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

Common Cause For Folding Diseases?

  April, 8 2002 8:14
your information resource in human molecular genetics
Diseases as diverse as Alzheimer's, diabetes and Creutzfeldt–Jacob disease (CJD) may have a common molecular foundation: protein misfolding. So suggests this week's Nature (Vol. 416, No. 6880, 04 Apr 02), hinting that breaking up rogue protein gangs could be a way to attack such diseases.

Small clumps of misshapen protein can damage cells, researchers have found. This is true for proteins in general and for the proteins that accumulate in the brains of Alzheimer's patients.

Christopher Dobson of the University of Cambridge, UK, and colleagues persuaded normally harmless proteins, one from bacteria and the other from cattle, to take on a new shape. This made them toxic to cells in culture. The rogue proteins were most damaging in small groups, before they formed into large insoluble clusters.

Meanwhile, Dennis Selkoe, of Harvard Medical School and the Brigham and Women’s Hospital, Boston, and colleagues, have found that small clusters of amyloid beta molecules, the misfolded protein that accumulates in much bigger clumps in the brains of Alzheimer's patients, disrupt the synapses in rat brains.

Researchers have argued over whether amyloid beta is toxic, or whether it is a consequence, rather than a cause of Alzheimer's. Pinning a specific form of damage on the molecule in living animals could help settle this debate.

"These ideas highlight the importance of understanding the cellular mechanisms that combat these potentially lethal mistakes, and identifying the precise cellular targets of those aggregates that escape such surveillance," say R. John Ellis and Teresa J. T. Pinheiro of the University of Warwick, UK, in an accompanying News and Views article.


Christopher Dobson
tel +44 1223 763 070
e-mail cmd44@cam.ac.uk

Dennis Selkoe
tel +1 617 525 5200
e-mail dselkoe@rics.bwh.harvard.edu

R. John Ellis
tel +44 2476 523509,
e-mail jellis@bio.warwick.ac.uk

(C) Nature 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 © 1995-2017 HUM-MOLGEN. All rights reserved. Liability, Copyright and Imprint.