New research suggests that age-related macular degeneration (AMD) decreases an essential fatty acid, preventing the formation of a class of protective molecules and reducing repair potential – a discovery that may open new therapeutic avenues for AMD.
The study shows that AMD decreases peripheral retinal docosahexaenoic acid (DHA) 22:6 in rod photoreceptor cells, limiting the elongation of fatty acids to form very-long-chain polyunsaturated fatty acids (VLC-PUFAs). VLC-PUFAs are precursors of elovanoids, bioactive chemical messengers made from omega-3 VLC-PUFAs.
Elovanoids have been shown to restore the structure and integrity of damaged photoreceptor cells by repairing, remodelling and regenerating healthy cells. The loss of the neuroprotective precursors of elovanoids in the retina periphery from AMD facilitates uncompensated stress and cell loss.
The research was led by Nicolas Bazan, Boyd Professor, Ernest C and Yvette C Villere Chair for the Study of Retinal Degeneration, and Director of the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine.
“Biosynthetic fatty acid pathway insufficiencies may be a fundamental factor in the onset and progression of macular degenerative diseases leading to blindness,” notes Dr Bazan. “These findings open important immediate avenues for therapeutic exploration for AMD.”
The research team also found major differences between genders. According to the National Institutes of Health, 66% of AMD-affected persons are female. Females have higher DHA 22:6 than males because of oestrogen effects. As they age and oestrogen decreases, so does DHA 22:6, and as a result, women can become increasingly susceptible to retinal degeneration.
“In AMD, the female retina loses peripheral rod VLC-PUFAs to about 33% less than in males, limiting elovanoid formation and its protective bioactivity,” adds Bazan.