home   genetic news   bioinformatics   biotechnology   literature   journals   ethics   positions   events   sitemap
 
  HUM-MOLGEN -> Genetic News | search  
 

A New Target For Alzheimer's Therapy

 
  September, 5 2001 19:57
your information resource in human molecular genetics
 
     
Many genetic mutations are known to increase the risk of Alzheimer's disease, but it remains controversial whether these mutations have common functional effects. One common site for mutations that predispose individuals to the early onset form of Alzheimer's disease is the gene for amyloid precursor protein. Previously characterized mutations of this type were known to result in increased production of the amyloid b-protein (Ab), a fragment of amyloid precursor protein that is a major component of the large 'amyloid plaques' found at lesions within the diseased brain. The increased production of Ab was thought to favor plaque formation and lead to disease onset.

A study by Lannfelt and colleagues in this issue (Nature Neuroscience, Vol. 4, No. 9, Sep 01) suggests, however, that this theory may need to be revised. The authors report that individuals expressing the 'arctic' Alzheimer's mutation (identified in a family from northern Sweden) actually show decreased production of Ab. The apparent paradox was resolved by further biochemical analysis, which revealed that 'arctic' mutant Ab (the mutation is located within the Ab sequence) actually displayed increased rates of protofibril formation. Protofibrils are small protein complexes that are an intermediate step in the formation of the larger amyloid plaques. Thus, even though patients with this mutation show reduced production of Ab, the pathway to plaque formation is still accelerated.

The authors conclude that it is not simply the levels of Ab that are important, but also the formation of protofibrils. This is an important distinction because it both unifies the mechanism of disease onset for a variety of different mutations and suggests a new target for therapeutic intervention, the formation of protofibrils.

Christian Haass and Harald Steiner discuss these findings in an accompanying News & Views article.

Contact:

Dr. Lars Lannfelt
Karolinska Institute
Department of Neurotec, Geriatric Medicine
Novum KFC
Huddinge, S-141 86
Sweden
tel: +46 8 585 864 72
fax: +46 8 585 838 80
e-mail: lars.lannfelt@kfcmail.hs.sll.se

Dr. Christian Haass
Ludvig-Maximilians-Universitat
Adolf-Butenandt-Institute
Department of Biochemistry
Schillerstrasse 44
D-80336 Muenchen
Germany
tel: +49 49 89 5996 471/472
fax: +49 89 5996 415
e-mail: chaass@pbm.med.uni-muenchen.de

(C) Nature Neuroscience press release.


Message posted by: Trevor M. D'Souza

print this article mail this article
Bookmark and Share this page (what is this?)

Social bookmarking allows users to save and categorise a personal collection of bookmarks and share them with others. This is different to using your own browser bookmarks which are available using the menus within your web browser.

Use the links below to share this article on the social bookmarking site of your choice.

Read more about social bookmarking at Wikipedia - Social Bookmarking

Latest News
Variants Associated with Pediatric Allergic Disorder

Mutations in PHF6 Found in T-Cell Leukemia

Genetic Risk Variant for Urinary Bladder Cancer

Antibody Has Therapeutic Effect on Mice with ALS

Regulating P53 Activity in Cancer Cells

Anti-RNA Therapy Counters Breast Cancer Spread

Mitochondrial DNA Diversity

The Power of RNA Sequencing

‘Pro-Ageing' Therapy for Cancer?

Niche Genetics Influence Leukaemia

Molecular Biology: Clinical Promise for RNA Interference

Chemoprevention Cocktail for Colon Cancer

more news ...

Generated by News Editor 2.0 by Kai Garlipp
WWW: Kai Garlipp, Frank S. Zollmann.
7.0 © 1995-2016 HUM-MOLGEN. All rights reserved. Liability, Copyright and Imprint.