Chief Supervisor

Dr Bin LIN

Project Title

Synopsis

Retinitis pigmentosa (RP) is an inherited eye disease that causes the progressive degeneration of photoreceptor cells in the retina and subsequent severe vision impairment. There are no effective treatments available to reverse the disease. It has been reported that microglia-mediated neuroinflammation contributes to neurodegeneration in RP. Therefore, reducing the microglia-mediated neuroinflammation in RP could be a meaningful therapeutic approach for RP patients.

The transmembrane protein CD33, one of the sialic acid-binding immunoglobulin (Ig) like family, is extensively expressed in microglia in the brain and regulates innate immunity. Sialic acid containing glycans and glycolipids adhered in the surface of mammalian cells and immune cells can distinguish themselves from others via CD33 by blinding to these kinds of endogenous glycans and glycolipids. Recent genome-wide association studies have identified CD33 as a risk factor for Alzheimer's disease (AD). CD33 is reported to contribute to the pathogenesis of AD by impairing microglial phagocytosis. However, the functional role of CD33 in RP remains unknown.

In this study, we would like to explore the important function of CD33 in regulating neuroinflammation and photoreceptor apoptosis in a mouse model of RP with hope to develop a novel therapeutic approach centered around CD33 inhibition for the treatment of RP patients