TESTING dementia drugs on people with Down Syndrome long before they show any symptoms could provide a major breakthrough for the treatment of the disease in the general population, a leading researcher has said.

Professor Anthony Holland, a psychiatrist and expert in intellectual disabilities at Cambridge University, said that an argument could be made to begin trialling Alzheimer's drugs in people with Down Syndrome in their 20s to determine whether they are effective at delaying or preventing the onset of dementia.

Around 50 to 70 per cent of individuals with Down Syndrome will develop dementia in their lifetime - a much higher incidence than the general population - and cognitive functions, such as memory, also begin to fail earlier in their 40s and 50s.

To date clinical trials of potential Alzheimer's drugs designed to target the build-up of protein clumps in the brain called beta amyloid plaques - thought to be one of the leading causes of the disease - have only been tested on patients once they have already been diagnosed with the disease, and never on people with Down Syndrome.

Results have been disappointing, but it is unclear whether this is because the amyloid hypothesis is wrong or because treatment is started too late, once the protein clusters have already taken hold.

Prof Holland, who was speaking at the World Down Syndrome Congress in Glasgow, said: "Most of the drug studies are in the general population.

"The problem with that is that you can't give them to healthy volunteers because a majority of people will never develop Alzheimer's, so you have to wait for them to have the early evidence of the disease.

"What makes Down Syndrome different is that 50-70 per cent of that population will develop dementia so there's an argument that you can justify starting treatment early because their risk is so high.

"You could start it in their 20s, because in generally once they are in their 50s the damage is done."

People with Down Syndrome are born with an extra copy of chromosome 21, which carries the APP gene responsible for generating the amyloid precursor protein (APP).

As a result, nearly all people with Down Syndrome will develop amyloid plaques by age 40, along with other Alzheimer's-related protein deposits called tau tangles, although not all will suffer dementia.

Prof Holland said people with Down Syndrome have the potential to make a "major contribution" to Alzheimer's science because of their unique genetic profile.

His research at Cambridge University is also seeking to identify biomarkers for Alzheimer's risk so that it might be easier to pinpoint at an early stage who is at increased risk of the condition.

One study has thrown up unexpected findings in relation to retinal screening.

Scientists already know that among the non-Down Syndrome population, the retina appears to thin out in the early stages of Alzheimer's.

However, researchers in Cambridge were surprised to discover the opposite - thickening of the retina - among study participants with Down Syndrome.

Prof Holland said: "We found the opposite of what we expected so we don't know what that means yet.

"We are really looking for biomarkers of the disease at an early stage.

"It could be that amyloids build up in the retina earlier than they do in the brain, so potentially retinal screening might offer us a cheaper and less invasive alternative to brain scans as well as an 'early indicator' of the disease before brain damage has set in."