Early symptoms of dementia explained in NHS video
Dementia affects more than 55 million people worldwide, with numbers expected to grow in the coming decades. It is a syndrome associated with the progressive decline of the brain, causing problems such as memory loss, personality changes and mobility issues. Currently there is no known cure for dementia.
But now researchers have found that an existing medication used to treat HIV patients could hold the key to creating a treatment.
A study, published in Neuron journal, revealed that maraviroc – sold under the brand name Celsentri – is able to clear rogue proteins in the brain which are linked to the development of dementia.
By clearing these proteins it prevents dangerous build up and slows the progression of the disease, scientists said.
Professor David Rubinsztein, a senior study author of the UK Dementia Research Institute at Cambridge University, said: “We’re very excited about these findings.
“We’ve not just found a new mechanism of how our microglia hasten neurodegeneration, we’ve also shown this can be interrupted, sinemet urine potentially even with an existing, safe treatment.”
The brain and central nervous system have their own specialist immune cells, known as microglia, which should protect against unwanted and toxic materials.
In dementia, they kick into action, but in such a way as to impair the process of autophagy – a process by which cells degrade and recycle their components.
As part of the study, the team used lab mice to show that during neurodegeneration microglia release a suite of molecules which in turn trigger a genetic switch, known as CCR5.
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It leads to a chemical called tau gathering in clumps, destroying brain cells.
Prof Rubinsztein said: “The microglia begin releasing these chemicals long before any physical signs of the disease are apparent.
“This suggests – much as we expected – that if we’re going to find effective treatments for diseases such as Huntington’s and dementia, these treatments will need to begin before an individual begins showing symptoms.”
The team tested mice that had been genetically-altered to develop forms of dementia characterised by the build-up of tau. When the action of CCR5 was knocked out, the animals were protected.
The gene is also used by HIV as a “doorway” into our cells. It is inhibited by maraviroc, which stops the virus making more copies of itself.
The team administered the drug for four weeks when the mice were two months old.
When the researchers looked at the animals’ brains, they found a significant reduction in the number of toxic proteins when compared to untreated peers.
The same effect was observed in mice with dementia and Huntington’s – a cognitive disorder that leads to dementia.
The drug reduced tau aggregates compared to untreated mice, but it also slowed down the loss of brain cells. The treated mice performed better at an object recognition test, suggesting that the drug slowed down memory loss.
Prof Rubinsztein added: “Maraviroc may not itself turn out to be the magic bullet, but it shows a possible way forward.
“During the development of this drug as a HIV treatment, there were a number of other candidates that failed along the way because they were not effective against HIV. We may find that one of these works effectively in humans to prevent neurodegenerative diseases.”
The findings come as a separate study, published in Neural Regeneration Research in January this year, found that maraviroc can aid in recovery from traumatic brain injury.
In the UK, maraviroc is currently available to HIV patients on prescription.
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