Potential new drug target to stop Alzheimer’’s progression identifiedMarch 20th, 2009 - 1:02 pm ICT by ANI
Washington, Mar 20 (ANI): Scientists have moved a step closer to developing a drug that could actually stop the progress of Alzheimer’’s disease.
They have identified a molecule that can form the basis for a new therapy for the neurodegenerative disease.
A typical characteristic of the brains of Alzheimer’’s patients is the presence of amyloid plaques, which are abnormal accumulations of the (c)!-amyloid protein between the neurons. The sticky (c)!-amyloid arises when the amyloid precursor protein is cut into pieces incorrectly.
The Y=a-secretase complex - which cuts proteins at a specific place - plays a major role in the creation of these plaques.
However, this complex (group of proteins that work together) is also involved in the regulation of a series of other essential proteins such as Notch, which plays a crucial role in the development of an embryo.
This is why many of the medicines in development that act on the whole ?-secretase complex run up against toxic side effects.
Under the direction of Bart De Strooper, and in collaboration with researchers in other countries, Lutgarde Serneels, Jerome Van Biervliet and their colleagues have been studying the Y=a-secretase complex in a variety of tissues.
They have now been able to demonstrate that the complex assumes a different shape and function according to the tissue in which the secretase is active.
For their research on Alzheimer’’s disease, the researchers used mouse models. They found that deactivating the variant, Aph1B Y=a-secretase, in Alzheimer mice leads to reduced formation of the plaques, without any harmful side effects.
With this discovery, the researchers are once again opening a way toward the development of medicines that deactivate Y=a-secretase.
By concentrating on a variant of the complex that cuts proteins specifically in the brain - the Aph1B Y=a-secretase complex - the formation of the plaques can be prevented, while the other functions of Y=a-secretase are not affected.
This raises hopes for a drug that, for the first time, will succeed in stopping Alzheimer’’s disease.
The journal Science is publishing the results of this research. (ANI)
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Tags: amyloid plaques, amyloid precursor protein, amyloid protein, bart, brains, deactivate, different shape, drug target, embryo, medicines, mice, molecule, mouse models, neurodegenerative disease, neurons, notch, proteins, specific place, tissues, toxic side effects