Although it was discovered in 1906, Alzheimer’s disease didn’t receive significant research attention until the 1970s. In 1984, scientists identified the plaque-like buildup of amyloid beta proteins in brain tissue that causes nerve damage and can lead to symptoms like memory loss, personality changes, and physical debility.
Now, researchers are learning why amyloid beta tends to collect in brain tissue like barnacles on a ship. It might not be rallying expressly to cause damage, but to protect the brain from another invader: the herpes simplex virus.
As The Atlantic recently noted, a number of studies have strengthened the notion that amyloid beta activity is working in response to herpes, the virus that travels along nerve pathways and typically causes cold sores around the mouth (HSV-1) or genitals (HSV-2). In a study involving mice, those engineered to produce more amyloid beta were more resistant to the herpes virus than those who were not.
But when too much amyloid beta is produced to combat the virus, the proteins can affect the brain’s neurons. And while herpes tends to target specific pathways in the body that result in external sores, it’s possible that the virus might act differently in an older population that is susceptible to more widespread infection. Roughly half of adults under age 50 in the U.S. are infected with HSV-1 and 12 percent with HSV-2, which suggests that a large swath of the population could be vulnerable to Alzheimer's disease. Two other strains of the virus, HHV-6A and HHV-7, have also been found to be more common in the brains of deceased Alzheimer’s patients than in the general population.
More research will be needed to further understand the possible relationship between the two. If more findings support the theory, then it’s possible that antiviral drugs or vaccines targeting herpes might also reduce the chances of amyloid beta buildup.