Publications by authors named "Beata Barabasi"
Article Synopsis
- This study explores how hypertriglyceridemia, linked to atherosclerosis, affects the function and structure of the blood-brain barrier (BBB) using a specific mouse model (APOB-100 transgenic).
- Researchers examined the role of interleukin (IL)-6, a pro-inflammatory cytokine, in impairing BBB characteristics and whether IL-10, an anti-inflammatory cytokine, could counteract these effects.
- Results showed that IL-6 increased permeability and decreased the activity of critical BBB proteins in the mice, while IL-10 helped mitigate these changes, indicating a potential therapeutic target for BBB dysfunction.
Background: Heat-shock protein B1 (HSPB1) is among the most well-known and versatile member of the evolutionarily conserved family of small heat-shock proteins. It has been implicated to serve a neuroprotective role against various neurological disorders via its modulatory activity on inflammation, yet its exact role in neuroinflammation is poorly understood. In order to shed light on the exact mechanism of inflammation modulation by HSPB1, we investigated the effect of HSPB1 on neuroinflammatory processes in an in vivo and in vitro model of acute brain injury.
View Article and Find Full Text PDFCerebrovascular Pathology in Hypertriglyceridemic APOB-100 Transgenic Mice.
Front Cell Neurosci
October 2018
Hypertriglyceridemia is not only a serious risk factor in the development of cardiovascular diseases, but it is linked to neurodegeneration, too. Previously, we generated transgenic mice overexpressing the human APOB-100 protein, a mouse model of human atherosclerosis. In this model we observed high plasma levels of triglycerides, oxidative stress, tau hyperphosphorylation, synaptic dysfunction, cognitive impairment, increased neural apoptosis and neurodegeneration.
View Article and Find Full Text PDF