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Are AGEs and Lipofuscin related? Could ALT-711 eliminate lipofuscin?

ufotruth at ix.netcom.com ufotruth at ix.netcom.com
Fri Jan 8 21:06:21 EST 1999


 
>I think it's likely that the people who wrote that were confusing
>age spots with another aspect of skin aging, one which certainly
>is thought to be largely due to AGE accumulation, namely wrinkles.
>They arise from loss of elasticity of the skin, due to excessive
>linking of the network of collagen fibres in the lower layer (the
>dermis).

You are correct. That is a very possible explanation.

>Anyway, if you surf a lot then you've probably learnt not to believe
>everything you read on the net, especially in medical matters!  If

Yep. I have learned not to believe everything I read on the internet.
There is a good bit of disinformation, lies, and misinformation all
over cyberspace. But on the other hand many things on the internet CAN
be believed, at least to some degree, that are not "mainstream".

>you can't confirm an assertion by searching Medline, the chances that
>it's wrong are pretty high.  Nevertheless I recommend that you start
>to make a habit of recording how you found things out -- scientists
>do that religiously, for the very same reason, ie that when they get
>conflicting information later on they can weigh up the strength of
>evidence on either side.

Eventually, when I obtain a better computer with a larger hard drive,
I want to get a database program to file information about virtually
everything I find on the internet. It would probably be a very good
habit to pick up since, one day, I want to become a scientist.


>You're absolutely right to focus on those questions.  The "generic"
>answer is that some things DO happen just as fast early on as late (or
>nearly as fast, anyway), but they don't have any serious effects until
>they have progressed quite a long way; at that time they start to have
>many other effects on systems that were hitherto working fine; as soon
>as that happens everything starts to accelerate rapidly, just as you
>describe.  So, any theory of aging involves identifying some damage

Perhaps it would be a good idea to find out which aspects of the aging
process cause harm at the same rate early and late in life. Then we
could possibly compare the two sets of aspects of the aging process
and figure out exactly why some of them accelerate as we grow older
and which ones occur at a gradual rate all through life.

>that accumulates throughout life and then exploring how it could have
>the late-onset effects.  This doesn't rule out any of the suspects,
>unfortunately: chromosomal mutations, telomere shortening, mitochondrial
>DNA mutations, lipofuscin accumulation, extracellular AGE accumulation,
>shrinking heterochromatin...  In other words, this:

I sure do wish that I had a laboratory and a formal education in
biology so I could do some of my own research into all of these
theories. 

>is definitely wrong.  Any of the above can, in theory, get cells into
>stress once they get far enough.

Yep. That is correct. But it just seems to me that perhaps one factor
of the aging process has the ability to accelerate all the others and
once we find this key factor of the aging process, we could find a way
to reverse it, and at the same time reverse all the other factors.

>
>The problem with blaming telomere shortening (as you know unless you
>have a very short memory!) is that the cells whose telomeres shorten

My memory is not really short, but when you are interested in so many
different subjects and read as much information on the internet as I
do it becomes difficult to recall individual bits and pieces of
information. So if I have forgotten anything that I should remember,
then I apologize.

>during aging are ones that don't actually appear to suffer any decline
>in function even in very old age -- with the possible exception of the
>immune system, whose decline may indeed be largely due to telomere
>shortening (see recent papers by Rita Effros).  Then there are "those
>damn mice", as Tom Mahoney calls them, whose lifespan is unaffected
>by their telomere length at birth; Tom has noted that this isn't a
>totally conclusive proof that telomere shortening is irrelevant to
>mammalian aging, but it certainly doesn't give the theory any support.
>I don't see much point in regurgitating this any further: see DejaNews.

Well, I appreciate all the information that you have already
regurgitated. Thank you for being willing to try and explain
somethings to me and letting me learn from you.

Probably the only way we will know for SURE if telomerase is the
biggest factor in the human aging process is when an inducer or viral
vector (which could carry the telomerase gene) is tested on an animal
or human. Until then, we probably will not know for sure.

Again, thanks for everything. Take care and have a great day.

Best Regards,
William


>
>> In your current
>> opinion, if you do not mind me asking, what do you believe is the
>> cause of the human aging process (or at least most of it)?  
>
>Personally I think that the theory with the most plausibility on
>current evidence is that mitochondrial DNA mutations are the main
>driving force.  But I must stress that that theory has an unfair
>advantage over a lot of others at the moment, namely that we don't
>yet have good tools for doing a proper test of it -- interventions
>that greatly retard or accelerate the rate of accumulation of those
>mutations, and which are therefore predicted (if this theory is right)
>to make a big difference to lifespan.  If someone develops a way to
>make mutations arise a lot faster in the mitochondria, and the mice
>(or whatever) that get this treatment live as long as ever, then this
>theory will be in the same amount of trouble as the telomere theory.
>
>Aubrey de Grey





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