Age-related macular degeneration involves damage to the retina and consequent encroaching blindness. One of the contributing causes is a buildup of metabolic waste products in long-lived retinal cells to form lipofuscin, something that the SENS Research Foundation focuses on in their lysoSENS program. Here researchers review the evidence for a different proximate cause, the malfunction of nervous system immune cells:
In the healthy retina, microglial cells represent a self-renewing population of innate immune cells, which constantly survey their microenvironment. Equipped with receptors, a microglial cell detects subtle cellular damage and rapidly responds with activation, migration, and increased phagocytic activity.
While the involvement of microglial cells has been well characterized in monogenic retinal disorders, it is still unclear how they contribute to the onset of retinal aging disorders including age-related macular degeneration (AMD). There is evidence, that microglial activation is not solely a secondary manifestation of retinal tissue damage in age-related disorders. Thus, work in the aging rodent and human retina suggests that long-lived and genetically predisposed microglia transform into a dystrophic state, with loss of neuroprotective functions. In this concept, malfunction of aging microglia can trigger a chronic low-grade inflammatory environment that favors the onset and progression of retinal degeneration.