Scientists find genetic variation drives up dementia risk

A GENETIC variation carried by 20 per cent of the population appears to accelerate the build-up of the toxic brain plaque which causes Alzheimer’s disease.

People who have the genetic variation start declining in mental performance up to 13 years before those who don’t carry it.

HEALTHY adults who carry a common genetic variation have a 2-3 times faster build up of the toxic plaque implicated in Alzheimer’s disease in their brain than those without it.

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In a new study scientists from the Florey Institute of Neuroscience and Mental Health and Stanford University in California confirm the crucial role the change in this gene — which occurs in one in five people — plays in driving up the risk of dementia.

The variation, known as APOE4, is the biggest risk factor, besides age, for developing Alzheimer’s disease and other forms of dementia.

Dr Yen Ying Lim from the Florey Institute of Neuroscience has identifed a genetic variant that appears to increase their risk of dementia.

Dr Yen Ying Lim said previous research shows it brings forth the diagnosis of dementia by about 10 years and those who carry APOE4 are five times more likely to develop memory problems due to dementia.

“We are starting to find evidence that Alzheimer’s disease is not an old person’s disease; these processes start in middle age,” Dr Lim said.

Drugs to stop the amyloid protein or plaque have been disappointing, and many believe it’s because treatments are being tested too late in the disease’s progression.

Dr Lim said finding a way to detect those at risk of dementia was vital because by the time plaque starts to build up and brain cells die it’s almost too late to intervene.

People who have the genetic variation start declining in mental performance up to 13 years before those who don’t carry it.

“Our findings suggest it will be important to study adults in middle age with this genetic variation to work out if they can intervene with medication or lifestyle changes, like sleep or exercise, before amyloid plaque levels become abnormal,” she said.

The study, in the journal Neurology, scanned the brains of more than 500 people over five years.

APOE4 carriers who were healthy and had normal levels of amyloid showed significantly faster rates of protein accumulation than those who did not carry the variant.

“It’s important to point out that we are looking at very small but significant amounts of plaque building up in their brain,” she said.

“It appears APOE4 plays an important role initially in the build-up of plaque, possibly by disrupting its clearance from the brain, but it doesn’t exert any further influence once the disease is established.”

The Florey is recruiting 5000 healthy Australians aged 40-65 to measure their mental performance and genetic risk

To join: brainproject.org.au or email: [e-mail]