Researchers from Tufts University and the University of Oxford have made a fascinating discovery about Alzheimer’s disease, a condition that often starts as simple forgetfulness in older age.
Their study has found a link between common viruses and the early stages of Alzheimer’s, offering new insights into what causes this mysterious disease.
The team focused on two viruses – varicella zoster virus (VZV), known for causing chickenpox and shingles, and herpes simplex virus (HSV), which is often associated with cold sores.
They discovered that VZV can activate HSV that lies dormant in the brain. This activation can lead to the buildup of harmful proteins and loss of brain cell function, which are classic signs of Alzheimer’s.
Dana Cairns, a research associate at Tufts, explained that an infection with VZV could trigger inflammation that wakes up dormant HSV in the brain.
This could be just one way Alzheimer’s starts, as other inflammatory events in the brain might also activate HSV and lead to the disease.
Published in the Journal of Alzheimer’s Disease, the study offers a fresh perspective on how Alzheimer’s develops.
David Kaplan from Tufts University and Ruth Itzhaki from the University of Oxford, who have long studied the link between herpes virus and Alzheimer’s, contributed to this research.
They believe that understanding the sequence of events leading to Alzheimer’s is crucial.
The World Health Organization reports that around 3.7 billion people under 50 have HSV-1, which typically remains inactive.
Similarly, about 95% of people are infected with VZV by age 20, usually appearing as chickenpox. Both viruses can stay dormant in the body and be reactivated later in life. It’s this reactivation, particularly of HSV-1, that’s linked to Alzheimer’s.
To investigate this link, the researchers created brain-like environments using silk protein and collagen sponges populated with neural stem cells. These cells grew into functioning neurons and glial cells, similar to those in the brain.
They found that while neurons infected with VZV didn’t immediately show Alzheimer’s markers, neurons with dormant HSV-1 did when exposed to VZV. This led to increased harmful proteins and slowed neuronal signals.
Cairns noted that while other factors like head trauma or obesity might also lead to Alzheimer’s, the reactivation of HSV in the brain could be a key pathway.
The study observed that VZV infection increased cytokine production, which can cause inflammation and potentially reactivate HSV.
Repeated activation of HSV-1 can cause more inflammation, plaque production, and brain damage.
Interestingly, a vaccine for VZV, which prevents chickenpox and shingles, has been shown to reduce dementia risk, possibly by stopping this cycle of viral reactivation and brain damage.
The researchers also mentioned the long-term neurological effects seen in some COVID-19 patients, particularly in the elderly, and the possibility of VZV and HSV-1 reactivation after COVID infection. Monitoring cognitive effects and neurodegeneration in these cases could be important.
This study opens up new possibilities for understanding and potentially treating Alzheimer’s, highlighting the unexpected role that common viruses might play in this complex disease.
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The research findings can be found in Journal of Alzheimer’s Disease.
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