Abstract 363: The Brain - Pancreas Axis: An Alzheimer Nanoplaque Study

التفاصيل البيبلوغرافية
العنوان: Abstract 363: The Brain - Pancreas Axis: An Alzheimer Nanoplaque Study
المؤلفون: Stephanie Hammersen, Irit Lubitz, Martin Malmsten, Dan Georgescu, R. Saunders, Angela Becker, Eugeny A. Ermilov, G. Siegel, Björn Lindman
المصدر: Circulation Research. 123
بيانات النشر: Ovid Technologies (Wolters Kluwer Health), 2018.
سنة النشر: 2018
مصطلحات موضوعية: medicine.medical_specialty, Physiology, business.industry, Insulin, medicine.medical_treatment, medicine.disease, medicine.anatomical_structure, Endocrinology, Internal medicine, Diabetes mellitus, Cortex (anatomy), medicine, Cardiology and Cardiovascular Medicine, Pancreas, business
الوصف: Background: The central-nervous regulation of blood glucose occurs purely neuroendocrine via the hypothalamus-hypophysis-adrenal cortex system. In this control loop, insulin is the adjustable and glucose the controlled variable. Methods: Ellipsometry, photometric methods and ELISAs were applied. Intracellular membrane potential and tension were recorded from human intracerebral arteries of consciousness areas. Results and discussion: Despite multiply feedback coupled and safeguarded control loops for maintenance of a constant blood glucose level, 4.7% of the world population suffered from diabetes mellitus (T2DM) in 1980 and already 8.5% in 2014. In parallel, the risk for cardiovascular (heart attack, stroke) and Alzheimer diseases (AD) has risen by a factor of four to eight. In ellipsometry measurements with polyanionic heparan sulfate proteoglycan (HS-PG), VLDLapoE4/E4 and IDLapoE4/E4, β-amyloid (1-42) and Ca 2+ -ions, we could show that non-enzymatic glycation of these substances leads to an Alzheimer nanoplaque formation increased by 20-30%. Since the viscoelastic polyelectrolyte HS-PG serves not only as lipoprotein receptor but also as blood flow sensor, we recorded with the same glycation a flow-dependent dilatation reduced by up to 80% in human brain arteries ex vivo (from neurosurgery) which express HS-PG in endothelial and smooth muscle cell membranes. The resulting O 2 -deficiency with certainty entails neuronal cell death. Postprandial, blood glucose levels can appear as were experimentally applied here. Conclusion: Also short-term distinctly increased blood glucose concentrations in apoE4 carriers can explain neuronal cell death like in AD.
تدمد: 1524-4571
0009-7330
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::e3e43d73de86e921b457daeafc475f0aTest
https://doi.org/10.1161/res.123.suppl_1.363Test
رقم الانضمام: edsair.doi...........e3e43d73de86e921b457daeafc475f0a
قاعدة البيانات: OpenAIRE