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Studies link 3 more genes to Alzheimer’s disease risk

David Brown Washington Post

Two European research teams have identified three genes that affect a person’s risk of developing Alzheimer’s disease, the most common cause of dementia in the elderly.

The new genes appear to have at least as big a role as four others discovered in the last 15 years that are known to play a role in Alzheimer’s.

“The message here is that genes are important in Alzheimer’s disease … and there may be multiple ways of reducing the risk that the genes produce,” said Julie Williams, a neuroscientist at Cardiff University in Wales who helped lead one of the teams.

All so-called “Alzheimer genes” have normal roles in brain physiology; they don’t exist solely to cause dementia. Instead, small variations in their DNA alter their function and, through processes only now being uncovered, increase or reduce a person’s risk of developing the disease.

Two of the genes described in the new research may be involved in determining the brain’s capacity to clear itself of toxic “amyloid” proteins that collect outside neurons, eventually poisoning them.

The new findings, reported Sunday in the journal Nature Genetics, will have no immediate consequence in either diagnosis or treatment of the disease. However, they will help illuminate a process that goes on for years or even decades before memory loss, the cardinal symptom of the disease, becomes apparent.

Neuroscientists believe 60 percent to 80 percent of a person’s risk of developing Alzheimer’s disease is attributable to genes. Knowing which they are and what they do may provide targets for drugs and other interventions.

In one of the studies, Williams and her collaborators scanned the genomes of about 4,000 people with Alzheimer’s and 7,800 people without it, looking for patterns of variation in half a million locations on the DNA chain. They found three that were far more common in the people with dementia.

One was a variation in the APOE gene – known since 1993 – that leads to the overproduction of amyloid protein. The other two genes – CLU and PICALM – were new.

CLU appears to be involved in “chaperoning” newly formed amyloid molecules and helping suppress their deposition in the brain.

PICALM, however, seems to play a role in maintaining healthy synapses. The loss of synapses is highly correlated with loss of mental function in Alzheimer patients.

A second research group, led by Philippe Amouyel, a neurologist and epidemiologist at the Institut Pasteur de Lille, in France, scanned the genomes of about 2,000 Alzheimer patients and 5,300 control cases.

In addition to APOE and CLU it found another gene, CR1, that is involved in the body’s inflammatory response and may specifically play a role in capturing and clearing away amyloid molecules.

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