Viral role discovered in Alzheimer’s disease

In the latest study, published today in the Journal of Alzheimer’s Disease, Professor Itzhaki, now working at the Oxford Institute of Population Aging, together with Tufts researchers, extended the study of viral roles in AD to include another type of herpes virus, varicella zoster virus ( VZV), which causes chickenpox and shingles.

They investigated whether VZV may play a similar role to HSV-1, which could implicate VZV directly in the development of AD. Using laboratory-grown brain cells and a 3D brain model, the researchers looked at whether VZV infection caused the accumulation of amyloid beta (Aβ) and abnormally phosphorylated tau (P-tau) and other AD-like features, such as this is the case of HSV-1.

They found that VZV infection of laboratory-cultured brain cells does not lead to the formation of Aβ and P-tau, the main components, respectively, of AD hallmark plaques and neurofibrillary tangles in the brain. However, they found that VZV infection resulted in gliosis and upregulation of inflammatory cytokines. This makes it unlikely that VZV could be a direct cause of AD, but suggests that it instead has an indirect effect by reactivating dormant HSV-1.

They also found that following VZV infection of cells containing latent HSV-1, HSV1 reactivation and a dramatic increase in Aβ and P-tau levels occurred, suggesting that severe VZV infection in humans, as in shingles, it could reactivate latent HSV-1 in the brain. , which, in turn, could lead to the formation of damage similar to AD.

Professor Itzhaki, Visiting Professor at the Oxford Institute of Population Aging and Emeritus Professor at the University of Manchester, said: “This surprising result seems to confirm that, in humans, infections such as VZV can cause increased inflammation. in the brain, which can reactivate dormant HSV-1

“Brain damage from repeated infections throughout life would eventually lead to the development of AD/dementia.

“This would mean that vaccines could play a more important role than just protecting against a single disease, because they could also indirectly, by reducing infections, provide some protection against Alzheimer’s.”

In fact, researchers at the University of Manchester in an epidemiological study, together with Professor Itzhaki, found that shingles vaccination reduced the risk of AD/dementia (Lophatananon et al., BMJ Open, 2021).

The results should help elucidate the pathways by which infections increase the risk of AD/dementia and the ways in which this disease could be combated through the use of appropriate antivirals for treatment or possibly prevention.

The three authors’ current studies, not on infections but using the same cell model system, support the likelihood that HSV1 reactivation in the brain is central to the brain’s response to damage and the development of AD.

The full article, ‘Potential involvement of varicella zoster virus in Alzheimer’s disease through reactivation of dormant herpes simplex virus type 1’it is publiched in the Journal of Alzheimer’s Disease.

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