University of Manchester biophysicist Dr. Ruth Itzhaki has suspected a link between Alzheimer's and herpes simplex virus type 1 (HSV1) for several years. She co-authored a paper in 1999 showing that brain cells grown in culture develop beta-amyloid plaques when HSV1 is introduced [source: Coghlan]. She demonstrated the same results in laboratory experiments that used the brains of mice.
Most recently, Itzhaki led a research team that found that 90 percent of the plaques found in the brains of Alzheimer's patients are infected with the herpes virus that leads to cold sores. The HSV1 virus has already been shown to induce beta-amyloid accumulation as it destroys nerve cells. The presence of the virus in the plaque in Alzheimer's brain tissue suggests that the virus might be responsible for the excessive memory loss and forgetfulness associated with the disease. The virus may move from the facial area to attack neurons in the brain as our immune systems deteriorate due to age.
As we further study human genetics, it becomes increasingly clear that genes play a major role in the prevalence of disease. It looks like Alzheimer's is no different.
In her research, Dr. Itzhaki found that all six of the Alzheimer's patients whose brain tissue she used as specimens in her research had a common variant of the APOE-4 gene. Itzhaki believes that mutation is responsible for an inability to dispose of the accumulating beta-amyloid deposits [source: Coghlan].
There are still questions over Itzhaki's findings. For one, how does one account for not only the plaques but also the tau protein tangles, which haven't been linked to the herpes virus? The research is hopeful, however. Itzhaki says that cheap, already available anti-viral medicines used to treat herpes can reduce the presence of beta-amyloid in human cells infected with HSV1.