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In concordance with previous investigations [ 10], it was found that the rate of lens compaction was not constant over time, and that the majority of compaction was observed before middle age.
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Our prior studies have shown that aging human lenses exhibit specific structural changes that contribute to significant, measurable lens compaction, especially in nuclear regions[ 16, 17].
Cells within each compartment traveled along similar trajectories (Fig. 7N, supplementary material Movie 8), with one exception: during pinwheel movement 12-144 hpf), the posteriormost lens cells stalled or moved anteriorly, initiating posterior lens compaction (data not shown).
This data suggests that, in rabbit lenses, compaction in the outer FN fibers precedes compaction in the older fibers of the inner FN and EN.
Compaction of lens fibers is of particular interest because it has been shown to begin before middle age[ 18], thus potentially contributing to presbyopia as well as age-related cataracts.
Taken together, these studies lead us to hypothesize that compaction of lens fibers occurs along the visual axis and may be a factor contributing to increased light scatter as a function of age.
Additionally, ultrastructural investigations have shown that compaction has specific, measurable effects on several aspects of lens fiber structure.
Observational studies of whole lenses from a variety of etiologies have provided evidence that compaction is an ongoing process affecting fibers at all stages of lens development, growth and aging[ 18, 19, 44- 46].
For confocal scanning of lens epithelium, left lenses were used.
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