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>> No.14527489 [View]
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14527489

>>14522104
I disagree with this in some parts, though your idea on longevity, evolution and reproductive age is interesting and a good observation.
However... We understand the overview of ageing enough that we know it can be fixed. It just may be really hard. Transposons can be silenced via targeted methyl transferase enzymes, telomers can be regrown through extopic expression of telomerase enzyme, epigenetic cellular rejuvination can be done through application of yamanaka factor, stem cell attrition may be solvable by forced expression of the PIWI-piRNA pathway, a unique marker of scenescence was recently identifyed which woul alow us to increase clearance, declining proteostasis is a hard one, but increased expression of proteosomes helps, sterile inflamatin can be reduiced via targeting cDNA...
We know the problems and have some solutions, all we need are more effective solutions, and a clearer ide as to what to focuse on most.
Evolution actually has cured ageing in some cases, like hydra vulgaris, some sponges, some acoels, planarians and all germlines. Also to understand ageing and evolution it is worth looking at the vast age difference between tha major wokers and reproductives of macrotermes bellicosus.
>>14522066
Yes, and no. It's actually really interesting. Copying errors are a factor of ageing, but if it were the only one, ageing would be linear. But ageing doesn't show linear growth. We can show this quantifiably but just think about it. How much do you age from 0-40 (keep in mind development is a totally different process from ageing). How much more do you age from 40-80, and how much more form 80-120. It's exponential.
There are two factors in this: one) the antagonistic haulmarks of ageing pass their tippingpoint, two) transposon expression is exponential and so it's DNA damageing effects are too.
Basically ageing is a series of hierarchical DNA damageing factors, each of which causes and is caused by the other.

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