Sunday, November 24, 2024

How to forestall Alzheimer’s: A plea for vaccines

According to the World Health Organization, there are about 10 million latest cases of Alzheimer’s and other types of dementia worldwide every year. That’s about one latest case every 3 seconds. As population trends allow people to live longer, the overall number of individuals affected by the disease is predicted to double in the following 20 years. New research now suggests that vaccination against common viruses can significantly reduce the danger of developing Alzheimer’s.

Alzheimer’s disease is characterised by the buildup of beta-amyloid plaques and tau neurofibrillary tangles, which ultimately result in brain atrophy or shrinkage. Changes within the brain often begin years before cognitive symptoms appear, making this disease particularly difficult to diagnose and treat. The pattern of structural damage observed within the brains of Alzheimer’s patients shows signs of great neuroinflammation. High levels of inflammation within the brain over several years could be each a cause and a consequence of the event of this disease.

Inflammation within the brain can occur any time you have been exposed to a virus. Even without directly infecting brain cells, viruses can trigger an inflammatory response so strong that it overwhelms your entire body. The Covid-19 virus, for instance, is especially good at triggering a powerful immune response. In some cases, inflammation-related damage to the brain can persist even after symptoms have subsided.

However, certain viruses never completely leave the body. For example, when someone is exposed to the varicella-zoster virus that causes chickenpox, a part of the virus becomes latent and stays within the body. Latent viruses can remain inactive for years and even a long time without multiplying within the body before being reactivated. Reactivation of a latent virus triggers a brand new infection and results in an inflammatory response. After a chickenpox infection, the virus reactivates in a single in three people and manifests itself as shingles, a painful skin rash.

A growing variety of reports suggest that exposure to chickenpox and subsequent reactivation of shingles could also 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 abnormally phosphorylated tau, which resemble the amyloid plaques and neurofibrillary tangles characteristic of Alzheimer’s disease. Administration of antiviral agents directed against chickenpox significantly reduces the buildup of beta-amyloid and phosphorylated tau. These findings reveal a possible mechanism for the event of Alzheimer’s disease and, more importantly, the way to prevent it.

How can exposure to the chickenpox virus trigger Alzheimer’s a lot later in life? One theory is that the latent varicella-zoster virus is continually reactivated in response to emphasize, causing cumulative damage within the brain over time. In this fashion, the presence of the reactivated virus directly triggers the formation of amyloid and tau aggregates within the brain. However, this theory is restricted by previous reports that reactivation of the varicella-zoster virus occurs just once, causing shingles.

Since Alzheimer’s disease develops over a long time, latest study from the University of Oxford suggested that this virus probably has an indirect effect by increasing inflammation within 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 triggers 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 didn’t observe the formation of beta-amyloid and tau proteins, the researchers measured increased levels of pro-inflammatory cytokines, confirming their hypothesis that the link between chickenpox and Alzheimer’s disease could also be not directly mediated by inflammation. Cumins et al. concluded that the pro-inflammatory cytokines triggered by the varicella-zoster virus can trigger repeated reactivation of latent viruses, which might eventually result in the event of Alzheimer’s disease.

These results are consistent with clinical reports showing that vaccination against chickenpox and shingles can significantly reduce the danger of Alzheimer’s disease. Vaccination against other common viruses, comparable to influenza, has been shown to have an identical protective effect. Recent study A study published within the Journal of Alzheimer’s found that a flu shot can reduce the danger of developing Alzheimer’s disease by 40% in people over 65.

Although the mechanism of how inflammation results in Alzheimer’s disease shouldn’t be yet clear, timely vaccination offers some protection. We are only starting to know the role of the immune system in Alzheimer’s. This shouldn’t be an isolated brain disease. It is evident that environmental aspects and lifestyle selections that increase your susceptibility to brain inflammation put you susceptible to developing this and other types of dementia.

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