UV light and other factors damage crystallin proteins in the eye lens, resulting in cataracts that scatter light and affect vision. Little information exists about protein structures within these disease-causing aggregates. We examined postmortem lens tissue from individuals with and without cataracts using 2D infrared (2DIR) spectroscopy. Amyloid β-sheet secondary structure was detected in cataract lenses along with denatured structures. No amyloid structures were found in lenses from juveniles, but mature lenses with no cataract diagnosis also contained amyloid, indicating that amyloid structures begin forming before diagnosis. Light scatters more strongly in regions with amyloid structure, and UV light induces amyloid β-sheet structures, linking the presence of amyloid structures to disease pathology. Establishing that age-related cataracts involve amyloid structures gives molecular insight into a common human affliction and provides a possible structural target for pharmaceuticals as an alternative to surgery.
https://doi.org/10.1073/pnas.1821534116
The paper is behind a paywall, but Ricki Lewis gives an interesting account of the development of the eye and significance of this finding. https://blogs.plos.org/dnascience/2019/ ... ug-target/
The crysallin membranes protect cells against stress and UV light, so maybe it is a good idea to have UV protection with replacement implant lenses. (Many of us have had cataract surgery, but I don't know of an association with ApoE4 status).
) I even buy big "Hollywood style" sunglasses that curve to minimize glare coming in from the side/top. So, it was disappointing to hear that despite that, cataracts seem to be forming anyway.