New defense strategy against Alzheimer's disease discovered

New defense strategy against Alzheimer's disease discovered

Researchers find possible approach for new drugs for Alzheimer's
Around 1.5 million people in Germany suffer from dementia, most of whom have Alzheimer's. Despite years of research, it is still unknown what exactly causes the disease and how it can be combated. Scientists in the USA have now discovered a possible attack strategy against Alzheimer's.

Incurable disease
In Germany alone, around 1.5 million people suffer from dementia, the majority of them from Alzheimer's. There are approximately 47 million dementia patients worldwide. And there are more and more: According to the World Alzheimer Report, another dementia diagnosis is made every 3.2 seconds. The disease has not yet been curable, but can be delayed with medication in the early stages. Researchers in the United States have now discovered a possible approach for new drugs for Alzheimer's.

The causes of Alzheimer's have not yet been clearly clarified
Numerous scientists around the world have spent the past few years trying to find out what triggers the disease. Even if the exact cause is still unclear, so-called “senile plaques”, harmful deposits of the compound amyloid-beta in the gray matter, play a role. These occur in high density in Alzheimer's patients and increase with progressing dementia, reports the news agency APA. A team of researchers led by Vienna-born US medicine Nobel Prize winner Eric Kandel (86) has now found in mice under what circumstances the protein PP2A reduces the negative effects of these deposits. This was how they discovered a target for therapies, the scientists explained in the journal "Proceedings of the National Academy of Sciences". ("PNAS")

Targeted approach to new drugs
It was previously known that the activity of PP2A is reduced by senile plaques. The researchers led by Kandel, who works at the Howard Hughes Medical Institute at Columbia University in New York (USA), discovered that PP2A does not directly control the activity of amyloid-beta, but does influence its pathological effects, according to the APA. When the scientists increased the activity of an enzyme in the mouse brain that removes methyl groups from PP2A, a high amyloid beta level was more harmful than before. However, if they suggested that PP2A was given more methyl groups by another enzyme, it became more effective and the brain damage was less. According to the researchers, the results suggest that PP2A methylation affects the severity of damage from high amyloid beta levels and makes it a potential drug target. (ad)

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