The Case for Virus Origin of Neurodegenerative Diseases Is Getting Stronger and More Important
Dr. Ruth Itzhaki, an emeritus professor of neurology at the University of Manchester today, was frequently demoralized by grant rejections in the 1990s. Scientists would not be able to pay and carry out their research without the grant money. No, scientists are not allowed to do study on whatever topic they choose. That is the funders’ prerogative.
Why were Itzhaki’s grant applications consistently turned down? It’s as a result of her unusual insights. The scientific community dismissed as ludicrous the idea that viruses cause or hasten the onset of neurological illnesses such as Alzheimer’s disease (AD).
To be fair, though, I would also be skeptical if you told me that an infection I had as a child would make me more likely to develop AD when I get older.
“My research on viruses as a potential cause of Alzheimer’s disease was met with a great deal of hostility in the following decades, and nearly all of my funding applications were denied: a hostility that has persisted for 25 years and which has only recently subsided, because of growing evidence,” Itzhaki wrote in her 2022 article for The Conversation.
In fact, strong evidence supporting the role of viruses in the onset of AD has emerged throughout the last ten years. For example, a 2020 meta-analysis of 47 cohort studies — some of which were carried out nationally — found that infections with several herpesviruses and the bacteria Chlamydia pneumoniae were associated with higher chances of AD.
I wrote a review paper on the topic of herpes simplex virus-1 (HSV-1) infection in a renowned journal in 2021, therefore I am well familiar with its role in AD. In that article, I discussed research demonstrating how HSV-1 genetic material was discovered in amyloid aggregates in the brains of AD patients after their deaths, as well as how HSV-1-infected animals started to exhibit memory loss symptoms and amyloid aggregates in their brains.
