- A new study finds that two very common viruses most people carry might interact to cause Alzheimer’s disease.
- Vaccines for one of the viruses appear to reduce the chances of developing Alzheimer’s.
- The research suggests that other common viruses may drive the development of the debilitating condition.
The virus responsible for chickenpox and shingles may activate a dormant herpes virus strongly associated in its active state with AD.
visiting professor at Oxford University and professor emeritus at Manchester University, told MNT that “age and the decline in the immune system with age, and immunosuppression” are factors that can reawaken VZV as shingles in an adult.
HSV-1 is also extremely common, with 50% to 80% of American adults carrying the virus. While either the oral or genital form of VZV is active, it can cause painful blisters at the site of infection.
“If we shift paradigms,” said Prof. Kaplan, “to focus efforts more on preventive strategies of treating these microbial species before they get a chance to wreak this havoc, we might have a better handle on preventing this disease.”
HSV-1 and Alzheimer’s disease
“Thirty years of evidence by my lab, and subsequently by many others, suggests that HSV-1 is a major cause of AD, though the disease is obviously multifactorial,”
According to Prof. Kaplan, “a range of factors has been reported to reactivate HSV-1 from the latent state, including stresses and disease states.”
“Interestingly,” he added, “this study suggests that this occurs independently of amyloid and tau deposition, which may support the notion that there are independent pathways of neuroinflammation leading to AD, or that the presence of inflammation decreases brain reserve making patients more susceptible to the development of AD.”
way to prevent Alzheimer’s?
have put much effort into the development of vaccines for HSV-1, but thus far, no successful vaccine exists. Some have suggested that mRNA vaccines may provide a more productive way forward.
“I am optimistic that we will have effective mRNA-based vaccines for different targets in the coming years using the knowledge acquired with COVID-19,” he told us.
“Any potential therapy needs to be evaluated in multiple, rigorous human studies. There are several ongoing studies using antivirals, including one funded by the Alzheimer’s Association through our Part on the Cloud initiative,” she noted.
virus
Professor Kaplan told MNT that he feels his study “also demonstrates how a 3D tissue model can be used to elucidate such interactions and synergies in relatively rapid methods.” Much AD research uses animal models.
VZV on inactive HSV-1, Prof. Kaplan and his colleagues created brain-like environments embedded in six millimeter-wide donut-shaped sponges made of silk protein and collagen Neural stem cells — some of which developed into functional neurons, and some of which became support brain glial cells — were delivered into the sponges.
VZV into the brain tissue, they found that, while the neurons became infected, there was no triggering of the development of AD’s characteristic amyloid plaques or tau-protein tangles. More importantly, the functionality of the neurons also remained unimpaired.
VZV to neurons with dormant HSV-1 present, the HSV-1 became reactivated, there was increased amyloid and tau protein growth, and the electrical signals from the neurons began to slow down as they would in AD.
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