Alzheimer’s, the most common form of dementia, is thought to affect 50 million people worldwide and usually starts after age 65 – Copyright AFP/File Philippe LOPEZ
Scientists at Oxford’s Institute of Population Ageing, Tufts University and the University of Manchester have discovered that common viruses appear to play a role in some cases of Alzheimer’s disease.
While the underlying causes of most cases of Alzheimer’s remain unknown, there is growing evidence to suggest viruses are involved. A central point of attention is the herpes simplex virus type 1 (HSV-1). This is the so-called cold sore virus.
This virus resides lifelong, after infection, in the peripheral nervous system. Typically, this is in a dormant form, although it can be reactivated by events such as stress and immune-mediated mechanisms.
The researchers have discovered that HSV-1 DNA is present in the human brain in a high proportion of older people. Research suggests that the virus, when in the brain, in combination with a specific genetic factor, confers a high risk of developing Alzheimer’s disease.
Other studies have revealed major links between the effects of the virus and the characteristic features of Alzheimer’s disease. This is demonstrated through the treating laboratory-grown HSV1-infected cells with antivirals protected against Alzheimer’s disease.
Further support for a major causal role for HSV-1 has been shown using a 3D bioengineered human brain tissue model. This study showed HSV-1 infection of human-induced neural stem cells caused changes that resembled changes observed in Alzheimer’s disease patients’ brains.
These changes are in the form of amyloid plaque-like formations, gliosis, neuroinflammation, and decreased functionality.
New research published in the Journal of Alzheimer’s Disease (“Potential Involvement of Varicella Zoster Virus in Alzheimer’s Disease via Reactivation of Quiescent Herpes Simplex Virus Type 1”), expands the viral roles in Alzheimer’s disease to include another type of herpes virus, varicella zoster virus (VZV), which causes chickenpox and shingles.
By using both laboratory-grown brain cells and a 3D brain model, the researchers examined whether VZV infection caused the accumulation of beta amyloid and abnormally phosphorylated tau (P-tau) and other Alzheimer’s disease -like features, as is the case with HSV-1.
It was found that VZV infection resulted in both gliosis and up-regulation of inflammatory cytokines. This makes it unlikely that VZV could be a direct cause of Alzheimer’s disease, but suggests instead it has an indirect effect by reactivating dormant HSV-1.
This means a severe VZV infection in humans, as in shingles, could reactivate latent HSV-1 in brain, which, in turn, could lead to formation of Alzheimer’s disease -like damage. It follows that the damage in the brain by repeated infections over a lifetime could lead eventually to the development of Alzheimer’s disease.