Antidepressant Slows Production Of Alzheimer’s Protein

Scientists in the US have found that an antidepressant slows production of a known Alzheimer’s protein, amyloid, in mice and in healthy younger people. The study is published on Wednesday 14 May in the journal Science Translational Medicine.

Researchers led by a team at the University of Pennsylvania tested the drug citalopram, which is commonly prescribed to people with depression, in mice that were bred to develop a build-up of amyloid in the brain – a known feature of Alzheimer’s disease. The researchers tested the interstitial fluid – the fluid surrounding nerve cells in the brain – of the mice after they had been given different doses of citalopram. They found mice that were given citalopram had a reduction in the amount of amyloid accumulating in the brain compared to mice that were not given the drug, with higher doses of citalopram leading to a greater reduction in the protein.

In a separate study, the researchers also recruited 23 healthy people aged between 21 and 50, none of whom had ever been prescribed an antidepressant before. Half the participants were given 60mg of citalopram, while the other half were given a placebo, and the researchers then took samples of their cerebrospinal fluid (CSF) on an hourly basis for up to 36 hours. The results showed that those who took citalopram had 38% less amyloid in their CSF than those who took the placebo, with a reduction in the amount of amyloid that was newly-produced.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“Amyloid build-up occurs many years before symptoms appear in Alzheimer’s, and understanding how to prevent or delay its accumulation early is a key goal for Alzheimer’s researchers. This study has yielded some interesting findings, and further research to understand the mechanisms responsible for these results could provide vital new clues about the disease and how to fight it. It’s important to note that the people involved in this study did not have Alzheimer’s, and these results don’t tell us whether antidepressants could prevent or delay the disease. To better understand the possible effects of these drugs for Alzheimer’s, we would need to see large-scale, long-term clinical trials.

“Currently half a million people in the UK are living with Alzheimer’s, the most common cause of dementia, and we urgently need treatments that can stop the disease in its tracks. Investment in research is crucial if we are to develop these treatments and provide better outcomes for people with the disease.”

 

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