05 November 2020

Destroy plaques in the bud

Experimental Alzheimer's therapy is better than all existing drugs

Svetlana Maslova, Hi-tech+

Scientists have managed to influence the early stages of the development of neurodegeneration, when proteins toxic to neurons begin to accumulate in the brain – they have learned to destroy the very basis of these formations. If an experimental drug shows similar results in humans, it will surpass all existing drugs in effectiveness today and, perhaps, will become the first tool that can reverse neurodegeneration.

The main sign of developing neurodegenation is the accumulation of beta-amyloid and tau protein proteins in the brain. These aggregations of proteins form into plaques, which as a result disrupt the transmission of signals between neurons and lead to their death. Experimental drugs currently being studied in clinical trials are trying to destroy these aggregations, but they cannot bind to the smallest clusters of proteins that are considered the most toxic to neurons.

A new approach was presented by a team from Uppsala University (Sweden). They have developed a treatment method that destroys the basis of future aggregates.

Article by Rofo et al. Enhanced neprilysin-mediated degradation of hippocampal Aß42 with a somatostatin peptide that enters the brain is published in the journal Theranostics – VM.

The new therapy allows to reduce the formation of toxic plaques of all types of proteins.

It is based on the peptide somatostatin, which can activate the body's own forces for the decomposition of plaques. This is a very promising protein for the treatment of neurodegeneration, but until now scientists could not preserve its properties for a long time.

The problem was that the half-life in the blood was too short. Within just a few minutes, it became ineffective and, moreover, could not penetrate the blood-brain barrier of the brain. To solve this problem, scientists connected it with a brain transport protein to deliver it through a protective barrier.

As a result, they were able to increase the time of the protein's presence in the brain to several days. Scientists called their achievements fiction.

When testing the therapy on mouse models, the greatest effect was observed in the hippocampus, a key part of the brain for memory.

"We hope that our treatment will act purposefully and thereby reduce the number of side effects to a minimum," concluded study author Greta Haltqvist. These are the problems that very often arose in previous clinical trials, she added.

The authors believe that somatostatin will have a similar effect in humans. If these assumptions are confirmed, then experimental therapy may become the most effective of all existing today.

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