Researchers find genetic cause of Alzheimer's disease

Brussels, 20 Apr 2006

Researchers from the Flanders Interuniversity Institute for Biotechnology (VIB) and Antwerp University in Belgium have found that the quantity of amyloid protein in brain cells plays a key role in the development of Alzheimer's disease - the greater the quantity of the protein, the younger the dementia can start.

Alzheimer's disease is a memory disorder that affects up to 70 per cent of all dementia patients. In Belgium alone, around 100,000 people suffer from the disease. As the disease develops, brain cells are gradually destroyed in the areas of the brain responsible for memory and knowledge. Unfortunately, all attempts to find a cure or treatment for Alzheimer's have so far been unsuccessful.

Previous research had illustrated a link between amyloid protein and the development of senile plaques and the loss of cells. People with Down Syndrome frequently develop Alzheimer's - a fact indicating that the quantity of the amyloid precursor protein contributes to the disease. Those with Down Syndrome have three copies of the gene for the amyloid precursor protein, and therefore produce 150 per cent of the normal amount of the protein.

With this in mind, the VIB scientists studied the hereditary code responsible for controlling the expression of the gene, and found variations in the promoter that increases gene expression, and thus the formation of the amyloid precursor protein, in Belgian and Dutch Alzheimer's patients below the age of 70.

Furthermore, the team found a connection between these variations and the age at which Alzheimer's symptoms are first detected: the higher the gene expression, the younger the patient. The results of the research mean that it is possible to identify those with an increased genetic risk of developing Alzheimer's by measuring the amount of amyloid precursor protein that an individual has.

The research was partly funded under the APOPIS project of the EU's Sixth Framework Programme (FP6)

CORDIS RTD-NEWS/© European Communities, 2005
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