A part is better than a whole

Experimental treatment reduces the main indicators of dementia

Svetlana Maslova, Hi-tech+

Therapy combats the accumulation of toxic plaques in the brain even at a progressive stage. The most interesting thing is that the drug is aimed at only one type of protein, however, as observations have shown, it also kills other protein aggregations that are toxic to neurons.

Article by Roda et al. Both Amyloid-β Peptide and Tau Protein Are Affected by an Anti-Amyloid-β Antibody Fragment in Elderly 3xTg-AD Mice published in the International Journal of Molecular Sciences – VM.

The main causes of the development of Alzheimer's disease and at the same time the main signs of the disease are clusters of beta-amyloid proteins and neurofibrillary tau tangles in the brain. These plaques accumulate around neurons, disrupt synaptic connections and gradually contribute to the death of nerve cells.

The experimental treatment proposed by scientists from Spain is based on a fragment of the antibody scFv-h3D6, which was previously developed by the team to attack beta-amyloids. Full-sized antibodies showed no improvement in cognitive functions and at the same time caused serious side effects, so the scientists slightly adjusted the approach.

They wanted to find out whether antibody fragment therapy could show efficacy in late-stage Alzheimer's disease, which had not yet been studied for this drug. Their assumptions were justified.

scFv-h3D6 led to a decrease in the accumulation of not only beta-amylodes, but also tau proteins, and also did not cause side effects.

In addition, the treatment showed a decrease in neuroinflammation in the brain. These first experiments were conducted on old mice with progressive neurodegeneration. The press release of Scientists succeed in reducing the levels of the molecules that kill neurons in elderly mice with Alzheimer's is published on the website of the Autonomous University of Barcelona.

"We have shown that antibody fragment therapy works at a late stage and is directed against two signs of the disease that ultimately kill neurons and provoke dementia," said Sandra Villegas, the author of the work.

So far, these are the first results and further studies should show the prospects of the findings for humans, she added.

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