New defense strategy against Alzheimer's Disease discovered

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

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

A special protein counteracts the harmful effects of Alzheimer's plaques. (Image: pict rider / fotolia.com)

Causes of Alzheimer's disease have not been clarified yet
Numerous scientists around the world have spent the past few years trying to figure out what causes the disease. Even though 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 are very dense in Alzheimer's patients and are on the increase as dementia progresses, reports APA. A research team led by Vienna-born US Nobel Laureate in Medicine Eric Kandel (86) found out in mice under what circumstances the protein PP2A reduces the negative effects of these deposits. This has discovered an attack target for therapies, the scientists said 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. Kandel, who works at the Howard Hughes Medical Institute at Columbia University, New York, USA, discovered that PP2A does not direct the activity of amyloid beta, but does affect its pathological effects. When scientists increased the activity of an enzyme in mouse brains that removed methyl groups from PP2A, a high amyloid beta level was more harmful than before. But when they suggested that PP2A was getting much more methyl from another enzyme, it became more effective and brain damage was lower. According to the researchers, the findings suggest that PP2A methylation affects the severity of high-amyloid beta-level damage, making it a potential drug target. (Ad)