ProHealth health Vitamin and Natural Supplement Store and Health
Home  |  Log In  |  My Account  |  View Cart  View Your ProHealth Vitamin and Supplement Shopping Cart
800-366-6056  |  Contact Us  |  Help
Facebook Google Plus
Fibromyalgia  Chronic Fatigue Syndrome & M.E.  Lyme Disease  Natural Wellness  Supplement News  Forums  Our Story
Store     Brands   |   A-Z Index   |   Best Sellers   |   New Products   |   Deals & Specials   |   Under $10   |   SmartSavings Club

Trending News

Vitamin D supplements, sleep could help manage pain

Bacopa: The Herb That May Increase Your Brain Power

Lilac Oil: More Than Just for Fragrance

Eat More Yogurt and Avoid Osteoporosis

Safflower: An Economically Important Herb That Can Benefit Humans and Animals Alike

What Is Bilberry Good For?

Coffee, herbal tea may help prevent liver fibrosis

Crafty Uses for Carrot Seed Oil

Higher omega 3 levels linked to improved brain blood flow

Curcumin, resveratrol, ursolic acid show promise against prostate cancer

 
Print Page
Email Article

Study Implicates Programmed Cell Death in Familial Alzheimer's Disease

  [ Not Yet Rated ]   [ Discuss This Article ]
By Press Release by the National Institute of Health • www.ProHealth.com • December 5, 1996


Scientists have found additional evidence that dysregulation of programmed cell death --the normal process by which old or superfluous cells self-destruct -- may underlie the earlier onset and more rapid downhill course of inherited forms of Alzheimer's disease.

As reported in the Dec. 6 issue of Science by scientists from the National Institutes of Health (NIH), Loyola University Medical Center in Maywood, Ill., and Harvard Medical School in Charlestown, Mass., the new findings may help explain the features that distinguish familial Alzheimer's disease, which clusters in families, from the more common, late-onset form of the disease. Luciano D'Adamio, M.D., Ph.D., chief of the T Cell and Molecular Biology Unit at the National Institute of Allergy and Infectious Diseases (NIAID), and Benjamin Wolozin, M.D., Ph.D., an Alzheimer's disease researcher formerly with the National Institute of Mental Health (NIMH) and now at Loyola, led the collaborative research study.

Alzheimer's disease is the single greatest cause of mental impairment in older people, affecting an estimated 4 million people in the United States. Familial Alzheimer's disease accounts for up to 10 percent of all cases. Recently it has been linked to the inheritance of specific mutations in any of three genes: presinilin-1 (PS1), PS2 and amyloid precursor protein (APP). An extremely aggressive form of the illness, familial Alzheimer's disease strikes people between ages 30 and 60 and progresses much more quickly than sporadic Alzheimer's disease, which generally develops after age 65.

Otherwise, however, the two types of the illness -- which strips away memories and leads to mental confusion -- are indistinguishable, characterized by the loss of neurons and the development of amyloid plaques and neurofibrillary tangles in the brain.

The new report extends the findings that the three NIAID co-authors published earlier this year in Science. In the course of investigating several genes they had identified as being involved in apoptosis, or programmed cell death -- the choreographed cell suicide that helps sculpt developing tissues and organs -- they stumbled across a gene fragment that is a piece of mouse PS2. It was the first objective evidence that part of the programmed cell death pathway might be involved in Alzheimer's disease.

In the current paper, the authors report the results of a series of experiments conducted with model neuronal cells to study PS2 function, to determine how the mutant PS2 found in familial Alzheimer's patients affects the role of PS2 in apoptosis. They also examined if PS2 might play a role in apoptosis induced by a mutant APP. APP gives rise to beta-amyloid peptide, which is toxic to cells and collects in the plaques found in Alzheimer brains. Finally, they investigated whether PS2 and APP -- which are transmembrane proteins, meaning each contains domains that cross the cell membrane -- might act via signalling through certain kinds of so-called G proteins, proteins lodged in the cell membrane that bind molecules involved in energy transfer.

"I think we have established pretty convincingly that PS2 is required for some form of apoptosis in different cell types," comments Dr. D'Adamio. "In the system we have studied, it is clear that mutation exacerbates this function." The results of their experiments demonstrate that:

1. PS2 is not only required for T-cell receptor triggered cell death (the finding of their earlier Science paper), but also for neuronal cell death

2. A PS2 mutant associated with familial Alzheimer's disease causes much more apoptotic activity than does normal PS2

3. PS2-mediated apopotosis can be blocked by pertussis toxin, an inhibitor of G proteins, suggesting that G proteins are required for PS2's function

4. APP and PS2 share the same membrane signalling pathway

5. PS2 dramatically increases the susceptibility of cells to apoptosis induced by beta amyloid peptide, without affecting the level of APP.

Although they only experimented with PS2 and APP, they speculate that since PS1 is very similar to PS2, it could involve the same pathway. The authors conclude, that the "activation of PS2 increases the susceptibility of neurons to apoptotic stimuli that could sensitize neurons to the harmful insults of aging, such as free radical-mediated oxidation and neurotoxicity resulting from aggregated beta-amyloid peptide. The accelerated rate of neuronal cell death that occurs in the brains of Alzheimer's patients may therefore result from the additive effects of activated apoptosis, aging and beta-amyloid peptide activity."

Furthermore, they note that activating PS2 also may indirectly contribute to the process of neurodegeneration by triggering a stress response that increases production of beta-amyloid peptide, as the authors note, "adding to the toxic burden in the brains of Alzheimer's patients and further accelerating the process of neurodegeneration."

Source:
National Institute of Health
Press Release
December 5, 1996

References:
Wolozin B, Iwasaki K, Vito P, Ganjei K, Lacana E, Sunderland T, Zhao B, Kusiak JW, Wasco W, and D'Adamio L. PS2 participates in cellular apoptosis: constitutive activity conferred by Alzheimer mutation. Science 1996;274:1710-13.
Vito P, Lacana E, and D'Adamio L. Interfering with apoptosis: Ca2+2+ -binding protein ALG-2 and Alzheimer's disease gene ALG-3. Science 1996;271:521-15.



Post a Comment

Featured Products From the ProHealth Store
Energy NADH™ 12.5mg Ultra ATP+, Double Strength FibroSleep™

Looking for Vitamins, Herbs and Supplements?
Search the ProHealth Store for Hundreds of Natural Health Products


Article Comments



Be the first to comment on this article!

Post a Comment


 
NAD+ Ignite with Niagen

Featured Products

Mitochondria Ignite™ with NT Factor® Mitochondria Ignite™ with NT Factor®
Reduce Fatigue up to 45%
Vitamin D3 Extreme™ Vitamin D3 Extreme™
50,000 IU Vitamin D3 - Prescription Strength
Energy NADH™ 12.5mg Energy NADH™ 12.5mg
Improve Energy & Cognitive Function
Optimized Curcumin Longvida® Optimized Curcumin Longvida®
Supports Cognition, Memory & Overall Health

Natural Remedies

Complete and Natural Menopause Relief Complete and Natural Menopause Relief
Relief for Dry, Itchy Skin Caused by Fibromyalgia Relief for Dry, Itchy Skin Caused by Fibromyalgia
Coenzyme Q10 - The Energy Maker Coenzyme Q10 - The Energy Maker
Mitochondria-Booster NIAGEN® Shows Promise in First Human Clinical Trial Mitochondria-Booster NIAGEN® Shows Promise in First Human Clinical Trial
Coconut Oil - Healthy Gifts from the 'Tree of Life' Coconut Oil - Healthy Gifts from the 'Tree of Life'

CONTACT US
ProHealth, Inc.
555 Maple Ave
Carpinteria, CA 93013
(800) 366-6056  |  Email

· Become a Wholesaler
· Vendor Inquiries
· Affiliate Program
SHOP WITH CONFIDENCE
Credit Card Processing
SUBSCRIBE TO OUR NEWSLETTERS
Get the latest news about Fibromyalgia, M.E/Chronic Fatigue Syndrome, Lyme Disease and Natural Wellness

CONNECT WITH US ProHealth on Facebook  ProHealth on Twitter  ProHealth on Pinterest  ProHealth on Google Plus

© 2017 ProHealth, Inc. All rights reserved. Pain Tracker App  |  Store  |  Customer Service  |  Guarantee  |  Privacy  |  Contact Us  |  Library  |  RSS  |  Site Map