Adaptation to intermittent hypoxia prevents the decrease in cerebral vascular density in rats with experimental Alzheimer’s disease
Autor: | H. F. Downey, Anna V. Goryacheva, Igor V. Barskov, Eu. B. Manukhina |
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Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Angiogenesis Hippocampus 03 medical and health sciences Cresyl violet chemistry.chemical_compound 0302 clinical medicine Internal medicine Cortex (anatomy) Medicine business.industry Neurodegeneration General Engineering Intermittent hypoxia Hypoxia (medical) medicine.disease Vascular endothelial growth factor 030104 developmental biology Endocrinology medicine.anatomical_structure nervous system chemistry medicine.symptom business 030217 neurology & neurosurgery |
Zdroj: | Regional blood circulation and microcirculation. 20:59-64 |
ISSN: | 2712-9756 1682-6655 |
DOI: | 10.24884/1682-6655-2021-20-2-59-64 |
Popis: | Introduction. Patients with Alzheimer’s disease (AD) have reduced cerebral vascular density (VD), which impairs blood flow to neurons and may contribute to progression of AD. Earlier we showed that prior adaptation to intermittent hypobaric hypoxia (IHH) prevented memory loss and degeneration of cortical neurons in rats with experimental AD (EAD). The aim of this study was to test if IHH might prevent EAD-induced vascular rarefaction in rats. Materials and methods. EAD was induced with bilateral injection of neurotoxic beta-amyloid peptide fragment (A) (25–35) into n. basalis magnocellularis. IHH was simulated at a 4,000 m altitude, for 4 hours a day, for 14 days. Brain blood vessels were stained by transcardiac infusion of Indian ink; brain sections were stained with 0.3 % cresyl violet by Nissle method. Vascular density was assessed in the cortex and hippocampus using the Infinity Analysis Software. Results. In the EAD rats, VD was significantly decreased in the hippocampus (13.3±0.9 vs 17.8±1.0 in field of view, FOV, pConclusion. One of the mechanisms of AIH beneficial effect in AD-related neurodegeneration is preserving the capability for compensatory angiogenesis in brain. |
Databáze: | OpenAIRE |
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