Cerebral Complications of Diabetes Mellitus
Abstract
A WHO adatai szerint a világon jelenleg több mint 180 millióan szenvednek diabetes mellitusban, és ez a szám 15 éven belül megduplázódik. Az agy működése a folyamatos glükózellátás függvénye, hypoglykaemiában a homeostasis megtartására irányuló ellenregulációs hormonok (glukagon, adrenalin, növekedési hormon, kortizol) termelődése fokozódik, a szimpatikus idegrendszer aktiválódik, neuroglykopenia tünetei jelennek meg. Az alarmírozó, az életet aktuálisan veszélyeztető állapotnak azonban még ismétlődés esetén sem olyan kifejezettek a hosszú távú szövődményei, mint a hyperglykaemiának. A hyperglykaemiára adott aktív neurális válasz a génexpresszió és génműködés megváltozása. A kezdetben adaptív, hyperosmolalitás elleni lépések a hypothalamicus magnocellularis neurosecretiós sejtek hiperaktivitásához, majd strukturális károsodásához vezetnek. Részben a hippocampalis géntranszkripciós változások állnak a deklaratív memória csökkenése hátterében. A neurológiailag passzív választ a cukorfölösleget elvezető metabolikus kerülőutak jelentik, melyek részben az atherogen, vascularis károsító tényezőkért, részben a szabadgyök-képződésért, leukoencephalopathia és cerebrális atrófia kialakulásáért felelősek, s ezúton okoznak kognitív deficitet. Fiziológiás körülmények között az inzulin neuroprotektív, azonban a perifériás inzulinrezisztenciával korreláló központi idegrendszeri inzulinrezisztencia miatt a protektív hatás csökken, az apoptoticus folyamatok, neurodegeneráció és a következményes kognitív hanyatlás kerül előtérbe. A diabetes mellitus az Alzheimer-kórral számos, még nem tisztázott összefüggést mutat, különösen az APOE-4 gént hordozó diabéteszeseknek nagyobb az esélyük az Alzheimer-kórban való megbetegedésre. Diabetes mellitusban a depresszió prevalenciája megnő, de a depresszió is kockázati tényező diabetes mellitusra nézve. A két kórkép egyidejű fennállása mindkettő kórlefolyását súlyosbítja.
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Very low glucose concentrations can immediately induce seizures, loss of consciousness, and death.
“Very low glucose concentrations can immediately induce seizures, loss of consciousness, and death, while chronic hyperglycemia would induce changes in hippocampal gene expression and function [12].”
From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [12]
Chronic hyperglycemia induces changes in hippocampal gene expression and function.
“Very low glucose concentrations can immediately induce seizures, loss of consciousness, and death, while chronic hyperglycemia would induce changes in hippocampal gene expression and function [12].”
From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [12]
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- Authors
- Aszalós, Z.
- Affiliations
- Semmelweis University (HU)
- Corresponding author
- Aszalós, Zsuzsa
- Venue
- Orvosi Hetilap
- Publisher
- Akademiai Kiado Zrt.
- Published
- 2007-12-01
- Volume
- 148
- Issue
- 50
- Pages
- 2371-2376
- ISSN
- 0030-6002 (ISSN-L)
- 1788-6120
- OpenAlex
- W2055228068
- Cited by
- 11
- References
- 20
- Citations by year
- 2021: 1 · 2020: 1 · 2018: 1 · 2013: 1 · 2012: 1
- FWCI
- 1.06
- Type
- journal article
- Language
- hu
- Open access
- closed
- Locations
- Orvosi Hetilap (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- diabetes mellitus, cerebral complications, hypoglycemia, neuroglycopenia, hyperglycemia, hyperosmolarity, declarative memory, leukoencephalopathy, brain atrophy, cognitive decline, insulin resistance, Alzheimer's disease, APOE ε4, depression, neurodegeneration
- MeSH terms
- Alzheimer Disease, Brain, Cognition Disorders, Depression, Hormones, Humans, Hyperglycemia, Hypoglycemia, Insulin, Insulin Resistance, Osmolar Concentration, Risk Factors, Diabetes Complications
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