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CarbonRobot CarbonRobot
wrote...
Posts: 393
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2 years ago
What causes the lens of the eye to stiffen with age? Does it accumulate extra material from somewhere?
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wrote...
Valued Member
Educator
2 years ago Edited: 2 years ago, bio_man
This is an age-related farsightedness, where parts of your body start to slow down simply due to aging. The lenses of your eyes become harder and less flexible with age, and your ciliary eye muscles probably become weaker too. As a result, the lenses can no longer change shape as easily. This means that it’s harder to see things close-up. But your ability to see faraway objects isn’t affected.

Why do some old people get it while others don't? Depends on your genetics; perhaps you've inherited a better gene for eye muscles than someone else, leading to better eye health overall.

Of course, things like exposure to radiation and drugs such as glucocorticoids could weaken those areas quicker than they should.
CarbonRobot Author
wrote...
2 years ago
Yes, I know what presbyopia is. I want to know the mechanics behind why it happens? Has nobody dissected the lens of old and young people?
wrote...
Valued Member
Educator
2 years ago
If it's the contractile capability that is affected with age, then if you'd compare a young person's eye muscles to an old person's, the muscles wouldn't look muscle different under a microscope, because a microscope can only zoom in so far. However, here's a look at what a muscle fiber looks like illustrated:



What affects elasticity is damage to the myofibrils, and so if it's a loss of elasticity that's the root cause, technically this is where you'd find the most difference.
Woo
wrote...
2 years ago
If you're looking for an anatomical comparison between a young human and older human, this might interest you:



Age-related change in the geometry of the sclera, ciliary body, and zonula: human. Note the deformation of the outer limbus (''notch,'' arrow) in the accommodated young eye compared to the unaccommodated eye. In the older eye there is a discernible depression or ''inward bowing'' contour to the sclera. The notch appearance in the young sclera and the ''inward bowing'' of the older sclera occur in the nasal, but not the temporal quadrant. In the older eye there is not much difference between the unaccommodated and accommodated state with regard to the ciliary body/muscle shape. The young accommodated muscle clearly is in the anterior inward position compared to the unaccommodated eye. The ''inward bowing'' phenomena also is present in the monkey eye (see Fig. 7), although this has not been observed as frequently due to iatrogenic conjunctival swelling in the monkey eye.
CarbonRobot Author
wrote...
2 years ago
If you're looking for an anatomical comparison between a young human and older human, this might interest you: Age-related change in the geometry of the sclera, ciliary body, and zonula: human. Note the deformation of the outer limbus (''notch,'' arrow) in the accommodated young eye compared to the unaccommodated eye. In the older eye there is a discernible depression or ''inward bowing'' contour to the sclera. The notch appearance in the young sclera and the ''inward bowing'' of the older sclera occur in the nasal, but not the temporal quadrant. In the older eye there is not much difference between the unaccommodated and accommodated state with regard to the ciliary body/muscle shape. The young accommodated muscle clearly is in the anterior inward position compared to the unaccommodated eye. The ''inward bowing'' phenomena also is present in the monkey eye (see Fig. 7), although this has not been observed as frequently due to iatrogenic conjunctival swelling in the monkey eye.

Interesting. I think some animals can regenerate their eye lens. I wonder how that works if there is no blood flow. Do humans have any lens maintenance processes?
Woo
wrote...
2 years ago
Yes, the lens epithelial cells do repair themselves as they are capable of dividing mitotically. Some epithelial cells lose their nuclei and other organelles, and become lens fiber cells. These lens fiber cells are filled with a 30% solution of protein, known as cytosol (soluble) lens protein. Because there is little protein turnover in the lens fiber cells, damage to lens protein accumulates throughout life.
Source  http://photobiology.info/Roberts.html
CarbonRobot Author
wrote...
2 years ago
Yes, the lens epithelial cells do repair themselves as they are capable of dividing mitotically. Some epithelial cells lose their nuclei and other organelles, and become lens fiber cells. These lens fiber cells are filled with a 30% solution of protein, known as cytosol (soluble) lens protein. Because there is little protein turnover in the lens fiber cells, damage to lens protein accumulates throughout life.

Why the low turn over? Does presbyopia happen gradually, or super slow until age 30, then faster after 40 or so? I heard NAD+ plays a major role in eye health. Wonder if it could reverse lens aging. Or if cellular senescence is a bigger threat to eye aging.
Woo
wrote...
2 years ago
Lens crystallins (specifically, alpha-crystalline, which comprises 40% of the proteins present in the lens) are structural proteins. They have little or no turnover because they are maintained throughout the lifetime of the host. In fact, post-translational alteration and protein unfolding continue throughout life, and transparency has to be maintained for decades.  The reason for this low-turnover is because the alpha-crystallin protein has a chaperone-like function that helps prevent the formation of large light-scattering aggregates and possibly cataract. This also makes them vulnerable to glycation, which is the attachment of sugars to the proteins, causing them to be less effective.

This is interesting stuff, and I recommend you read the following two articles for more information.

https://www.sciencedirect.com/science/article/pii/B9780124017177000150
https://www.nature.com/articles/eye1999114.pdf
CarbonRobot Author
wrote...
2 years ago
Lens crystallins (specifically, alpha-crystalline, which comprises 40% of the proteins present in the lens) are structural proteins. They have little or no turnover because they are maintained throughout the lifetime of the host. In fact, post-translational alteration and protein unfolding continue throughout life, and transparency has to be maintained for decades. The reason for this low-turnover is because the alpha-crystallin protein has a chaperone-like function that helps prevent the formation of large light-scattering aggregates and possibly cataract. This also makes them vulnerable to glycation, which is the attachment of sugars to the proteins, causing them to be less effective. This is interesting stuff, and I recommend you read the following two articles for more information. https://www.sciencedirect.com/science/article/pii/B9780124017177000150 https://www.nature.com/articles/eye1999114.pdf

Cool. Thanks.
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