Protein may be key in treatment of dementia, say Scots scientists

Alzheimer’s disease, the most common form of dementia, affects one in 10 people over the age of 65.

Study lead researcher Professor TaraSpires Jones, at Edinburgh University, said: “A key knowledge gap blocking development of effective therapeutics for Alzheimer’s disease is the lack of understanding of how proteins cooperate in causing disease phenotypes.

“More work is needed to take what we’ve learned in this study and find therapeutics – but this is a step in the right direction, giving us new targets to work towards.”

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Researchers used mice to study how certain proteins – called “amyloid beta and tau” – work together.

The team found the proteins stopped communication between brain cells by working together to change how genes are expressed in the brain.

Prof Jones said: “In both the mouse model and in brain tissue from people with Alzheimer’s disease, we found clumps of amyloid beta and tau proteins in synapses.

“When both amyloid beta and tau were present in the brain, genes that control the function of synapses were less active.”

They also found that the brain produced more “immune cells”, which are known to block synapses in people with Alzheimer’s.

Dementia affects around 850,000 people in the UK and is expected to reach over a million by 2025.

Over 70,000 Scots live with dementia with Alzheimer’s causing two-thirds of cases.

Their research is focussing on microscopic connection points between nerve cells in the brain.

They are essential for thinking, learning and memory. Damage of these causes the symptoms of dementia.

There is no known cure for the syndrome, which causes problems with memory loss, thinking speed, movement, mood, hallucinations and language.

Last week it was revealed that a drug that can slow down the progression of Alzheimer’s disease has been found.

Researchers at Biogen pharmaceutical company released the results of a final phase trial in 3,000 people which showed that the drug Aducanumab can reduce “decline in function” by 40 per cent compared with a placebo, over 18 months.

Participants reported significant improvements in memory and the ability to carry out everyday tasks, such as dressing and eating.

Hopes that Aducanumab could be helpful for dementia were dashed in March when the company announced it was stopping trials after seeing no beneficial results.

But after reanalysing the results they realised those on a higher dose for longer had shown marked improvements.

Dementia charities said it was now crucial for the drug to be approved so that it could start helping people slow down the devastating decline of Alzheimer’s.

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Dr Carol Routledge, director of research at Alzheimer’s Research UK, said: “The positive news is that, given the long wait for a disease-modifying drug for Alzheimer’s, Aducanumab shows a clear effect on key hallmarks of the disease.”

Experts said regulators now had a “critical decision to make” in deciding whether to license the drug.

“We are now in uncharted territory for an Alzheimer’s drug, and there will be huge anticipation,” she added.

There is currently no drug that can prevent, slow down or reverse the impact of Alzheimer’s and dementia for sufferers.

The new treatment is said to work by lowering levels of amyloid protein in the brain, which clumps together and prevents brain cells from communicating.