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

Ultrasound Therapy for Fibromyalgia and Lyme Disease

Curcumin: The All In One Solution, Part 2

What Are the Benefits of Vitamin K2?

Vitamin D deficiency + high fat diet = metabolic syndrome

Why You Should Take Your Apple Cider Vinegar at Night

Use Burdock Oil to Promote Healthy Hair Growth

Meet Your Weight Loss Goals

People with forms of early-onset Parkinson's disease may benefit from boosting niacin in diet, resea...

AMA journal associates iron deficiency with hearing loss

Why the Mediterranean Diet Is so Successful

 
Print Page
Email Article

Mitochondrial Genome Lesions in the Pathogenesis of Sporadic Alzheimer's Disease.

  [ 5 votes ]   [ Discuss This Article ]
By Meier-Ruge WA, Bertoni-Freddari C • www.ProHealth.com • October 1, 1999


BACKGROUND: The recent, magnificent results of molecular biology concerning beta-amyloid (betaA) metabolism in early onset Alzheimer's disease (AD) have generated a series of new findings and, in turn, a new etiological concept. Attention on the early events in the pathogenesis of AD has been shifted from the chromosomal abnormalities in the nucleus of nerve cells onto genetic changes in the mitochondrial genome. This offers a new pathogenetic approach which also opens new pharmacological challenges particularly for the episodic forms of AD.

OBJECTIVE: Alterations occurring at the mitochondrial genome result in major consequences of oxidative phosphorylation and, if a specific threshold is exceeded, they may constitute important causative events in the apoptosis of selected nerve cells. The fact that the main source of mitochondrial metabolism is its glucose turnover allows monitoring brain changes in glucose metabolism by 18F-2 deoxyglucose positron emission tomography. In the demented brain, a low glucose turnover causes a cholinergic deficit by decreasing the synthetic rate of acetyl coenzyme A (AcCoA). AcCoA represents the key substrate for the acetylation of choline to acetylcholine by choline acetyltransferase. The consistent energy need for AcCoA synthesis appears obvious when considering that 1 molecule of glucose generates just 2 molecules of AcCoA, but 38 molecules of ATP. In the brain, AcCoA is exclusively synthesized in the glycolitic pathway. Generation of betaA is increased if the synthetic rate of ATP drops below a critical threshold: under these conditions, the betaA precursor protein (betaAPP) is inserted only in part into synaptic membranes which have the highest betaAPP turnover. In conditions of short ATP supply, betaAPP is not split at the beta region by an ATP-activated protease and this results in a substantial increase in uncleaved betaA molecules.

CONCLUSION: Peroxidative alterations in mitochondrial DNA are of importance in degenerative diseases of postmitotic tissues, particularly in degenerative diseases. This offers a new pharmacological approach for the treatment of AD. Neurotrophic factors and estrogen seem to be the first pharmacological leads.

Source: Gerontology 1999 Oct;45(5):289-297
PMID: 10460992

(Division of Gerontological Brain Research, Department of Pathology, University Medical School, Basel, Switzerland)




Post a Comment

Featured Products From the ProHealth Store
Optimized Curcumin Longvida® Ultra ATP+, Double Strength Ultra EPA  - Fish Oil

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%
Ultra EPA  - Fish Oil Ultra EPA - Fish Oil
Ultra concentrated source of essential fish oils
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

Break Free From Fibromyalgia Break Free From Fibromyalgia
Cocoa's Polyphenol Riches - All the Health Benefits without the Sugar, Calories or Guilt Cocoa's Polyphenol Riches - All the Health Benefits without the Sugar, Calories or Guilt
Coenzyme Q10 - The Energy Maker Coenzyme Q10 - The Energy Maker
Complete and Natural Menopause Relief Complete and Natural Menopause Relief
Fatigue & Fibro Fog: Could You Have a B-12 Deficiency? Fatigue & Fibro Fog: Could You Have a B-12 Deficiency?

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