Two thirds of all patients with dementia suffer from Alzheimer's disease. Estimates indicate that by 2010 our country will have more than 150,000 Alzheimer's patients. 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 targe
|Contact: Pieter Van Dooren|
VIB (the Flanders Institute for Biotechnology)