New mechanism of Alzheimer's disease found

Hitherto unknown mechanism with significant effect on Alzheimer's disease?
Alzheimer's disease is much more known today than it was just a few years ago. However, the mechanisms of the disease have still not been completely deciphered. A research team from the University of Bonn has now identified a previously unknown mechanism that may contribute significantly to the development of Alzheimer's disease.

The scientists found that the so-called beta-amyloid plaques (also known as Alzheimer's plaques) affect the power of the cells (mitochondria) in their function. These are paralyzed by the Alzheimer's toxins and stop their energy supply, whereby the cells are doomed, according to the announcement of the University of Bonn. The researchers have published their latest study results in the journal "Molecular Biology of the Cell".

Beta-amyloid, which accumulates in the brains of Alzheimer's patients, destroys the cell power plants, which could be the cause of neuronal death. (Image: goa novi / fotolia.com)

Beta amyloid deposits in the brain of the patients
In Alzheimer's disease, characteristic deposits are formed in the brain between the nerve cells, the so-called plaques, which consist of beta-amyloid peptides. These protein deposits also occur in the brains of healthy people, but are rapidly degraded there, explain the scientists. In Alzheimer's patients, on the other hand, there is an accumulation and in the plaques large amounts of entangled beta-amyloids would be found, according to the University.

Toxic effect within the cells?
For a long time, it has been suggested that these extracellular deposits damage and eventually kill the nerve cells - so the plaques are the cause of progressive dementia. But in the meantime, more and more doubts are expressed on this thesis, reports the University of Bonn. Today, it is known that "beta-amyloids also occur within the nerve cells" and many researchers would suspect "that they develop their toxic effects there by damaging certain components of the cell." A thesis to which, according to the researchers, a Another finding fits: In the nerve cells of Alzheimer's patients, the mitochondria are often defective.

Damage to mitochondria investigated
In their latest study, the researchers have investigated "whether beta-amyloids can damage the mitochondria," reports Professor Dr. med. Wolfgang Voos from the Institute of Biochemistry and Molecular Biology of the University of Bonn. For this purpose, among other things, isolated mitochondria were mixed with beta-amyloids and then tested which processes are disturbed by it. Although the scientists could not detect any direct damage to the mitochondria by the beta-amyloid and the cell power plants were completely intact. "But we have found another effect," Prof. Voos emphasizes: Thus, the beta-amyloids prevented the transport of proteins into the mitochondria.

Protein transport inhibited in the mitochondria
The mitochondria depend on around 1,000 different proteins for their complex task, and they can produce just 13 of them, the researchers explain. The remaining proteins would be produced in the cytoplasm of the cell and picked up by mitochondria on their surface using special transporter molecules. The beta-amyloids inhibit this intake - and extremely effective. "During my research career, I have rarely seen such a strong blockade of protein transport," says Professor Voos.

Cell power plants paralyzed by Alzheimer's toxins
By blocking the protein transport, the mitochondria lack the necessary enzymes they need to produce energy, and eventually the energy production collapses completely, causing cell death. This mechanism may, according to Professor Voos, "possibly contribute significantly to the mass demise of neurons that is characteristic of Alzheimer's dementia." However, it remains unclear to what extent the results from the test tube are transferred to whole cells or even people with Alzheimer's disease let restrict the researchers. Further investigations are now needed to find out whether the blockade of protein transport is also found in the nerve cells of patients, explains Professor Voos. (Fp)