Senescent cells are created constantly, but only begin to linger and accumulate in tissues in later life, as the pace of creation accelerates and the mechanisms of clearance decline in effectiveness. A senescent cell secretes a mix of moleculers that spurs chronic inflammation and disrupts the processes of tissue maintenance and function. They contribute directly to numerous age-related conditions, including forms of retinal degeneration, as noted here. The most direct approach to therapy is probably the best: periodic destruction of senescent cells, delivering senolytic therapies that force these cells into apoptosis or steer the immune system to destroy them. In old mice, senolytic treatments produce robust and significant rejuvenation, including reduced chronic inflammation, and reversal of many age-related conditions.
Age-related macular degeneration (AMD), a degenerative disease in the central macula area of the neuroretina and the supporting retinal pigment epithelium, is the most common cause of vision loss in the elderly. Although advances have been made, treatment to prevent the progressive degeneration is lacking. Besides the association of innate immune pathway genes with AMD susceptibility, environmental stress- and cellular senescence-induced alterations in pathways such as metabolic functions and inflammatory responses are also implicated
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