From: LEF Email List1 ddye@lifeextension.com
Sent: Friday, January 05, 2001 11:50 AM
Subject: LIFE EXTENSION UPDATE JANUARY 5 2001
LEF Email List1 - http://www.lef.org
LIFE EXTENSION UPDATE, JANUARY 5 2001
IN THIS ISSUE, JANUARY 5, 2001: LIFE EXTENSION UPDATE EXCLUSIVE: Vaccine
halts Alzheimer's disease in mice; WHAT'S HOT: Alzheimer's plaques
probable cause, not effect; PROTOCOL: Alzheimer's disease; FEATURED
PRODUCTS OF THE WEEK: Melatonin capsules, Huperzine-A; JANUARY LIFE
EXTENSION MAGAZINE NOW ONLINE; SUPER SALE GOOD THROUGH THE END OF THIS
MONTH
LIFE EXTENSION UPDATE EXCLUSIVE: Each week, "Life Extension Update
Exclusive" features an article not found on Life Extension's website or in
Life Extension Magazine.
Vaccine halts Alzheimer's disease in mice
Alzheimer's disease effects almost one out of every ten people over age
sixty-five, and people over eighty have four times this risk. The disease
is characterized by severe memory loss and the formation in the brain of
what are known as senile plaques, containing the protein beta-amyloid.
Mutations to the gene that codes for this protein have been found to cause
an overproduction of beta-amyloid peptide in the brain and resultant
plaque formation. It had not been known whether these plaques are
causative of dementia, but a recent study published in The Journal of
Neuroscience indicates they are. (See "What's Hot" below.) In research
published in the journal Nature last year, mice genetically modified to
overproduce beta-amyloid who show the symptoms of Alzheimer's disease were
vaccinated with beta-amyloid peptide. The mice developed antibodies to
the protein which caused the disappearance of senile plaques in the brain.
Now researchers have found that the vaccine appears to arrest memory loss
as well in this animal model. The December 21 2000 issue of Nature
published two papers that confirm that Alzheimer's model mice who were
immunized with beta-amyloid demonstrated a reduction in memory and
learning deficit when performing certain tests over a period of time,
compared to nonimmunized controls. The immunized mice experienced the
expected reduction in beta-amyloid as well.
Alzheimer's authority Paul Chapman of Cardiff University stated, "This is
big news. If the results had gone the other way then a lot of people would
have been forced to rethink . . . The really significant aspect of this
work to me is not so much the result but the process they use. Other
treatment studies tend to create the pathology of Alzheimer's and then try
to make them go away. Tests of behaviour like this are critical."
Researcher Dave Morgan of the University of South Florida in Tampa who
coauthored one of the Nature papers feels that this evidence supports the
hypothesis that beta-amyloid-containing deposits are related to the
dementia experienced by these patients.. Large scale clinical trials are
planned in hopes that treatments based on the vaccine will prevent or
postpone the development on Alzheimer's symptoms in humans.
WHAT'S HOT
Alzheimer's plaques probable cause, not effect
The Journal of Neuroscience (volume 21, 2001) published a report of
research conducted by the National Institute of Environmental Health
Sciences (NIEHS) that the plaques found in the brains of Alzheimer's
patients disrupt brain signals which may contribute to the memory loss
experienced by this group. These plaques contain a protein called
beta-amyloid and their presence is confirmative of an Alzheimer's
diagnosis upon autopsy of the brain. The beta-amyloid peptide has been
found in the brains of both humans and animals. Although it had been
frequently speculated, it had not been known whether these plaques were
causative of the disease's symptoms.
Working with rats, the NIEHS team of Jerrel L. Yakel, PhD, Diana L.
Pettitt, Ph.D., and Zuoyi Shao, Ph.D, working from NIEHS' headquarters and
laboratory in Research Triangle Park, North Carolina, discovered that
beta-amyloid binds to the nicotinic acetylcholine receptor, a key
signalling receptor in the brain's hippocampus, which is the area of the
brain involved in emotion, memory and motivation. This blocks the
transmission of signals involved in learning and memory. According to the
researchers this is the first time that a link between Alzheimer's plaques
and failed brain function has been established.
Although several treatments are available which can temporarily relieve
some of the symptoms Alzheimer's disease, there is no cure, and with a
longer-lived population the disease's incidence in the U.S. is on the
rise. Dr Yakel stated, "Knowing how the disease process works makes it
more likely that medical science can find ways to slow, halt or even
reverse the process." He predicted that improved therapies could result
from finding chemicals that prevent the binding of beta-amyloid to the
nicotinic acetylcholine receptor.
http://www.lef.org/cgi-local/welcome.cgi/id=151061356/sgroup_id=699/welcome.
html
PROTOCOL
Alzheimer's disease
The only two FDA-approved drugs for treatment of Alzheimer's disease are
both acetylcholinesterase inhibitors: tacrine (Cognex) and donepezil
(Aricept). Huperzine-A, metrifonate, and rivastigmine are also
acetylcholinesterase inhibitors-and the last two may receive FDA approval
soon. Huperzine-A has been used for centuries in China as an herbal
medicine prepared from the moss Huperzia serrata. Side effects from
tacrine, including liver toxicity, make donepezil (Aricept) the first drug
of choice.
Although acetylcholinesterase inhibitors can apparently reverse symptoms
by several months, they have not been shown to slow the progress of neuron
degeneration. By contrast, a double-blind, placebo-controlled clinical
trial with daily doses of 10 mg deprenyl (selegiline), 2000 IU vitamin E,
or both showed a 25% slowing of the progress of the disease, but without
any cognitive improvement. There was no advantage to using both deprenyl
and vitamin E, so vitamin E alone would be a less expensive and more
convenient therapy for most patients.
Treatment of cultured neurons with vitamin E has been shown to protect
them from beta-amyloid toxicity. This suggests that vitamin E and other
antioxidants such as vitamin C (which regenerates vitamin E) and coenzyme
Q10 may be of value in preventing Alzheimer's disease. In fact, melatonin
has been shown to protect cell cultures from beta-amyloid toxicity.
N-acetylcysteine has protected cultured cells from oxidative stress due to
AGE-modified tau-protein. (Advanced glycation end-products, AGEs, lead to
the formation of toxic hydroxyl free radicals and impaired ion and glucose
transport, which cause neuron degeneration. This is discussed in detail
further in the text.)
http://www.lef.org/cgi-local/welcome.cgi/id=151061357/sgroup_id=699/welcome.
html
FEATURED PRODUCTS OF THE WEEK
Melatonin 3 mg capsules
Melatonin is the most effective antioxidant yet studied because it easily
penetrates cell membranes (especially in the brain) to provide protection
against free radicals throughout all our cells. Melatonin crosses the
blood-brain barrier very effectively. It appears to protect the central
nervous system against injury, disease, and aging better than any other
substance.
The Life Extension Foundation believes that melatonin is the single most
effective antiaging therapy in the world. It has been shown, in thousands
of published studies, to protect against almost every disease associated
with aging including cardiovascular disease, osteoporosis, age-associated
immune impairment, and Alzheimer's and Parkinson's disease, as well as
against aging itself. The Life Extension Foundation uses only
pharmaceutical-quality melatonin that has been assayed for purity.
http://www.lef.org/cgi-local/welcome.cgi/id=151061358/sgroup_id=699/welcome.
html
Huperzine A with vitamin E
Huperzine A standardized extract is an all natural herbal supplement that
has been clinically shown to enhance memory, focus and concentration.
Huperzine A should be taken consistently for best results. Do not take
this product if you have heart or pulmonary problems without first
consulting your physician.
http://www.lef.org/cgi-local/welcome.cgi/id=151061359/sgroup_id=699/welcome.
html
JANUARY LIFE EXTENSION MAGAZINE NOW ONLINE!
As We See It
Inflammation and heart disease
http://www.lef.org/magazine/mag2001/jan2001_awsi.html
Cover Story
Carnosine: nature's pluripotent life extension agent by Karin Granstrom
Jordan, MD
http://www.lef.org/magazine/mag2001/jan2001_report_carnosine_1.html
Carnosine and cellular senescence
http://www.lef.org/magazine/mag2001/jan2001_report_carnosine2_1.html
Report
The scales tilt on the side of nature
http://www.lef.org/magazine/mag2001/jan2001_report_cox2_1.html
Childhood nutrition, the road to lifelong health
http://www.lef.org/magazine/mag2001/jan2001_report_child_1.html
In the News
C-reactive protein is a heart disease culprit, not just a marker
http://www.lef.org/magazine/mag2001/jan2001_itn.html
Profile
Taking charge
http://www.lef.org/magazine/mag2001/jan2001_profile.html
Q & A
The link between homocysteine levels and SAMe, plus . . .
http://www.lef.org/magazine/mag2001/jan2001_qanda.html
January 2001 Medical Updates
http://www.lef.org/magazine/mag2001/jan2001_medup.html
January 2001 Abstracts
http://www.lef.org/magazine/mag2001/jan2001_abs.html
SUPER SALE GOOD THROUGH THE END OF THE MONTH
Don't forget, Super Sale is only good through the end of this month.
Order your supply of life extension supplements for 2001 now to receive
the 10% Super Sale discount. (Super Sale discount not valid for some
overseas countries.) To view the list of products available from Life
Extension, go to
http://www.lef.org/cgi-local/welcome.cgi/id=151061360/sgroup_id=699/welcome.
html
If you have any questions or comments concerning this issue or back issues
of Life Extension Update, or on any other life extension topics, email me
at ddye@lifeextension.com
Long life and happy 2001,
Dayna Dye
Editor, Life Extension Update
ddye@lifeextension.com
Life Extension Foundation
www.lef.org
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