Alzheimer’s disease (AD) accounts for 60-70% of the cases of dementia1 with an estimated 5 million in the America currently. The number of cases is expected to exceed 13 million by 2050.2 This makes AD the single fastest growing psychiatric illness. The Alzheimer’s Association estimates that the annual expenses for the care and medical needs of patients with AD exceed $410 billion in America alone.3
The definitive diagnosis of AD is made at autopsy, based on the findings of amyloid plaques, neurofibrillary tangles, and neuronal degeneration. The clinical diagnosis is largely based on conjecture, because depression, overuse of benzodiazepines, and other dementias can have similar symptoms. Recent advances in neuroimaging have provided an earlier opportunity to recognize a dementing process and begin interventions.1
Current efforts to develop drugs that treat AD are focused on reducing amyloid protein, but anti-amyloid medications have, by and large, failed to show significant clinical improvement. Yet, if recent research is correct and a shift in intrinsic assumptions about AD can occur, then treatments that are currently available could significantly impact the incidence of AD.
A group in Sweden4 recently completed a longitudinal study of the association between immunoreactivity to herpes simplex virus 1 (HSV1) and Alzheimer’s disease. While the finding attracted considerable media attention, it also attracted criticism. In part, the criticism comes from the assumption that most individuals have HSV1 antibodies.
One physician is quoted as saying, “More than 90% of the population has antibodies to herpes, and they are not all destined to develop Alzheimer’s disease.”5 This is not entirely accurate. The incidence of HSV1 in the United States is approximately 34%6. HSV1 is a particularly tenacious virus and if a person is exposed, then the virus will most likely be present in their body, albeit quiescent.
HSV1 , which causes cold sores, generally lives in the trigeminal ganglion, a group of neurons embedded in the skull at the base of the brain. The trigeminal ganglion provides touch sensation for the face, the teeth, and part of the scalp. It also provides nerves to the blood vessels and the meninges (lining) of the brain. The parts of the trigeminal ganglion that innervate the lip are only millimeters from the parts that innervate the lining of the brain.
In other words, it is a short trip for this virus to gain access to the brain.