New mechanism of Alzheimer's disease found

New mechanism of Alzheimer's disease found

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So far unknown mechanism with a significant effect on the development of Alzheimer's?
Much more is known today about the development of Alzheimer's than a few years ago. However, the mechanisms of the disease have not yet been fully deciphered. A team of researchers from the University of Bonn has now identified a hitherto unknown mechanism that may make a decisive contribution to the development of Alzheimer's disease.

The scientists found that the so-called beta-amyloid plaques (also known as Alzheimer's plaques) impair the function of the cell power plants (mitochondria). These are virtually paralyzed by the Alzheimer's toxins and stop their energy supply, with which the cells are doomed, according to the University of Bonn. The researchers have published their latest study results in the specialist magazine “Molecular Biology of the Cell”.

Beta-amyloid deposits in the patient's brain
In Alzheimer's disease, characteristic deposits, known as plaques, are formed in the brain between the nerve cells, which consist of beta-amyloid peptides. These protein deposits also occur in the brains of healthy people, but are broken down there quickly, the scientists explain. In contrast, Alzheimer's patients show an accumulation and there are large amounts of entangled beta-amyloids in the plaques, the university said.

Toxic effects within the cells?
For a long time it was suspected that these extracellular deposits damage the nerve cells and ultimately kill them - in other words, the plaques trigger progressive dementia. However, doubts about this thesis are now being raised, 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, which the researchers also agree on further finding fits: Mitochondria in the nerve cells of people with Alzheimer's are often defective.

Mitochondrial damage examined
In their current study, the researchers examined “whether beta-amyloids can damage the mitochondria,” reports Professor Dr. Wolfgang Voos from the Institute of Biochemistry and Molecular Biology at the University of Bonn. For this purpose, isolated mitochondria were mixed with beta-amyloids and then it was tested which processes are disturbed. The scientists were unable to determine any direct damage to the mitochondria caused by the beta amyloid, and the cell power plants were completely intact. "But we found another effect," emphasizes Prof. Voos: The beta-amyloids prevented the transport of proteins into the mitochondria.

Inhibited protein transport to the mitochondria
The mitochondria rely on around 1,000 different proteins for their complex task, and only 13 of them can produce themselves, the researchers explain. The remaining proteins would be produced in the cell's cytoplasm and would be taken up by the mitochondria with the help of special transporter molecules. This absorption is inhibited by the beta-amyloids - and extremely effectively. "I have rarely seen such a strong blockage of protein transport during my research life," reports Professor Voos.

Cell power plants paralyzed by Alzheimer's toxins
By blocking protein transport, the mitochondria lack the enzymes they need to generate energy and at some point the energy production breaks down completely, resulting in cell death. According to Professor Voos, this mechanism can "possibly make a decisive contribution to the massive decline of neurons, which 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 allow, restrict the researchers. In further studies, it is now necessary to find out whether the blockage of protein transport can also be found in the nerve cells of patients, explains Professor Voos. (fp)

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Video: Alzheimers Disease - Pathology, Tangles, Beta Amyloids (August 2022).