Impact of common viral infections on Alzheimer’s progression
A recent study highlights the potential role of common viral infections in promoting the development of Alzheimer’s.
Previous research has established a relationship between varicella zoster virus (VZV), herpes simplex virus (HSV) and Alzheimer’s; however, there is little known about how these viruses may promote disease progression. A recent study from Tufts University (MA, US) and University of Oxford (UK) reports that exposure to VZV may activate HSV, which in turn promotes the early stages of Alzheimer’s, specifically accumulation of amyloid protein.
The study utilized sponges composed of silk protein and collagen, forming the scaffolding to house neural stem cells that could differentiate and grow within the sponge structure. The differentiated, functional neurons form connections with other neurons and supporting brain cells including glial cells. This brain model allowed researchers to study the effect of VZV infection on neuron function.
Researchers reported that exposure to VZV in the absence of a dormant HSV variant (HSV-1) had no impact on neuron function. However, in neurons that had been previously infected with HSV-1, exposure to VZV resulted in reactivation of HSV-1 and increased accumulation of amyloid protein, diminishing neuronal signaling. The “results suggest one pathway to Alzheimer’s disease, caused by a VZV infection which creates inflammatory triggers that awaken HSV in the brain,” commented first author Dana Cairns (Tufts University).
The authors of the study provided further evidence to support this, demonstrating that VZV infected samples produced higher levels of cytokines, small molecules involved in inflammatory signaling. Subsequent inflammation in the brain model led to reactivation of quiescent HSV. “It’s still possible that other infections and other pathways of cause and effect could lead to Alzheimer’s disease, and risk factors such as head trauma, obesity, or alcohol consumption suggest they may intersect at the re-emergence of HSV in the brain” added Cairns.
Previous research suggests that vaccines to protect against VZV, currently used to prevent chickenpox and shingles, may be beneficial in reducing risk of inflammation in the brain and therefore risk of Alzheimer’s. It is suggested that this is achieved by preventing reactivation of HSV and may therefore provide an effective treatment in slowing the onset of symptoms by preventing protein build up.
The researchers emphasize the relevance of these findings in current society as the virus that results in COVID-19 infection (SARS-Cov-2) has been shown to reactivate both VZV and HSV in elderly patients. Dementia is a disorder highly associated with aging, and the increased susceptibility of elderly patients to COVID-19 may further increase their risk of Alzheimer’s progression. This study highlights the need for further research into Alzheimer’s pathogenesis, as the more we understand about what causes the symptoms to arise, the greater potential there is to create targeted treatments to slow the onset of this degenerative disease.