Dementia: Researchers ‘solve decade-long puzzle’ in major new step to preventing disease


Alzheimer’s disease – the most common form of dementia – has become a major public health concern as the world’s populations age. Slow and chronic in nature, the condition affects emotional control, memory, social behaviour and thinking. A new breakthrough study, however, has identified one crucial target which could help the way towards more efficient therapy.

Senior author Xiaolu Yangm professor of Cancer Biology in the Perelman School of Medicine, at the University of Pennsylvania, and his team showed how restoring levels of protein DAXX and a large group of similar proteins could prevent the misfolding of proteins known to drive Alzheimer’s disease.

He said: “We solve a decades-long puzzle by showing this group of proteins actually constitute a major protein quality control system in cells and a never-before seen enable of proper folding of various proteins, including proteins prone to misfolding associated with various diseases.

“Keep that family of proteins functioning properly and the angling of rogue proteins may be diminished or stopped altogether.”

The brain of an Alzheimer’s patient typically harbours two kinds of pathology.

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First, plaques, or deposits, that are scattered between nerve cells.Second; fibres that form tangles inside the cells.

The plaques consist of protein fragments called amyloid, while the tangles consist of a protein known as tau.

Researchers have long speculated that these two substances are the underlying cause of Alzheimer’s disease.

However, it is beta-amyloid that has garnered most interest in recent years, following suggestions that excessive build of the protein is the cause of Alzheimer’s.

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For their study, researchers looked at a death-associated protein DAXX, which is a member of a large family of human proteins.

There is growing research discussing the role of DAXX in cell processes, but their role as a protein quality control system – a “chaperone” that directs protein folding – was unanticipated.

The researchers showed that DAXX, and other polyD/E proteins which facilitate the folding of proteins, reverse protein aggregates and unfold misfolded proteins.

This helps prevent the formation of neurodegeneration-associated proteins from misfolding, tangling and forming extracellular plaques, the researchers found.

The team also showed DAXX’s potential role in treating cancer; as the protein restores function to tumour-associated proteins, reducing their cancer properties.

Yang added: “The findings give us a better understanding of a new biochemical activity that effectively contends with protein misfiling seen in Alzheimer’s and other neurodegenerative diseases, as well as in cancer, and represent an opportunity to develop new approaches to treat these diseases.”

Although some existing drugs alleviate symptoms of Alzheimer’s, they do so feebly.

In June, the US Food and Drug Administration (FDA) approved the first Alzheimer’s drug in 18 years; aducanumab.

Unlike other drugs, aducanumab attempts to get at the underlying cause of the disease.

How to prevent amyloid formation Studies have found that diets rich in omega-3 fatty acids could help prevent neurodegenerative illnesses.

There is growing evidence that these healthy fats may prevent Alzheimer’s disease and dementia by reducing plaque.

Sources of omega-3 fatty acids include cold-water fish such as salmon, tuna, trout, mackerel, seaweed and sardines.





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