The shingles virus may play a role in the development of Alzheimer’s disease (AD) by reactivating another dormant virus, and triggering the development of AD-related plaques in the brain, a study has suggested.
Researchers from the University of Manchester, Tufts University in Massachusetts and the University of Oxford have shown that infections such as varicella zoster virus (VZV), which causes chickenpox and shingles, may activate dormant herpes viruses, leading to the accumulation of AD-associated proteins in the brain.
A complete understanding of the causes of Alzheimer’s disease is still to be found, but there is increasing evidence to suggest microbial organisms are involved – in particular, the herpes simplex virus type 1 (HSV-1), the so-called cold sore virus, they said.
After infection, HSV-1 resides in the peripheral nervous system, usually in a dormant form and can be reactivated by events such as stress and immune-mediated mechanisms.
The new research has now suggested that dormant HSV-1 can be activated by another type of herpes virus, VZV, which could in turn lead to AD-like damage.
This study expanded the study of viral roles in AD to include the chickenpox and shingles virus. The results were published in the Journal of Alzheimer’s Disease.
Using both laboratory-grown brain cells and a 3D brain model, lead researcher Professor Ruth Itzhaki and her team looked at whether VZV infection caused AD-like features, such as beta-amyloid (Aβ) and abnormally phosphorylated tau (P-tau).
These are the main components of the characteristic AD plaques and neurofibrillary tangles seen in Alzheimer’s patients, and also seen in HSV-1.
The results showed that VZV did not lead to the build-up of plaques in the brain and, therefore, was unlikely to be a direct cause of AD. However, severe VZV infection, such as shingles, was shown to reactivate dormant HSV-1 in the brain, which can lead to the formation of AD-like damage.
Professor Itzhaki said: ‘This striking result appears to confirm that, in humans, infections such as VZV can cause an increase in inflammation in the brain, which can reactivate dormant HSV-1. The damage in the brain by repeated infections over a lifetime would lead eventually to the development of AD/dementia.’
The findings also suggest a potential role for common vaccines in managing Alzheimer’s disease.
Professor Itzhaki added: ‘This would mean vaccines could play a greater role than just protecting against a single disease because they could also indirectly, by reducing infections, provide some protection against Alzheimer’s.’
In previous research also led by Professor Itzhaki, visiting professorial fellow at the University of Oxford and emeritus professor at the University of Manchester, found that the DNA of the cold sore virus (herpes simplex virus type 1 or HSV-1) is present in the brain of a high proportion of older people.
When combined with a specific genetic factor, there is a high chance of developing Alzheimer’s, they found.
This comes after research last year found that difficulty hearing spoken conversations is associated with a 91% increase in the risk of dementia.