TYPE3DIABETESMELLITUS:BIOLOGICALMECHANISMSANDITSRELATIONSHIPWITHALZHEIMER'SDISEASE

Zenodo (CERN European Organization for Nuclear Research) 2026 Dataset Open access

Read full text
Authors: LutfullayevOltinOybekugl
DOI: 10.5281/zenodo.18790220
Cited by: 0

Abstract

Type3diabetesmellitusisanemergingconceptualframeworkthatlinksmetabolicdysfunctionwithneurodegenerativeprocesses,particularlyAlzheimer’sdisease.Unlikeclassicaldiabetestypesthatprimarilyaffectperipheralglucoseregulation,type3diabetesdescribesinsulinresistanceandrelativeinsulindeficiencylocalizedwithinthebrain.Thisimpairmentdisruptsneuronalglucosemetabolism,leadingtocellularenergydeficits,oxidativestress,neuroinflammation,andprogressivesynapticdysfunction.CentraltothispathologyisalteredinsulinsignalingthroughthePI3K/Aktpathway,whichcontributestoamyloid-βaccumulation,tauhyperphosphorylation,mitochondrialdysfunction,andneuronalloss.Epidemiologicalevidenceindicatesthatindividualswithtype2diabeteshaveasignificantlyelevatedriskofdevelopingAlzheimer’sdisease,supportingthehypothesisthatmetabolicandneurodegenerativepathwaysarecloselyinterconnected.Understandingthesemechanismshighlightstheimportanceofinsulinsensitivity,metabolicregulation,andanti-inflammatorystrategiesinpreservingcognitivefunction.Althoughtype3diabetesisnotyetformallyrecognizedasaclinicaldiagnosis,growingexperimentalandclinicaldataunderscoreitsrelevanceinexplainingAlzheimer’spathophysiologyandguidingfuturetherapeuticapproaches.Continuedresearchmayopennewpreventiveandtreatmentstrategiesaimedatprotectingbrainhealththroughmetabolicintervention.

Fields of Study & Subjects

Alzheimer's disease research and treatments Dementia and Cognitive Impairment Research Neuroinflammation and Neurodegeneration Mechanisms

Publication details

Journal / source
Zenodo (CERN European Organization for Nuclear Research)
Publication date
26 February 2026
Language
EN
Document type
Dataset