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New Target For Medicine To Combat Alzheimer's: Scientists Confirm Protein's Key Role

Date:
February 13, 2009
Source:
VIB (the Flanders Institute for Biotechnology)
Summary:
Scientists have demonstrated that a particular protein is extremely well suited to be a target for a new medicine against Alzheimer's disease.

VIB scientists connected to the Center for Human Heredity have demonstrated that a particular protein is extremely well suited to be a target for a new medicine against Alzheimer's disease. Their findings are published in the journal Science.

The research has been conducted in collaboration with Galapagos, the biotechnology company that discovered the protein's role in Alzheimer's disease and that will now further the search for an appropriate medicine.

Two thirds of all patients with dementia suffer from Alzheimer's disease. Alzheimer's is a disease that gradually destroys brain cells, with the result that the mental capacity of patients with Alzheimer's gradually declines. At first, memory begins to fail, but the patient's cognitive capabilities also deteriorate as the disease progresses.

Today, this disease cannot yet be cured. Current medicines for Alzheimer's patients sustain the memory functions for a short time, but they are unable to stop the brain cells from dying off. At best, they are able to limit the loss of memory during the early phases of the disease.

The β-amyloid cascade

The brains of Alzheimer's patients typically show the presence of amyloid plaques, which are abnormal accumulations of a protein (β-amyloid) between the neurons. The sticky β-amyloid develops when the precursor protein (amyloid precursor protein or APP) is cut into pieces incorrectly.

GPR3: target for new medicine

Several years ago, Bart De Strooper and other researchers elucidated the way in which these plaques originate and discovered that secretases play a large role in this process. Now, under the direction of Bart De Strooper, and in collaboration with researchers from the biotech company Galapagos, Amantha Thathiah and her colleagues have investigated whether additional substances are also involved in the development of the plaques. Which is apparently the case: Galapagos has identified the GPR3 protein as a new player. The VIB researchers have been able to show − in vitro (in cells isolated and studied in the laboratory) as well as in vivo (in living animals − mice, in this instance) − that blocking GPR3 leads to reduction of the plaques.

Importance of this research

The GPR3 protein is an important target molecule for the eventual development of a new medicine against Alzheimer's disease. The majority of all of the medicines that are available in pharmacies − regardless of the disease that they work against − act on proteins of a specific type. GPR3 is one of these − which, at this time, cannot be said for any other protein implicated in Alzheimer's.

Further research and development of this medicine will be carried out by the Flemish biotechnology company Galapagos. It is possible that 'the cure for Alzheimer's' will never be able to restore a patient's memory − but, hopefully, the disorder can be arrested, saving as many brain cells as possible.


Story Source:

The above story is based on materials provided by VIB (the Flanders Institute for Biotechnology). Note: Materials may be edited for content and length.


Cite This Page:

VIB (the Flanders Institute for Biotechnology). "New Target For Medicine To Combat Alzheimer's: Scientists Confirm Protein's Key Role." ScienceDaily. ScienceDaily, 13 February 2009. <www.sciencedaily.com/releases/2009/02/090212141251.htm>.
VIB (the Flanders Institute for Biotechnology). (2009, February 13). New Target For Medicine To Combat Alzheimer's: Scientists Confirm Protein's Key Role. ScienceDaily. Retrieved July 30, 2014 from www.sciencedaily.com/releases/2009/02/090212141251.htm
VIB (the Flanders Institute for Biotechnology). "New Target For Medicine To Combat Alzheimer's: Scientists Confirm Protein's Key Role." ScienceDaily. www.sciencedaily.com/releases/2009/02/090212141251.htm (accessed July 30, 2014).

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