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Pathophysiological Mechanisms Linking Type 2 Diabetes and Dementia: Review of Evidence from Clinical, Translational and Epidemiological Research

dc.rights.licenseopenen_US
dc.contributor.authorBELLO-CHAVOLLA, O. Y.
dc.contributor.authorANTONIO-VILLA, N. E.
dc.contributor.authorVARGAS-VAZQUEZ, A.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorAVILA-FUNES, Jose Alberto
dc.contributor.authorAGUILAR-SALINAS, C. A.
dc.date.accessioned2020-05-13T12:58:32Z
dc.date.available2020-05-13T12:58:32Z
dc.date.issued2019
dc.identifier.issn1573-3998en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/7560
dc.description.abstractEnBACKGROUND: Type 2 diabetes represents an increasing health burden world-wide and its prevalence in particularly higher in elderly population. Consistent epidemiological evidence suggests an increased risk of dementia associated to type 2 diabetes; the mechanisms underlying these associations, however, remain unclear. OBJECTIVE: The study aims to review epidemiological, clinical and pre-clinical data that weigh on pathophysiological links, mechanisms of disease and associations between type 2 diabetes and dementia to identify areas of opportunity for future research. METHODS: We searched the following electronic bibliographic databases: PUBMED, EMBASE, SCIELO, MEDLINE and OVID for clinical, translational and epidemiological research literature that summarize diabetes-related risk factors for dementia, metabolic and neurological changes associated to T2D, evidence of therapeutic approaches in type 2 diabetes and its pathophysiological implications for dementia. RESULTS: Type 2 diabetes mellitus increases risk for all-cause dementia, vascular dementia and Alzheimer's disease. The most evaluated mechanisms linking both disorders in pre-clinical studies include an increase in neuronal insulin resistance, impaired insulin signaling, pro-inflammatory state, mitochondrial dysfunction and vascular damage which increase deposition of beta-amyloid, tau proteins and GSK3beta, leading to an earlier onset of dementia in individuals with impairment in the glucose metabolism. Neuroimaging and neuropathology evidence linking cerebrovascular lesions, neurodegeneration and particularly small-vessel disease in the onset of dementia is consistent with the increased risk of incident dementia in type 2 diabetes, but consistent evidence of AD-related pathology is scarce. Epidemiological data shows increased risk of dementia related to hypoglycemic episodes, glycemic control, metabolic syndrome, insulin resistance and genetic predisposition, but the evidence is not consistent and statistical analysis might be affected by inconsistent covariate controlling. Therapeutic approaches for T2D have shown inconsistent result in relation to dementia prevention and delay of cognitive decline; lifestyle intervention, particularly physical activity, is a promising alternative to ameliorate the impact of disability and frailty on T2D-related dementia. CONCLUSION: Vascular disease, inflammation and impaired brain insulin signaling might occur in T2D and contribute to dementia risk. Evidence from epidemiological studies has not consistently reported associations that could integrate a unified mechanism of disease in humans. Evaluation of the effect of antidiabetic medications and non-pharmacological interventions in dementia prevention in type 2 diabetes is promising but has thus far offered inconsistent results.
dc.language.isoENen_US
dc.subject.enSEPIA
dc.title.enPathophysiological Mechanisms Linking Type 2 Diabetes and Dementia: Review of Evidence from Clinical, Translational and Epidemiological Research
dc.title.alternativeCurr Diabetes Reven_US
dc.typeArticle de revueen_US
dc.identifier.doi10.2174/1573399815666190129155654en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed30648514en_US
bordeaux.journalCurrent Diabetes Reviewsen_US
bordeaux.page456-470en_US
bordeaux.volume15en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - UMR 1219en_US
bordeaux.issue6en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03210806
hal.version1
hal.date.transferred2021-04-28T08:40:52Z
hal.exporttrue
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