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 In Elderly

Researchers at the University of Cambridge have designed antibodies that target the protein deposits in the brain associated with Alzheimer’s disease, and stop their production.

The researchers used computer-based methods to develop antibodies – the star players of the body’s natural defence system – to target the deposits of misfolded proteins which are a hallmark of Alzheimer’s disease. Early tests of the antibodies in test tubes and in nematode worms showed an almost complete elimination of these pathogens.

The antibodies were designed to systematically scan the sequence of amyloid-beta, the main component of the toxic deposits associated with Alzheimer’s disease. By targeting specific regions, or epitopes, of the amyloid-beta sequence, the different antibodies were able to block amyloid-beta’s ability to stick together, or aggregate. Their results are reported in the journal, Science Advances.

Alzheimer’s disease is the most common form of dementia, which affects nearly one million people in the UK and about 50 million worldwide. One of the hallmarks of Alzheimer’s disease is the build-up of protein deposits, known as plaques and tangles, in the brains of affected individuals. These deposits, which accumulate when naturally-occurring proteins in the body fold into the wrong shape and aggregate, are formed primarily of two proteins: amyloid-beta and tau.

The process of protein aggregation also creates smaller clusters called oligomers, which are highly toxic to nerve cells and are thought to be responsible for brain damage in Alzheimer’s disease. Researchers around the world have spent decades attempting to unravel the processes that cause Alzheimer’s disease, and to target the misfolding proteins before they are able to aggregate.

Developing antibody-based therapies is costly and time-consuming, but if we can find better and cheaper ways of producing antibodies, we would increase the chances of finding treatments for patients – making them by design can create opportunities to achieve this goal,’ said Professor Michele Vendruscolo, from the Centre for Misfolding Diseases in Cambridge, and the paper’s senior author.

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