Alzheimer’s hope as researchers find nine genes that may PROTECT against the memory-robbing disorder

  • Researchers looked at DNA of 10,000 people, half of whom had Alzheimer’s
  • Those without condition had genes which stop a protein from functioning
  • The proteins, called tyrosine phosphatases, are involved in cell death
  • They encourage a protein called tau to build up and destroy cells and memory

Scientists have identified key genes that may protect against Alzheimer’s, raising hope of a drug to slash the risk of the cruel disorder 

A study by University College London Genetics Institute looked at the DNA of 10,000 people over 60, half of whom had Alzheimer’s. 

Those who did not have the memory-robbing disease were more likely to have nine specific genes.

They reduce the function of proteins called tyrosine phosphatases – known to be involved in the development of Alzheimer’s by encouraging brain cell death.

It’s the first time the genes have been found in people. Campaigners said the findings could ‘pave the way’ for a treatment to prevent or slow down Alzheimer’s.

Animal studies have suggested Alzheimer’s could be prevented by stopping tyrosine phosphatases from growing. 

The hopes millions of Alzheimer’s sufferers have been raised after scientists identified genes that may protect against the memory-robbing disorder (stock image) 

Professor David Curtis, who led the study, which was published in the journal Annals of Human Genetics, said: ‘These results are quite encouraging. 

‘It looks as though when naturally-occurring genetic variants reduce the activity of tyrosine phosphatases then this makes Alzheimer’s disease less likely to develop, suggesting that drugs which have the same effect might also be protective.’

Alzheimer’s disease is the most common form of dementia, affecting some 850,000 people in the UK.

This figure is predicted to rise to more than one million by 2025. There is currently no cure.

In the US there are 5.8million people living with Alzheimer’s and the number of people dying from the condition more than doubled (145 per cent increase) between 2000 and 2017.

A predicted 13.8m Americans over the age of 65 will have the disease by 2050.

However, the latest research raises hopes that scientists may be able to identify people who will go on to suffer from the disease.

In the study, Dr Curtis and his colleagues looked at more than 15,000 genes, and more than a million variations which affect how genes work. 

They found those with a lower risk of Alzheimer’s displayed more variants that disrupt how tyrosine phosphatases work. 

Tyrosine phosphatases hamper the functioning of a cell-signalling pathway which is important for cell survival, called PI3K/Akt/GSK-3β.

When this pathway does not work properly, tau is allowed to build up and cause Alzheimer’s.  

As it builds up, it forms tangles which kill brain cells and destroy memory. This is thought to cause Alzheimer’s.

Therefore, the variations in some people’s genes which damage how tysorine phosphatases work, or stop them from being made at all, could help prevent the disease.

Dr Curtis said: ‘Here’s a natural experiment in people that helps us understand how Alzheimer’s disease develops.

‘As some people have these genetic variants and some don’t, we can see that the impact of having particular variants is a reduced likelihood of developing Alzheimer’s disease.

‘Finding DNA variants which modify the risk of Alzheimer’s disease is useful as it may help us develop drugs which target the same proteins.’  

Scientists said treatments could work in a way that blocks the functioning of tyrosine phosphatases. 

Dr Curtis and his colleagues noted that one drug candidate is berginin, a chemical which exists in a medicinal herb used by traditional Indian healers.

It has not been proven to work in people but has shown some protective affects on brain cells in rat studies. 

The study also found evidence implicating a gene not previously known to affect Alzheimer’s risk, called C1R.

The gene is already known to be involved in periodontal Ehlers-Danlos syndrome, a disease which causes symptoms including chronic gum inflammation by affecting the connective tissue in the body.

Previous research suggests that gum infections may increase the risk of Alzheimer’s disease.

And Professor Curtis speculated there may be a mechanism whereby genetic variants in C1R lead to some degree of gum disease, which in turn predisposes people to Alzheimer’s disease. 

Fiona Carragher, chief policy and research officer at the Alzheimer’s Society, said: ‘This is the first time we’ve been able to show this gene variant, may reduce risk of Alzheimer’s disease in humans. 

‘Researchers will now look to target the proteins coded for by this gene variant with drugs to try and replicate the same reduction in risk.’

Ms Carragher said the research brings science ‘one step closer’ to decoding how genes determine Alzheimer’s risk.

‘[It] could pave the way for the first treatment to prevent or slow it down.

‘Dementia is devastating. We owe it to the 850,000 people in the UK currently living with dementia to understand the condition better and find a cure.’

Dr Katy Stubbs, of the charity Alzheimer’s Research UK, said more research will need to look into whether these genes are worthy of drug investment.

She said: ‘These findings suggest that certain changes to genes involved in maintaining the delicate energy balance in our cells may increase our risk of Alzheimer’s, while others may help protect against the disease.

‘While genetic discoveries are often an important starting point for research into new treatments, it is too early to say whether drugs that target this genetic pathway in people could help tackle Alzheimer’s without hampering other crucial cellular processes.’

Source: Dailymail

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