New research published in the Proceedings of the National Academy of Sciences suggests that melanin chemiexcitation could prevent the accumulation of lipofuscin associated with age-related macular degeneration (AMD) development.
What is chemiexcitation?
Chemiexcitation is the term for when electrons are excited to a high-energy state. These excited states can provoke chemical reactions that are otherwise impossible.
Talk about the study.
The study included two subject groups of albino Abca4-/- and pigmented mice given subretinal injections:
- The first group was given Ad-Tyr, an adenoviral vector carrying the inserted human tyrosinase cDNA, a compound that can directly excite electrons without melanin.
- The second group was given intravitreal injections of SIN-1 (3-morpholinosydnonimine) dissolved in PBS, a compound that can block chemiexcited melanin.
To note: melanin, a pigment found in hair, skin, and eyes, is not present in albino mice (hence their white coloring).
Following the injections, researchers acquired images via fundus autofluorescence and electron microscopy.
What did they find?
Decreased lipofuscin levels in the albino Abca4-/- mice following the restoration of melanosomes compared to the areas without pigmentation.
What does this mean?
Outer segment photoreceptor digestion, also referred to as disc turnover, is the process by which photoreceptors degrade and regrow throughout a person’s life. Lipofuscin is created as a byproduct of incomplete outer segment photoreceptor digestion, when material can’t be recycled into creating new discs.
As lipofuscin levels increase, it causes damage to the retinal cell epithelium (RPE) and eventually can result in AMD.
Melanin could contribute to potentially successful and safe photoreceptor disc turnover to lessen excess lipofuscin accumulation.
While the mechanism by which melanin supports safe photoreceptor disc turnover is still unclear, these findings suggest chemiexcitation could be key to exploring new avenues for AMD treatment.