You are here

Common mutation makes Alzheimer’s drugs ineffective in 3 out of 4 patients

Common mutation makes Alzheimer’s drugs ineffective in 3 out of 4 patients
22nd July 2019

Many Alzheimer’s drugs may be ineffective in individuals because of their DNA, new research suggests. Scientists at the University of Buffalo in the US have discovered that three quarters of people appear to carry a genetic mutation that renders some medications useless.

The gene in question is called CHRFAM7A and codes for a receptor for acetylcholine, which is involved in memory. It transmits impulses throughout the nervous system and has been investigated as part of Alzheimer’s research for a long time.

Of the Alzheimer’s drugs that are already on the market, three out of four are designed to stimulate acetylcholine receptors. Even more treatments that are still in the development stages also work on this principle.

The problem therefore lies in the latest findings that the CHRFAM7A gene is mutated in three out of four people. This makes them less receptive to the drugs that target acetylcholine receptors and therefore in need of personalised treatments that would be much more expensive and time consuming to develop.

Alzheimer’s is a big problem, with 62 per cent of dementia sufferers in the UK having this form of the disease. There is currently no cure, as treatments that catch the symptoms early on work to slow its progression to give individuals a better quality of life for longer.

Billions of pounds are being invested in research into Alzheimer’s drugs, with dozens being developed. Despite this, the field is notorious for its setbacks and the discovery of this mutation and its potential to disrupt treatments is the latest in a long line of hurdles scientists must overcome.

Analysing data from a ten-year study that took 345 patients into consideration, the scientists in Buffalo came to the conclusion that CHRFAM7A comes in two ‘flavours’. While the functioning gene is only present in a quarter of people, the other three quarters of the population live with a mutated version.

Dr James Pickett, head of research at the Alzheimer's Society, told MailOnline: “We are learning there are important genetic differences between people with dementia that might mean they will respond differently to treatments. 

“Clinical trials of drugs that target this particular receptor have already shown they don't work in Alzheimer's disease, but this study suggests there may be a group of people who could benefit. This idea of personalised medicine - where medicines are individualised to each of us - is a hot and developing topic at the moment.”