau), altered Ca 2+ regulation, elevated glucocorticoids and increased 11beta hydroxysteroid dehydrogenase activity (Awad et al, 2004; Benedict et al, 2007; Biessels et al, 2008; Biessels et al, 2006; Craft and Watson, 2004; Gasparini et al, 2002; Korol and Gold, 1998; Kulstad et al, 2006; Messier et al, 2003; Ott et al, 1999; Reagan, 2002; Reger et al, 2008; Ryan and Geckle, 2000; Seckl and Walker, 2004; Stranahan et al, 2008a; To et al, 2011; Yaffe et al, 2004; Zhao et al, 1999). However, because of the complexity of interacting factors and likely contributions from multiple processes, it remains unclear which diabetes-related mechanisms may be linked to cognitive decline and onset of AD.…”

Section: 0 Metabolic Syndrome/diabetes As a Risk Factor For Cognitimentioning

confidence: 99%

Hippocampal calcium dysregulation at the nexus of diabetes and brain aging

Thibault

Anderson

DeMoll

et al. 2013

European Journal of Pharmacology

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Accumulating evidence is associating disorders of lipid and glucose metabolism, including the overlapping conditions of insulin resistance/metabolic syndrome, obesity and diabetes, with moderate cognitive impairment in normal aging and elevated risk of Alzheimer’s disease. It appears that a common feature of these conditions is deficient insulin signaling, likely affecting the brain as well as canonical peripheral target tissues. A number of studies have documented that insulin directly affects brain processes and that reduced insulin signaling results in impaired learning and memory. Several studies have also shown that deficient insulin signaling induces Ca2+ dysregulation in neurons. Because brain aging is associated with substantial Ca2+ dyshomeostasis, it has been proposed that deficient insulin signaling exacerbates or accelerates aging-related Ca2+ dyshomeostasis. However, there have been few studies examining insulin interactions with Ca2+ regulation in aging animals. We have been testing predictions of the Ca2+ dysregulation/diabetes/brain aging hypothesis and have found that insulin and insulin sensitizers (thiazolidinediones) target several hippocampal Ca2+-related processes affected by aging, including larger Ca2+ transients and Ca2+-dependent afterhyperpolarizations, and counteract the effects of aging on those processes. Thus, while additional testing is needed, the results to date are consistent with the view that effects of deficient insulin signaling on brain aging are mediated in part by neuronal Ca2+ dyshomeostasis.

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“…Measurement of blood glucose and insulin will provide a measure of baseline glucoregulatory efficiency and control, which may contribute to age-related cognitive decline [66]. At both baseline and selected follow-up time points, biochemical markers of oxidative stress, inflammation and safety profiling will be measured through high sensitivity C-Reactive Protein, F2-Isoprostanes, inflammatory cytokines (e.g.…”

Section: Design and Methodologymentioning

confidence: 99%

A randomized controlled trial investigating the effect of Pycnogenol and BacopaCDRI08 herbal medicines on cognitive, cardiovascular, and biochemical functioning in cognitively healthy elderly people: the Australian Research Council Longevity Intervention (ARCLI) study protocol (ANZCTR12611000487910)

Stough

Pase

Cropley

et al. 2012

Nutr J

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BackgroundOne of the major challenges associated with our ageing population is the increasing incidence of age-associated cognitive decline, which has significant implications for an individual's ability to lead a productive and fulfilling life. In pure economic terms the costs of ageing reflects decreased productivity and engagement with the workforce. The maintenance of brain health underpinning intact cognition is a key factor to maintaining a positive, engaged, and productive lifestyle. In light of this, the role of diet, including supplementation with nutritional and even pharmacological interventions capable of ameliorating the neurocognitive changes that occur with age constitute vital areas of research.MethodsIn order to reduce cognitive ageing, the ARC longevity intervention (ARCLI) was developed to examine the effects of two promising natural pharmacologically active supplements on cognitive performance. ARCLI is a randomized, placebo-controlled, double-blind, 3-arm clinical trial in which 465 participants will be randomized to receive an extract of Bacopa monnieri (CDRI08 300 mg/day), Pycnogenol (150 mg/day), or placebo daily for 12 months. Participants will be tested at baseline and then at 3, 6 and 12 months post-randomization on a wide battery of cognitive, neuropsychological and mood measures, cardiovascular (brachial and aortic systolic and diastolic blood pressures as well as arterial stiffness), biochemical (assays to measure inflammation, oxidative stress and safety) as well as genetic assessments (telomere length and several Single Nucleotide Polymorphisms). The primary aim is to investigate the effects of these supplements on cognitive performance. The secondary aims are to explore the time-course of cognitive enhancement as well as potential cardiovascular and biochemical mechanisms underpinning cognitive enhancement over the 12 months of administration.ARCLI will represent one of the largest and most comprehensive experimental clinical trials in which supplements are administered to elderly participants. Results from ARCLI may help develop novel preventative health practices and nutritional/pharmacological targets in the elderly for cognitive and brain health.Trial registrationAustralia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12611000487910

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Effect of age and glucoregulation on cognitive performance

Cited by 84 publications

References 67 publications

High “Normal” Blood Glucose Is Associated with Decreased Brain Volume and Cognitive Performance in the 60s: The PATH through Life Study

High “Normal” Blood Glucose Is Associated with Decreased Brain Volume and Cognitive Performance in the 60s: The PATH through Life Study

Hippocampal calcium dysregulation at the nexus of diabetes and brain aging

A randomized controlled trial investigating the effect of Pycnogenol and BacopaCDRI08 herbal medicines on cognitive, cardiovascular, and biochemical functioning in cognitively healthy elderly people: the Australian Research Council Longevity Intervention (ARCLI) study protocol (ANZCTR12611000487910)

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