Alzheimer’s disease could appear following infection with the varicella zoster virus

Researchers from Tufts University in the United States present recent findings that support the hypothesis that Alzheimer’s disease may be triggered by a virus. The strain in question is very common since it is the varicella zoster virus (VZV)

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[EN VIDÉO] What are the differences between bacteria and viruses?
They are microbes. They are very small and they are quite easily confused. However, bacteria and viruses are two very different things. And to fight effectively against those that cause disease, it is better to identify them clearly.

Nearly 225,000 people in France declare Alzheimer’s disease each year, most after age 65. Although this form of dementia is common, its origin is still hotly debated among specialists. There are nevertheless points of consensus: amyloid plaques and aggregates of tau protein in the neurons are involved in the onset of the typical symptoms of Alzheimer’s disease, and theinflammation who seizes the brain patients exacerbates this toxicity.

To explain these observations, several hypotheses are proposed by scientists. Factors genetic seem to have an important role in sporadic cases of Alzheimer’s, the most frequent, but a deregulation of the synthesis of amyloid proteins or the intervention of a microorganism – a virus most of the time – could also have an implication.

Experiences in vitro on cultured neurons

A team from Tufts University, in the United States, presents results falling within the framework of the “viral hypothesis” on the origin of Alzheimer’s disease. The latter states that a virus sleeping in the brain – most often herpes virus 1 or HSV-1 – is “awakened” by still poorly defined factors, and induces the symptoms of Alzheimer’s disease. ” Our results suggest a pathway that leads to Alzheimer’s disease, caused by infection with the virus VZV that triggers inflammation waking up the HSV-1 virus in the brain “says Dana Cairnsfirst author ofstudy published in Journal of Alzheimer’s Disease.

To corroborate this hypothesis, they infected stem cells human neural cells with the two viruses and looked for the presence of markers specific to Alzheimer’s: amyloid plaques and Tau aggregates, gliosis (proliferation of glial cells in the brain) and neuroinflammation. Their results show that the VZV virus alone does not cause the formation of amyloid plaques and Tau aggregates, like HSV-1, but neuroinflammation and gliosis. This suggests, according to scientists, an indirect action of the VZV virus. In addition, they observed that infection of cells, in which HSV-1 is dormant, by the VZV virus reactivates the latter and causes changes typical of Alzheimer’s. ” It’s a double punch of two viruses that are very common and generally harmless, but lab studies suggest that if further exposure to VZV awakens dormant HSV-1, it could cause problems. “says Dana Cairns.

These experiments alone are not robust enough to confirm a causal link between Alzheimer’s disease and the VZV and HSV-1 viruses, even if the observations point in this direction. Moreover, the different hypotheses being studied on the origin of Alzheimer’s disease are not necessarily mutually exclusive. Viral infection could be a factor to consider in Alzheimer’s disease, among others.

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