Thesis supervisor: Tamás Kovács-Öller
Location of studies (in Hungarian): PTE Abbreviation of location of studies: PTE
Description of the research topic:
Diabetes is a major cause of severe disease and is associated with cognitive decline (CD). The constant rise in worldwide numbers calls for a better understanding of the pathological changes to help with early diagnosis and treatment, based on either genetic or drug-based approaches.
Using the retina, the most accessible brain area as an indicator for CD can be easily translated, however, this has never been addressed in relation to diabetes. Therefore, our aims are the following:
I. We will show how the status of the retinal tissue can be utilized as a direct indicator of cognitive decline in diabetes.
II. We will describe the functional and structural interactions between neuronal, vascular, and glial cells in diabetes with a focus on gap junction connections.
III. We aim to reveal the interaction between impaired glucose transporter trafficking and the loss of cellular communication and BBB integrity.
IV. We will use the drug sitagliptin for early neuroprotection and we will describe its applicability to preserve neuronal function in diabetes.
Our experiments are based on mouse models for both Type 1 & 2 diabetes (STZ & db/db). The anticipated outcomes will help the in-depth understanding of how the neurocellular interactions are changing and could be used directly for medical translation.