RELEVANCE OF VASCULAR ABNORMALITIES IN NEURODEGENERATIVE DEMYELINATION

Introduction: Until recently, pathological vascular events and neurodegenerative diseases were considered separate phenomena. However, a growing body of research suggests that these conditions are not independent of one another. Vascular dementia is characterized by a circulatory pathology that eventually leads to a cognitive deficit. In Alzheimer’s disease, neuronal alterations have been shown to be accompanied by evident vascular alterations.
In our study, we raised the possibility that demyelinating events may lead to changes in the vascularization of nervous tissue.
Materials and Methods: In our study, we used a murine model of demyelination induced by cuprizone. This model is based on the premise that there is no inflammatory component. After achieving demyelination, we assessed the presence of alterations related to glial populations and vascular elements using different histological techniques.
Results: Preliminary results indicate evident alterations in IB4-positive elements (a blood capillary marker) in the striatum of cuprizone-treated animals. At the glial level, we observed an astrocytic reaction in relation to the blood vessels and microglial phagocytosis of endothelial cells. For example, alterations in Aquaporin4 expression appear in areas of vascular abnormality.
Discussion/Conclusions: The different pattern of IB4 labelling indicates that, as in other pathologies, the neurodegenerative process is accompanied by a vascular disorder. In our model of non-inflammatory demyelination, we believe the astrocyte response is aimed at preserving the integrity of the blood-brain barrier to avoid the entry of the immune system, which could worsen the pathological process.