Research advances in recent years have given us a detailed knowledge of the molecular mechanisms behind Alzheimer’s disease. The spotlight has fallen on beta amyloid, a peptide formed from a special protein in the brain. The prevailing hypothesis is that the protein clumps together into plaques, which damage the brain’s nerve cells and causes the characteristic symptoms of Alzheimer’s.
The amyloid theory has spawned a large number of potential drugs which attempt to delay the development of the disease by slowing down the formation of, or even clearing, plaques. However, several major clinical trials have shown that this type of medication is not at all effective.
Kaj Blennow, a professor at the University of Gothenburg’s Sahlgrenska Academy and one of the world’s leading dementia researchers, is now taking research into new Alzheimer’s medication in a brand new direction.
“It’s important that we constantly question research results, including in Alzheimer’s research,” says Blennow. “And to do this we have to come up with new analytical methods.”
Blennow and his research colleagues believe that the solution lies in being able to test different drugs directly on living patients instead of on mice as has been the case to date.
“The mouse models currently being used have a very tenuous link to the most common form of Alzheimer’s,” says Blennow. “This is particularly obvious when new drug candidates are tested on real people – we have now identified over 100 molecules that reduce the formation of plaques in mice with Alzheimer’s, but unfortunately none have led to a single drug that slows down the illness in humans.”
Blennow and his research colleagues at the Clinical Neurochemistry Laboratory are trying instead to come up with new analytical methods that use biomarkers to monitor biochemical changes in patients with Alzheimer’s. It is hoped that the biomarkers can be used both to make an accurate and early diagnosis and to establish and monitor the effects of new drugs.
“Our studies on patients with Alzheimer’s and other age-related disorders would suggest that beta-amyloid is perhaps not the direct cause of the illness, but instead the brain’s response to different types of stress,” says Blennow. “This could completely change the way we view the illness and could play a crucial role in future treatments.”