Newly discovered brain protein leads to new model for Alzheimers diseaseFebruary 20th, 2009 - 6:14 pm ICT by ANI
London, Feb 20 (ANI): While trying to unravel the normal function of a protein implicated in Alzheimers disease (AD), scientists have discovered a naturally occurring protein that provides a new therapeutic target for the disease.
The new finding, by scientists in California and France, rules out the current theory that AD is a disease of toxicity stemming from damage caused by sticky plaques that collect in the brain.
However, the Buck Institute for Age Research and the CNRS (Centre Nationale de la Recherche Scientifique) study points to the condition as a disorder involving an imbalance in signalling between neurons.
One of the mysteries of AD has been the normal function of the amyloid precursor protein (APP) that are concentrated at the points where neurons connect.
Although the sticky amyloid plaques are believed to be the biggest characteristic of AD resulting from APP, but theres not much evidence to prove that APP exists simply to cause Alzheimers disease.
In the study, scientists have shown that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive.
When netrin-1 was given to mice that have a gene for Alzheimers disease their symptoms were reversed, and the sticky amyloid was reduced.
The results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong.
Instead, the disease apparently stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections both by binding to APP and activating normal cell programs.
It was found that netrin-1, not only binds to APP keep the nerve cells alive and connected, but it also shut down the production of the amyloid, all of which makes it an interesting potential therapeutic.
We now believe that APP is part of a plasticity module that functions in normal memory and forgetting, and that netrin-1 gives us an important starting point to restore the normal balance, Nature quoted Buck Institute Faculty Member Dale Bredesen, MD, who led the California half of the French-Californian collaborative research, as saying.
The study appears online in the Nature publication Cell Death and Differentiation. (ANI)
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Tags: amyloid plaques, amyloid precursor protein, belief that, brain cell damage, brain protein, buck institute, cnrs, london feb, mice, mysteries, nerve cells, nerves, neurons, new model, recherche scientifique, scientists, therapeutic target, toxicity