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In the early 1990s, researchers, including Itzhaki, found evidence suggesting that as we age, the herpes virus begins moving from its hideout near the bottom of the skull directly into the brain (possibly because our immune systems lose some bite). Indeed, one Journal of Pathology study found the virus in a high proportion of postmortem brain samples taken from people who'd died in their later decades, while it was absent in those from people who'd died in youth or middle age.

What effect does the virus have when it reaches your brain? The short answer: That depends. In certain people it seems to do much less damage than in others; just as some of us never develop cold sores, some of us can have the herpes virus inside our brains without any horribly ill effects. But Itzhaki believes that in other people—specifically those who carry APOE e4, a gene form, or allele, strongly linked to Alzheimer's—the virus is not only reactivated by triggers like stress or a weakened immune system, but also actually begins to create the proteins that form the plaques and tangles presumed to be responsible for Alzheimer's.

If you're looking for evidence, Itzhaki can show you a stack of it. In two studies, for example, she and several colleagues took brain samples from 109 deceased people—61 of whom had had Alzheimer's, 48 of whom hadn't—to search for any correlation between herpes, APOE e4, and Alzheimer's.

Their results: People who had both the APOE e4 gene and the herpes virus in their brains were 15 times more likely to have Alzheimer's than people who had neither. (The researchers also found, intriguingly, that people who suffered from recurrent cold sores were almost six times as likely to have the APOE e4 gene as those who didn't get cold sores.)
A decade later, Dr. Federoff, then working at the University of Rochester, administered the herpes virus to four different groups of mice, each of which had a different variation or absence of the APOE gene. He found that in mice with the specific APOE e4 variation, the virus was slower to become dormant than it was in mice with APOE e2, APOE e3, or no APOE gene, suggesting that the virus could be replicating faster in the e4 mice. "The results definitely suggest there's something different about having APOE e4," says Dr. Federoff.

Still other research shows the direct impact of HSV-1 itself. In 2007, a study by Itzhaki and Wozniak found that infecting lab samples of brain cells with the virus caused a buildup of the protein (beta amyloid) that's the primary component of the plaque clogging the brains of Alzheimer's patients. The same study also found a similar result in the brains of mice that had been infected with HSV-1.

Then there was January's study in the Journal of Pathology. In it, Itzhaki and Wozniak looked at brain samples from 11 deceased people; six had had Alzheimer's and five hadn't. While both groups had plaques (not surprisingly, the Alzheimer's group had far more) and evidence of the herpes virus in their brains, there was a crucial difference in the concentration of the virus: In the Alzheimer's patients, 72 percent of the virus's DNA was found in the plaques, compared with only 24 percent that was found in the plaques of the non-Alzheimer's brains. Not surprisingly, all but one of the Alzheimer's sufferers also carried the APOE e4 gene, compared with none of the samples from the non-Alzheimer's people.

Wozniak is confident that these last two studies point to the same conclusion: "The results strongly suggest that HSV-1 is a major cause of amyloid plaques—and probably of Alzheimer's disease."

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