X-Message-Number: 2469
From: whscad1!kqb (Kevin Q Brown +1 201 386 7344)
Subject: CRYONICS Anti-Aging Gene

The following recent sci.life-extension message announces intriguing
progress toward identifying the genetics of some aging mechanisms,
and potentially Alzheimer's and Parkinson's diseases, too.
Even if other aging mechanisms eventually take you down, therapies
derived from this work may ensure that at the time of suspension
you still possess a mind to preserve.
                              Kevin Q. Brown
PS: Even though the message below contains a copyrighted ClariNet article,
    permission for reposting to USENET was granted, so, as I understand it,
    distribution here should be OK, too.
> Newsgroups: sci.life-extension
> From:  (Daniel Marvin Garrett)
> Subject: Article: Anti-aging Gene
> Date: Fri, 19 Nov 93 02:58:09 GMT

I found the following article extremely interesting.  If you or your system
is not on ClariNet, I'd strongly suggest you lobby for it.

Copyright 199? by <UPI/Newsbytes/Whoever>
Reposted with permission from the ClariNet Electronic Newspaper newsgroup
clari.<groupname>.  For more info on ClariNet, write to  or
phone 1-800-USE-NETS.

> Article 5548 of clari.tw.health:
> From:  (LIDIA WASOWICZ, UPI Science Writer)
> Newsgroups: clari.tw.health,clari.news.group
> Subject: Finding may lead to treatments for aging diseases
> Keywords: health, seniors, special interest
> Copyright: 1993 by UPI, R
> Date: Thu, 18 Nov 93 15:08:05 PST
> Slugword: us-aging
> ANPA: Wc: 480/455; Id: a1109; Sel: na--w; Adate: 11-18-N/A

	Scientists said Thursday they have uncovered the mechanisms by which
an anti-aging gene prevents death of brain cells, findings with critical
implications for future treatments of such diseases as Alzheimer's and
	In a report published in the journal Science, the researchers from
the University of California, Los Angeles, said the gene BCL-2 thwarts
the entire cycle of neuron damage, degeneration and death.
	``The study is important because it sheds light on the pathology of
degenerative neurological diseases that often accompany aging and
suggests a possible therapeutic approach,'' said head researcher Dr.
Dale Bredesen.
	The scientists found BCL-2 decreases brain cells' production of
reactive oxidants, free radical molecules derived from oxygen but with
an unpaired electron that pose a lethal threat to cells.
	``The exciting thing about this finding is that BCL-2 prevents cell
death from conditions that are analogous to Alzheimer's, Parkinson's and
other degenerative diseases,'' Bredesen said.
	``In addition, we now understand for the first time how BCL-2's
protective influence works.''
	The study has key implications for future therapies, from gene
manipulation to replace BCL-2 in brain cells to increasing anti-oxidant
levels in other, simpler ways, the researchers said.
	``At least now we know where to focus our efforts,'' Bredesen said.
	The UCLA team previously had found the gene protects neurons from
death, but until now the specific mechanisms were not understood.
	The new study showed BCL-2 prevents cell death by decreasing the
cells' production of so-called ``reactive oxygen species,'' Bredesen
	``Typically, 1 to 5 percent of oxygen molecules utilized by cells
become super-oxides -- a type of free radical -- which are responsible for
aging and which have been linked to many degenerative neurological
diseases,'' he said.
	The study also for the first time conclusively links apoptosis --
programmed cell death -- with aging.
	And it proves the source of the cell damage that eventually causes
apoptosis, the researchers said.
	``These cells 'blow out' like worn tires,'' Bredesen said. ``What
we've found is that the cell membrane becomes damaged by a process
called lipid peroxidation. This happens when hydrogen peroxide, produced
by the oxygen-based free radicals, weakens the membrane and causes it to
	While damage to cells without BCL-2 rises dramatically, those with
the gene are fully protected, the scientists found in the study, which
was funded by the National Institutes of Health.
	``The whole process of cell damage, degeneration and death is now
more clear, and BCL-2 prevents the whole cycle,'' Bredesen said. ``We
believe it is a very important gene.''

Dan Garrett           Stanford Economics        

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