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      Glucose regulation and cognitive functions: relation to Alzheimer's disease and diabetes

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      Behavioural Brain Research
      Elsevier BV

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          Abstract

          Glucose has been found to improve memory in animals and humans. Animal research has revealed that glucose may improve memory through a facilitation of acetylcholine (ACh) synthesis and release in the brain. This glucose-related memory improvement has prompted research in elderly humans. These studies have shown that the memory-improving action of glucose depends on each individuals' blood glucose regulation. Based on these data, researchers have evaluated the effect of glucose on memory in patients with Alzheimer's disease (AD). Results demonstrated that glucose could improve memory in a subset of patients that had abnormalities in their blood glucose regulation. Interestingly, these alterations in blood glucose regulation were believed to depend on the severity of the disease process. Another line of investigation has focused on alterations in brain glucose metabolism. Both animal models and studies with Type II diabetic elderly patients have shown that altered glucose regulation impairs learning and memory processes. It is possible that in AD patients, hyperglycemia exerts a deleterious effect by potentiating the neuronal death produced by other pathological processes taking place such as amyloid deposition. Based on these data, it appears important to find the prevalence of altered glucoregulation at various stages of AD. Secondly, it may be of interest to determine prospectively whether altered glucoregulation is linked to a faster progression of the disease. Finally, if such a relationship is observed, the next logical step would be to determine whether AD patients could benefit from treatments aimed at normalizing blood glucose regulation and improving insulin sensitivity.

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          Author and article information

          Journal
          Behavioural Brain Research
          Behavioural Brain Research
          Elsevier BV
          01664328
          February 1996
          February 1996
          : 75
          : 1-2
          : 1-11
          Article
          10.1016/0166-4328(95)00153-0
          8800646
          33308461-5fa1-462d-8dab-9e6b72b948c9
          © 1996

          https://www.elsevier.com/tdm/userlicense/1.0/

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