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Scientists are gaining ever more insight into the causative mechanisms involved in Alzheimer's disease. Thus, they can identify possible attack points for a targeted, causative treatment of this severe brain disorder which affects millions of people worldwide, as reported at the international conference "Neurodegenerative Diseases: Molecular Mechanisms in a Functional Genomics Framework" in the Max Delbrück Communications Center (MDC.C) in Berlin-Buch (Germany). Alzheimer's, like Huntington's disease and Parkinson's disease, belongs to the group of neurodegenerative diseases caused by misfolded proteins.
"Alzheimer's is a disease of old age," Dr. Christian Haass, Professor at the Ludwig Maximilian University Munich said at the Berlin conference. In 1992, he succeeded in showing that the insoluble protein fragments that are deposited in the brains of Alzheimer's patients, the so-called amyloid beta, are continually formed in the brain throughout life and are part of the normal aging process. The scientist is convinced that all people, if they lived long enough, would fall ill with this severe degenerative disorder of the brain.
Amyloid beta develops when the so-called amyloid precursor protein (APP) is broken into fragments. It quickly became clear that Amyloid beta is generated by proteolytic processing involving two types of proteases, beta-, and gamma-secretase. "Inhibiting the activity of these two enzymes should slow down nerve cell degeneration," Dr. Haass said in Berlin. These enzymes could, therefore, be potential drug targets.
Yet Alzheimer's disease still baffles scientists: while they have a good understanding of how protein fragments develop, they cannot explain how these fragments prove to be toxic to nerve cells. Dr. Roberto Cappai, Professor at the University of Melbourne, Victoria, Australia, reported in Berlin that copper ions influence the formation of harmful protein deposits. The higher the level of copper in the brain, the less amyloid beta (which is neurotoxic) is formed. Scientists have been able to show that the level of copper in Alzheimer's patients is very low.
Around 200 genome researchers and clinicians from Europe, Japan, Canada, and the US attended the four-day conference in Berlin, which ended on Saturday, September 9th. The conference focused on the investigation of the causes of neurodegenerative diseases with the aid of systems biology, which seeks to piece together single aspects of research that have, until now, been analyzed separately - (e.g., proteins, protein interactions, signal pathways, and cells) in order to obtain an overall picture. It was the first conference of its kind organized by the Max Delbrück Center for Molecular Medicine (MDC) Berlin Buch together with the Charité -University Medical School Berlin and the University of Bonn under the umbrella of the National Genome Research Network (NGFN).
Press and Public Affairs
Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch
Barbara Bachtler
Robert-Rössle-Straße 10
13125 Berlin
Germany
Phone: 0049/30/94 06 - 38 96
Fax: 0049/30/94 06 - 38 33
e-mail: presse@mdc-berlin.de
http://www.mdc-berlin.de/englisch/about_the_mdc/public_relations/e_index.htm
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