After what seemed like months without a front-page story about Alzheimer's disease, the New York Times ran an important piece last April. It described two studies which analyzed the genes of over 50,000 people in the United States and Europe.

The discoveries double the number of genes involved in Alzheimer's from 5 to 10. The research also sheds new light on contributing factors, such as cholesterol, inflammation, and the concept of innate immunity.

The newly discovered genes don't seem to increase a person's risk of developing Alzheimer's, however, as much as having one or two copies of the APOE 4 gene, but they are likely to be helpful in understanding the disease and maybe in developing treatments. Researchers say the studies, leave little doubt that the five genes make the disease more likely in the elderly and have something important to reveal about the disease’s process. They may also lead to ways to delay its onset or slow its progress.

“The level of evidence is very, very strong,” said Dr. Michael Boehnke, a professor of biostatistics at the University of Michigan and an outside adviser on the research.

For years, there have been unproven information, but hints that cholesterol and inflammation are part of the disease process. People with high cholesterol are more likely to get the disease. Strokes and head injuries, which make Alzheimer’s more likely, also cause brain inflammation.

Now, some of the newly discovered genes appear to bolster this thought, because some are involved with cholesterol and others are linked to inflammation inside cells.

An estimated 5.4 million Americans have the incurable Alzheimer’s disease, most of whom are elderly. According to the Alzheimer’s Association, one in eight people over age 65 have the disease. Its annual cost to the country is $183 billion, health experts have estimated.

By themselves, the genes are not nearly as important a factor as APOE, a gene discovered in 1995 that greatly increases risk for the disease: by 400 percent if a person inherits a copy from one parent, by 1,000 percent if inherited from both parents.

In contrast, each of the new genes increases risk by no more than 10 to 15 percent; for that reason, they will not be used to decide if a person is likely to develop Alzheimer’s. APOE, which is a protein involved in metabolizing cholesterol, “is in a class of its own,” said Dr. Rudolph Tanzi, a neurology professor at Harvard Medical School and an author of one of the papers.

Of the 10 genes now known to be associated with Alzheimer’s in old age, four were found in the past few years and are confirmed by the new studies. APOE may have other roles in the disease, perhaps involved in clearing the brain of amyloids that pile up in plaques, the barnacle-like particles that dot the brain of Alzheimer’s patients. They are the one unique pathological feature of the disease, the Times story said.

It is known that one of the first signs of Alzheimer’s disease is an accumulation of beta amyloid, or a-beta, a protein that forms plaques. And it is known that later in the disease, twisted and tangled proteins — called tau — appear in dead and dying nerve cells.

But what is not known is why a-beta starts to build up, why the brains of people with Alzheimer’s cannot get rid of its excess, or what is the link between amyloid and tau. One of the new papers, by American investigators, analyzed the genes of 54,000 people, some with Alzheimer’s and others the same age but without the disease. They found four new genes.

The other paper is by researchers in Britain, France and other European countries with contributions from the United States. They confirmed the genes found by the American researchers and added one more gene.

One of the researchers, Dr. Schellenberg set out to gather all the data he could on Alzheimer’s patients and on healthy people of the same ages. The idea was to compare one million positions on each person’s genome to determine whether some genes were more common in those who had Alzheimer’s.

“I spent a lot of time being nice to people on the phone,” Dr. Schellenberg said, according to the Times.

He got what he wanted: nearly every Alzheimer’s center and Alzheimer’s geneticist in the country cooperated. Dr. Schellenberg and his colleagues used the mass of genetic data to perform an analysis and find the genes. Then, using two different populations, they confirmed that the same genes were conferring the risk.

That helped assure the investigators that they were not looking at a chance association. It was a huge effort, Dr. Mayeux said. Many medical centers had Alzheimer’s patients’ tissue sitting in freezers. They had to extract the DNA and do genome scans.

“One of my jobs was to make sure the Alzheimer’s cases really were cases — that they had used some reasonable criteria” for diagnosis, Dr. Mayeux said. “And I had to be sure that people who were unaffected really were unaffected.”

Meanwhile, the European group, led by Dr. Julie Williams of the School of Medicine at Cardiff University, was engaged in a similar effort. Dr. Schellenberg said the two groups compared their results and were reassured that they were largely finding the same genes.

“If there were mistakes, we wouldn’t see the same things,” he added.

Now the European and American groups are pooling their data to do an enormous study, looking for genes in the combined samples. “We are upping the sample size,” Dr. Schellenberg said.

“We are pretty sure more stuff will pop out.”

Tait Trussell is an old guy and fourth-generation professional journalist who writes extensively about aging issues among a myriad of diverse topics.

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