A rare mutation of a gene thatā€™s normally linked to inflammation could triple the risk of Alzheimerā€™s disease, according to new research from an international team of scientists.

Less than 1 per cent of the population has the gene variant, called TREM2. Scientists hope that by studying the gene they will better understand how Alzheimerā€™s attacks the brain -- and find a way to stop it.

Their findings were published Wednesday in the New England Journal of Medicine.

About 30 million people around the world have Alzheimerā€™s, and that number is expected to rise to 35 million in the next three years.

The incurable disease first destroys the mindā€™s ability to remember. Over time, as brain cells are attacked, symptoms worsen and patients lose more of their mental abilities until they are entirely dependent on caregivers.

Until now, itā€™s been commonly thought that the disease is caused by Amyloid plaques -- a sticky, toxic material. Based on this theory, pharmaceutical companies have spent hundreds of millions of dollars testing medications to treat Alzheimerā€™s, but most attempts have failed clinical studies.

The new research suggests those experimental treatments were pointed in the wrong direction, and that TREM2ā€™s role suggests inflammation could be the main culprit.

ā€œWhat we are now finding out from genetic study is that inflammation is an important part of the disease itself,ā€ Dr. Peter St. George-Hyslop of the University of Toronto told Ā鶹“«Ć½. ā€œIt starts early, and it is part of the way the disease actually happens.ā€

TREM2 has been previously linked to other forms of dementia, and was first found by researchers with Iceland-based deCODE Genetics Inc., who mapped the genetic code of 2,200 people.

Other scientists searched for the gene variant in 3,550 Alzheimerā€™s patients and people suffering from other types of dementia, and found it was more common in those with Alzheimerā€™s.

Study subjects who were found to have TREM2, but did not suffer from Alzheimerā€™s, still had lower mental function than those without the gene variant.

Dr. Lili-Naz Hazrati, of the University Health network, is hopeful that studying TREM2 could lead to a major breakthrough in fighting the disease.

ā€œWe are finding different components of the disease and yes, we are very optimistic that we are going towards a treatment for Alzheimerā€™s.ā€

However, Dr. Rudolph Tanzi, a Harvard Medical School geneticist, was more cautious.

He told The Associated Press he would prefer to ā€œsee more evidenceā€ that TREM2 was linked to Alzheimerā€™s and not one of the other forms of dementia already connected to the gene variant.

With a report by CTVā€™s medical specialist Avis Favaro and producer Elizabeth St. Philip, and files from The Associated Press