How To Prevent Alzheimer’s Disease: A Case For Vaccines

(Posted on Thursday, May 23, 2024)

According to the World Health Organization, there are approximately 10 million new cases of Alzheimer’s disease and other forms of dementia around the world each year. That corresponds with about 1 new case every 3 seconds. As demographic shifts enable people to live longer, the total number of people living with this disease is expected to double over the next 20 years. Now, emerging research suggests that vaccination against common viruses can significantly reduce your risk of developing Alzheimer’s disease. 

Alzheimer’s disease is characterized by the accumulation of beta-amyloid plaques and tau neurofibrillary tangles that ultimately lead to brain atrophy or shrinkage. Changes in the brain often begin years before the onset of cognitive symptoms, making this a particularly challenging disease to diagnose and treat. The pattern of structural damage observed in the brains of those with Alzheimer’s shows signs of significant neuroinflammation. High levels of inflammation in the brain over several years may be both a cause and a consequence of developing this disease. 

Inflammation in the brain can occur any time you have been exposed to a virus. Even without directly infecting brain cells, viruses are capable of triggering such a strong inflammatory response that it overwhelms the whole body. The Covid-19 virus, for example, is particularly adept at triggering a robust immune response. In some cases, inflammation-induced damage to the brain can persist even after symptoms are cleared. 

Certain viruses, however, never fully leave the body. For instance, when someone is exposed to the varicella-zoster virus that causes chickenpox, some of the virus becomes latent and remains in the body. Latent viruses can remain dormant, without replicating in the body for years, even decades, before they are reactivated. Reactivation of a latent virus triggers a new infection and prompts an inflammatory response. After a chickenpox infection, the virus reactivates in one out of every three people and presents as shingles, a painful skin rash. 

Increasing reports now suggest that exposure to chickenpox and subsequent shingles reactivation may be linked to Alzheimer’s disease. In brain tissue samples, researchers have observed that exposure to the varicella-zoster virus triggers the formation of beta-amyloid aggregates and abnormality phosphorylated tau, resembling the amyloid plaques and neurofibrillary tangles that are characteristic of Alzheimer’s disease. Administering chickenpox-targeting antivirals considerably reduces the accumulation of beta-amyloid and phosphorylated tau. These findings reveal a possible mechanism for how Alzheimer’s disease develops, and more importantly, how to prevent it. 

How does exposure to the chickenpox virus cause Alzheimer’s disease so much later in life? One theory argues that the latent varicella-zoster virus is continuously reactivated in response to stress, leading to cumulative damage in the brain over time. In this way, the presence of the reactivated virus directly triggers the formation of amyloid and tau aggregates in the brain. However, this theory is limited by previous reports that reactivation of the varicella-zoster virus only occurs once to cause shingles.

Given that Alzheimer’s disease develops over decades, a new study from the University of Oxford suggests that this virus likely has an indirect effect by increasing inflammation in the brain. The team speculated that reactivation of the chickenpox virus only develops into shingles in severe cases. An inflammatory response to the newly activated virus then induces a cascade of additional neuroinflammation that damages brain cells. 

In this study, Cumin et al. began by obtaining human stem cells that resemble brain tissue. These cells were then exposed to the varicella-zoster virus. Although they did not observe the formation of beta-amyloid and tau proteins, researchers measured increased levels of proinflammatory cytokines, confirming their hypothesis that the correlation between chickenpox and Alzheimer’s disease may be indirectly driven by inflammation. Cumins et. al concluded that the proinflammatory cytokines triggered by the varicella-zoster virus may induce recurrent reactivation of latent viruses that eventually can lead to the development of Alzheimer’s disease. 

These findings are consistent with clinical reports that vaccinating against chickenpox and shingles can significantly reduce the risk of Alzheimer’s disease. Vaccinating against other common viruses, such as the flu, has been shown to have a similar protective effect. A recent study published in the Journal of Alzheimer’s found that getting one flu vaccine can reduce the risk of developing Alzheimer’s disease by 40% in individuals above the age of 65 years old. 

Although the mechanism of how inflammation leads to Alzheimer’s disease is not yet clear, getting your vaccinations on time offers some protection. We are only just beginning to understand the role that the immune system plays in Alzheimer’s. This is not an isolated brain disease. It is evident that environmental factors and lifestyle choices that increase your vulnerability to brain inflammation can put you at risk of developing this and other forms of dementia.

Read the article online on Forbes.