[메디컬투데이TV] Alzheimer’s disease is caused by a decrease, not an increase, in the amyloid-beta protein.

[메디컬투데이=최재백 기자] Research has shown that cognitive decline associated with Alzheimer’s disease is caused by a decrease in amyloid-beta protein in the brain.

Research results showing that cognitive decline associated with Alzheimer’s disease is due to a reduction in amyloid-beta protein in the brain have been published in the academic journal ‘Brain’.

The cause of Alzheimer’s disease is not yet clearly known, but a representative hypothesis is that it is due to the accumulation of amyloid-beta protein in the brain.

However, a recent research team at the University of Cincinnati said that most patients with amyloid plaques found in the brain do not develop Alzheimer’s disease, and that the cause of cognitive decline is a decrease in amyloid-beta protein in the brain. that it was because of this.

The research team analyzed data from approximately 26,000 participants from 24 randomized clinical trials involving new monoclonal antibody therapies approved for the treatment of Alzheimer’s disease.

They say that only 20% of people under the age of 85 who have amyloid plaques develop Alzheimer’s disease, and that what is important is not the amount of amyloid plaques in the brain, but the ability to produce Aβ42, protein important for brain. Cheers.

Aβ42 protein is a protein that protects the brain in response to various toxic and infectious substances. In the process of protecting the brain, it is converted into amyloid plaques and stops working, so amyloid plaques can be seen as Aβ42 tombstone. New monoclonal antibody therapies unexpectedly increased Aβ42 levels in the brain.

According to the research team’s study, ‘high levels of Aβ42’ after monoclonal antibody treatment were independently associated with ‘slow cognitive impairment and cognitive decline’.

The research team said that the brain of Alzheimer’s disease continues to split regardless of the number of amyloid plaques, and concluded that Alzheimer’s disease is not caused by an increase in amyloid plaques, but by loss of Aβ42 protein.

They predicted that future treatment should focus on increasing Aβ42 directly, moving away from the idea that amyloid protein is the cause of Alzheimer’s disease.

Meanwhile, experts say it will be refreshing to the neuroscience community that an increase in amyloid plaque levels is an ‘unintended consequence’ of a new monoclonal antibody treatment and may in fact be part of a process that help delay Alzheimer’s disease.

Medical Today Video Editing Team ([email protected])

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