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Un traitement prolongé par l'ubiquinol et l'acide ascorbique dans le modèle murin 3 × Tg-AD de la maladie d'Alzheimer permet d'inverser la cooccurrence de l'hypoxie et des plaques β-amyloïdes dans l'hippocampe et le cortex entorhinal.

Des anomalies structurelles et fonctionnelles du système microvasculaire cérébral ont été observées chez des patients atteints de la maladie d'Alzheimer (AD) et des modèles animaux. Une des causes de l'hypoperfusion est l'épaississement de la membrane basale cérébrovasculaire (CVBM) en raison d'une augmentation des dépôts de collagène IV autour des capillaires. Cette étude a cherché à savoir si ces altérations et d'autres altérations du système cérébrovasculaire associées à la MA peuvent être prévenues par une supplémentation alimentaire à long terme avec l'ubiquinol (Ub), un antioxydant stabilisé avec de la poudre de Kaneka QH P30 contenant de l'acide ascorbique (ASC) dans un modèle murin de la MA. (Souris 3xTg-AD âgées de 12 mois). Les animaux ont été traités aux stades précurseurs de la maladie (âgés de 3 mois) avec de la nourriture standard sans ou avec un véhicule contenant Ub + ASC ou ASC et comparés à des souris de type sauvage (WT). Le nombre de plaques bêta-amyloïdes (Abeta) dans l'hippocampe et le cortex entorhinal était plus élevé chez les souris femelles que chez les souris mâles 3xTg-AD. Les régions étendues d'hypoxie étaient caractérisées par une charge de plaque supérieure chez les femelles seulement. Ceci a été aboli par Ub + ASC et, dans une moindre mesure, par le traitement ASC. Indépendamment de la charge Abeta, une augmentation du dépôt de collagène IV dans le CVBM a été observée chez les souris mâles et femelles 3xTg-AD par rapport aux animaux WT; cela a également été abrogé chez les souris traitées avec Ub + et ASC. L'inflammation chronique dans l'hippocampe et le stress oxydatif dans les leucocytes périphériques de souris 3xTg-AD ont également été inversés par un traitement antioxydant. Ces résultats fournissent des preuves solides qu'un traitement antioxydant à long terme peut atténuer le stress oxydatif plasmatique, la charge amyloïde et l'hypoxie dans le parenchyme cérébral de la MA.


Source: https://www.ncbi.nlm.nih.gov/pubmed/29953929


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