Presbyopia is an age-related
vision disorder that is a global public health problem. Up to 85% of people aged ≥40 years develop
presbyopia. In 2015, 1.8 billion people globally had
presbyopia. Of those with significant near
vision disabilities due to uncorrected
presbyopia, 94% live in developing countries.
Presbyopia is undercorrected in many countries, with reading glasses available for only 6-45% of patients living in developing countries. The high prevalence of uncorrected
presbyopia in these parts of the world is due to the lack of adequate diagnosis and affordable treatment. The formation of
advanced glycation end products (AGEs) is a non-enzymatic process known as the Maillard reaction. The accumulation of AGEs in the lens contributes to lens aging (leading to
presbyopia and
cataract formation). Non-enzymatic lens protein glycation induces the gradual accumulation of AGEs in aging
lenses. AGE-reducing compounds may be effective at preventing and treating AGE-related processes.
Fructosyl-amino acid oxidase (FAOD) is active on both
fructosyl lysine and fructosyl
valine. As the crosslinks encountered in
presbyopia are mainly non-
disulfide bridges, and based on the positive results of deglycating
enzymes in
cataracts (another disease caused by glycation of
lens proteins), we studied the ex vivo effects of topical FAOD treatment on the power of human
lenses as a new potential non-invasive treatment for
presbyopia. This study demonstrated that topical FAOD treatment resulted in an increase in lens power, which is approximately equivalent to the correction obtained by most reading glasses. The best results were obtained for the newer
lenses. Simultaneously, a decrease in
lens opacity was observed, which improved lens quality. We also demonstrated that topical FAOD treatment results in a breakdown of AGEs, as evidenced by gel permeation chromatography and a marked reduction in autofluorescence. This study demonstrated the therapeutic potential of topical FAOD treatment in
presbyopia.