6 replies to this topic

[VidX]

Ugh, I'm so eager to read it, I'll probably get a subscribtion, though if anyone already has - definitely take a look (and report back haha)

http://www.landesbio.../article/13120/


Some more interesting/related txts:

http://www.ncbi.nlm....pubmed/17975792

http://www.ncbi.nlm....pubmed/17012837


http://www.ncbi.nlm....pubmed/18156807



Rapamycin and quasi-programmed aging: Four years later.

http://www.ncbi.nlm....pubmed/20436272


Growth and aging: a common molecular mechanism (open access)


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806018/

Edited by VidX, 24 August 2010 - 01:37 AM.

[1101]

Thanks for posting this, lots of interesting things I didn't know before. The theory itself seems pretty sound. It is reasonable that a protein that is needed/beneficial during puberty or embryonic development could have detrimental side effects later on. But what I'm not understanding is why these side effects aren't always visible? If we have some protein that is necessary for a fetus to develop why is it only when we are older (as opposed to all our lives) that we start seeing detrimental side effects? This theory doesn't have any sense of time to it. In order for this theory to work some other biological process needs to signal for the expression of genes that are detrimental in late life. Now several things could keep track of time in the body and cause the expression of these genes. For instance telomere length, accumulation of molecular garbage, and menopause in women. But really that makes these genes a side-effect rather than a root cause of aging. So rather than fight the symptoms fight the cause at its simplest level of complexity. Something has to signal the late life expression of these genes so it seems like it'd be easier to stop this signal than to prevent the expression of every detrimental gene. I mean the theory works, it makes senses, but it is an explanation for the symptoms of aging rather than its cause.

[VidX]

This is how I see it: the timing you talk about is just a statistical approximation for a human specie (and it's pretty short - 20 years more or less). I mean - it takes about that time for the beneficial/SLASH/deleterious genes to do their "job". It's not intentional probably, more like an unfinished software, development program on a free run. The pattern is clear and it exists, but not because it was intended, more like - alternative wasn't achieved for one reason or another.

You mentioned female menopause. I red one article, it actually based the explanation of the cause on the same antagonistic theory. Can't remember the details, but estrogen signaling that's beneficial during puberty/maturing becomes harmful on the long run as it "numbs" the feedback mechanism between brain and ovaries (again - I'm not sure about the details).. So it's not a specific time, just a time that it takes for a system to go wacko.

[1101]

Ah, that makes sense then. A 'bad' gene might constantly be expressed it just takes x amount of years of buildup of whatever protein/RNA it codes for for its detrimental effects to occur/be noticed. I don't think that this causes all the symptoms of senescence but it could definitely be responsible for many.

[VidX]

I guess it just causes the damage that it causes and there aren't the right "code" to counteract it. So basically the lack of the missing "software" is the cause, the instructions for a system, how to act after a certain phase, the one that runs may be considered a cause too, but it's absolutely crucial for us in the first phase of development . At least how I understand that at this moment with the knowledge I acquired.

[Sillewater]

J Comp Pathol. 2010 Jan;142 Suppl 1:S4-9. Epub 2009 Dec 1.The law of mortality revisited: interspecies comparisons of mortality.Olshansky SJ.

This paper is somewhat related.

[xEva]

You can read most of it for free here: http://www.impactaging.com/contents

It's the journal he publishes.