Development of BIOnanotechnologies based on Extracellular Vesicles for early diagnosis, prognosis and therapy of atherosclerotic disease (BIOVEA)
Various biomarkers have been proposed for the diagnosis and prognosis of acute coronary syndrome, however none for stable coronary disease. Identification of biomarkers that augment established clinical indicators, may allow earlier diagnosis of coronary disease, as well as improved recognition of the risk of complications and cardiovascular death. Additionally, this would pave the way for biomarkers, such as extracellular vesicles, to be employed as precise therapeutic agents in these diseases.
Alteration of the brain barriers in aging and relevance of CD36 for the progress of neurodegeneration
The CD36 antigen is an integral membrane protein known to bind various ligands at cell surface levels, including oxidized low density lipoprotein, native lipoproteins, oxidized phospholipids and long-chain fatty acids. Previously known to be involved in atherosclerosis, arterial hypertension, diabetes and cardiomyopathy, more recent hypotheses postulate a link between altered CD36-mediated lipid metabolism at brain level and neurodegeneration. In this context, our project aims to identify the role that CD36 has in modulating lipoprotein traffic in the blood brain barrier (BBB). The working hypothesis of the project assumes that inhibiting the intake of fatty acids in the brain, by specifically blocking the CD36 transporter, can lead to a decrease in the synthesis of brain lipoproteins that clog brain barriers.
This project aims are:
mapping the cellular distribution of CD36 at BBB level, in normal conditions and in case of increased lipid intake;
mapping the spatial and temporal distribution of neurodegenerative modifications in aging in order to identify early lesions that affect BBB;
identify the role of CD36 in modulating lipoprotein trafficking in BBB.
Some of the expected results of this project are:
enrich the current knowledge in neurodegeneration and brain barriers modification, in both aging and altered lipid metabolism;
establish a protocol for modulating lipid intake at brain level by inhibiting CD36.
Laser scanning microscopy showing CD36 expression in the mouse brain, sagittal section.
Project funded by the Ministry of Education and Research, PN-NUCLEU Ctr. no. 01N/2019-19.29.01.02.