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Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia

dc.contributor.authorGonzález-Reyes R.E.
dc.contributor.authorAliev G.
dc.contributor.authorÁvila-Rodrigues M.
dc.contributor.authorBarreto G.E.
dc.date.accessioned2020-09-02T22:19:24Z
dc.date.available2020-09-02T22:19:24Z
dc.date.issued2016
dc.identifier10.2174/1381612822666151209152013
dc.identifier.citation22, 7, 812-818
dc.identifier.issn13816128
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4730
dc.descriptionThe use of the carbohydrate glucose as an energetic source is essential for an adequate function of the human body. The complex regulation of this molecule involves the coordinated action of various organs such as pancreas, liver and brain. Any disruption of this physiological balance may result in a dangerous compromise of general metabolic activities increasing the possibility of developing T1DM, T2DM and possibly AD. Astrocytes convert glucose into lactate and transfer it to neurons. This lactate is essential for neuronal metabolism and for various processes including the formation of synapses, dendrites and the expression of genes involved in memory. The brain is highly susceptible to variations in glucose blood levels, and both hypoglycemia and hyperglycemia can be dangerous. Pathological hyperglycemia induces changes in plasmatic osmotic pressure, mitochondrial production of free radicals, oxidative stress and activation of neuronal apoptosis, among others. Both AD and diabetes are chronic diseases having age as an important risk factor. As the brain ages, it seems to become much more susceptible to cellular damage induced by excess of circulating glucose and this could explain the appearance of cognitive changes observed in some patients with diabetes. Excessive circulation of pro-inflammatory agents has been observed in insulin resistance and is likely that some of these mediators may cross the bloodbrain barrier and induce abnormal neuroinflammation. GSK-3 is overexpressed in diabetes and also has been reported to regulate tau phosphorylation and production of A peptides in the brain. Currently, diabetes (hyperglycemia) is considered as a risk factor for the de- velopment of AD. A novel therapeutic approach, using intranasal insulin and anti-diabetic medications in patients suffering from AD is being explored and is discussed in this review. © 2016 Bentham Science Publishers.
dc.language.isoen
dc.publisherBentham Science Publishers
dc.subjectAlzheimer disease
dc.subjectAntidiabetic drugs
dc.subjectDementia
dc.subjectDiabetes
dc.subjectInsulin resistance
dc.subjectamyloid beta protein
dc.subjectamyloid precursor protein
dc.subjectantidiabetic agent
dc.subjectfree radical
dc.subjectglucagon like peptide 1
dc.subjectglucose transporter 1
dc.subjectintranasal insulin
dc.subjectlactic acid
dc.subjecttau protein
dc.subjectunclassified drug
dc.subjectantidiabetic agent
dc.subjectglucose
dc.subjectinsulin
dc.subjectAlzheimer disease
dc.subjectapoptosis
dc.subjectArticle
dc.subjectastrocyte
dc.subjectbrain function
dc.subjectbrain metabolism
dc.subjectcarbohydrate metabolism
dc.subjectcell activation
dc.subjectcell metabolism
dc.subjectcognition
dc.subjectdementia
dc.subjectdendrite
dc.subjectdiabetes mellitus
dc.subjectdisease association
dc.subjectgene expression
dc.subjectglucose blood level
dc.subjectglucose brain level
dc.subjectglucose metabolism
dc.subjecthuman
dc.subjecthyperglycemia
dc.subjecthypoglycemia
dc.subjectinsulin dependent diabetes mellitus
dc.subjectinsulin resistance
dc.subjectmemory
dc.subjectnervous system inflammation
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectosmotic pressure
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectprotein phosphorylation
dc.subjectsynapse
dc.subjectAlzheimer disease
dc.subjectanimal
dc.subjectcomplication
dc.subjectdementia
dc.subjectDiabetes Mellitus, Type 1
dc.subjectDiabetes Mellitus, Type 2
dc.subjectmetabolism
dc.subjectpathophysiology
dc.subjectrisk factor
dc.subjectAlzheimer Disease
dc.subjectAnimals
dc.subjectDementia
dc.subjectDiabetes Mellitus, Type 1
dc.subjectDiabetes Mellitus, Type 2
dc.subjectGlucose
dc.subjectHumans
dc.subjectHypoglycemic Agents
dc.subjectInsulin
dc.subjectRisk Factors
dc.titleAlterations in glucose metabolism on cognition: A possible link between diabetes and dementia
dc.typeArticle


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