The new suggests that repeated head injuries, such as concussions, a known risk factor for Alzheimer青瓜视频檚 disease (AD), may reactivate a common dormant virus in the brain, increasing the risk of AD and other neurodegenerative conditions. Researchers found that even mild brain trauma can trigger this chain reaction, leading to harmful changes associated with memory loss and cognitive decline.

, the researchers demonstrated the roles that common viruses, such as herpes simplex virus type 1 (HSV-1) (the so-called cold sore virus) and varicella zoster virus (VZV) (which causes chickenpox and shingles) play in the development of AD. HSV-1 can lie dormant in human cells for a lifetime, but when it re-awakens it can cause changes that resemble changes observed in AD patients青瓜视频� brains - amyloid plaque-like formations (PLFs), gliosis, neuroinflammation, and decreased functionality.

In the latest study, published today in Science Signaling, the researchers once again used their small, 3D, bioengineered human brain tissue model to test the effects of physical trauma on the brain cells. When the brain tissues were exposed to repeated "mild blows," similar to concussions, the previously dormant HSV-1 virus became active. This reactivation triggered inflammation, beta-amyloid plaque build-up, and the formation of harmful tau proteins, which can damage brain cells and impair memory.

Importantly, the researchers also found that blocking an inflammatory molecule called Interleukin-1 beta (IL-1尾) prevented many of these harmful effects in lab models, opening the door to potential new treatments for those at risk. 

Professor Ruth Itzhaki, who led the research with Drs Cairns and Kaplan at Tufts, has been researching the potential role of HSV-1 in AD for more than 30 years, beginning at the University of Manchester, where her team discovered HSV-1 DNA is present in the human brain in a high proportion of older people - the first microbe to be detected definitively in normal human brains. 

Professor Itzhaki, Visiting Professorial Fellow at the Oxford Institute of Population Ageing and Emeritus Professor at the University of Manchester, said: 青瓜视频淗ead injuries are already recognised as a major risk factor, as are the cumulative effect of common infections, for conditions such as Alzheimer青瓜视频檚 and dementia, but this is the first time we have been able to demonstrate a mechanism for that process.

青瓜视频淲hat we青瓜视频檝e discovered is that in the brain model these injuries can reactivate a dormant virus, HSV1, setting off inflammation which, in the brain, would lead to the very changes we see in Alzheimer青瓜视频檚 patients.

青瓜视频淯nderstanding both the risk factors for dementia and Alzheimer青瓜视频檚, and the mechanism by which they develop, is important in being able to target treatment and prevention at as early a point as possible.青瓜视频�

The researchers hope their work will pave the way for new treatments to protect against neurodegeneration, particularly for those at high risk due to repeated concussions.

The full paper, 青瓜视频楻epetitive injury induces phenotypes associated with Alzheimer青瓜视频檚 disease by reactivating HSV-1 in a human brain tissue model青瓜视频�, is published in.

Ruth Itzhaki, , Professor Emeritus of Molecular Neurobiology (and now visiting Professorial Fellow, University of Oxford) received the Alzgerm Quest prize, for research on Alzheimer’s disease aiming at showing the involvement of an infectious agent in the disease.

The eight individuals divided the "$1 Million Challenge", which lasted three years, ending December 31, 2020.

None of the challengers provided enough evidence to persuade the judges that a particular infectious agent was the sole cause of Alzheimer's disease, so the grand prize of $1 million was .

However Professor Itzhaki was awarded the highest sum of $35,00 for her work on Herpes Simplex Virus.

The challenge initially attracted 81 would-be entrants, of whom 40 were authorized to submit formal entries. Eight did so.

The other finalists were  Hugo Lovheim, Umea, Sweden; Richard Lathe, Edinburgh; Rima McCleod, Chicago, Tom Dowd, Wisconsin; Alan MacDonald, Naples; May Bedoun, Baltimore, and Steven Dominy, San Francisco.

Six microorganisms were nominated: herpes, toxoplasma, Borrelia, mycobacteria, H. pylori, and P. gingivalis.

Professor Itzhaki said: “I am delighted that our work has been recognised in this way and would like to thank the judges for their work, highlighting this area of research

"It was as long ago as 1991 when we discovered that, in many elderly people infected with HSV1, the virus is present also in the brain, and then in 1997 that it confers a strong risk of Alzheimer’s disease in the brain of people who have a specific genetic factor.

“In 2009, we went on to show that HSV DNA is inside amyloid plaques in Alzheimer’s patients’ brains.

“We suggested that the virus in brain is reactivated by certain events such as stress, immunosuppression, and infection/inflammation elsewhere.

“So we believe the cycle of HSV1 reactivation in the brain eventually causes Alzheimer’s in at least some patients.”

Dr Leslie Norins, from Alzheimer's Germ Quest said: “The plausible evidence submitted incriminating six different organisms means no one convincingly proved their nominee was the sole microbe triggering Alzheimer's disease.

“ This demonstrates that there may not be a single "Alzheimer's germ". Perhaps several microbes can cause the disease.

“If true, Alzheimer's will become an "umbrella" term like pneumonia, diarrhea, and hepatitis. It will signify cognition infection, but further tests would be needed to identify the troublemaking organism. The Challenge added recognition and momentum to the need to investigate microbes."