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gene network theory of aging

aging theories

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#1 sholay75

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Posted 06 June 2021 - 06:55 AM


 
Multi cellular organisms are governed by gene networks right from embryogenesis till death. I say death because i feel aging is also controlled by a gene network, which comes in to being at puberty. I also feel that morphogenesis does not end at birth, it continues till the end of the pubertal phase. Morphogenetic pace not phase varies across species with varying intervals of growth pace.
 
A gene network has function not individual genes, I mean genes have multiple functions depending on the gene network they are part of, i.e an individual gene can be part of many gene networks in the same organisms(for e.g serotonin). it is the gene network that morphs at various tissue growth milestones or organ boundary milestone and acquires different forms and function at those milestones. It does this by inhibiting some of its member genes and/or adding new genes to its network.
 
Aging is one such network which is activated at the morphogenetic milestone of puberty. The activation of this network, results in a program which controls 
1 the repair functions of the cell at the individual level, such as autophagy,dna repair, protein digestion, mitochondria repair etc. 
2 the recruitment of the immune system in response to cell damage and 
3 the  renewal  provided by resident stem cells.
 
The network does this by degrading the above at the aging rate of the species.
 
The gene network which was in control of the above functions during the growth and the final morphogenetic turn at puberty, is modified by activation of some unidentified genes, which in turn inhibit some genes, which played a key role in the previous iteration of the network. Due to this, the whole network modifies itself to implement the aging program.
And therefore, various genes which were found to be beneficial in the previous avatar of the network turn deleterious in the new network, leading to the so called phenomenon 'antagonistic pleiotropy'.
 
Various supplements which have proven to be beneficial are just perturbing small parts of the overall network. However, with the epigenetic clock showing lock step epigenetic modification across various organs and tissues in the organism. the presence of signalling factors in the communication medium can be hypothesized. Hence plasma exchange/dilution are probably effective because the perturb the whole network.
Also according to me partial reprogramming is an unnatural way of changing the dynamics of the aging gene network by introducing elite transcription factors, which supersede the key transcription factors controlling the aging network.
 

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#2 sholay75

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Posted 08 June 2021 - 03:19 PM

The evidence of Non Randomness in age span after maturity is evidence of an aging program.

The evidence of Antagonistic Pleiotropy is evidence of an Aging Gene network


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#3 sholay75

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Posted 16 January 2022 - 07:34 AM

An individual gene is modified at the RNA level i.e it may have one or many RNA variants, it is also modified at the protein level, where its protein product is modified depending on the path way it is part of and moreover the protein product forms a complex with other gene protein products. Most of the research focusses on individual genes rather than  gene pathways, which are activated based on stimuli external to the cell or on internal signalling.


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#4 sensei

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Posted 02 February 2022 - 11:21 PM

Ageing is driven by MTORC1. Regardless of gene network, if you inhibit MTORC1 you increase lifespan and healthspan.

Regardless of genes, if you turn MTORC1 on chronically, you get premature ageing and death.

MTORC1 inhibition even extends the lifespan of progeroid mice ( mice engineered to get progeria)

https://onlinelibrar...1111/acel.13457

Yes the inhibited MTOR genetically in this study, because it was easier to ensure MTOR was inhibited, not because they had to.

Edited by sensei, 02 February 2022 - 11:23 PM.






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