Development of Neuroprotective Molecule for the Treatment of Atophic Age-Related Macular Degeneration

Investigator: Matthew M. Lavail, PhD
Sponsor: Johns Hopkins University

Location(s): United States


Neuroinflammation is important in the pathoetiology of AMD. However, whether inflammation is neurotoxic and/or neuroprotective during the development of the wet and dry forms of AMD is unresolved. At the center of this debate is the role of retinal microglia versus infiltrating macrophages. Since these two cell subpopulations express the same surface markers, researchers have been unable to differentiate between resident retinal microglia and infiltrating monocytes, and there are no known microglia specific genes that encode cell surface proteins. This is particularly important since the evidence suggests that resident microglia and macrophages may have separate and distinct immune functions. As a result, it has not been possible to specifically target and immunomodulate CNS microglia or recruited monocytes, which is essential for therapeutic intervention to amplify neuroprotective effects, and/or inhibit neurotoxic effects. A recent discovery of specific biomarkers for resident microglia and recruited inflammatory monocytes provides a unique opportunity to investigate their role in pathoetiology of AMD