New research found that tau protein in the brain, considered a hallmark of Alzheimer’s disease, may initially play a protective role against viral infections.
With the number of people with dementia expected to hit 153 million globally by 2050 Trusted Source. Researchers are focused on identifying health conditions and diseases that may increase a person’s risk for dementia, particularly Alzheimer’s disease. Alzheimer’s disease is the most common type of dementia.
“Identifying health conditions that raise a person’s risk for Alzheimer’s disease is crucial because it allows for early intervention, targeted prevention strategies, and personalized treatment approaches,” Or Shemesh, PHD, assistant professor in the Department of Ophthalmology at The University of Pittsburgh explained to Medical News Today.
“By understanding the risk factors, researchers can develop strategies to mitigate these risks, potentially delaying or preventing the onset of Alzheimer’s. Additionally, this knowledge contributes to the broader understanding of the disease’s mechanisms, which can lead to the discovery of novel therapeutic targets and improved diagnostic tools,” he noted.
Shemesh is the senior author of a new study recently published in the journal Cell Reports Trusted Source that identified a potential link between Alzheimer’s disease and the herpes simples virus-1 (HSV-1).
The new study also found that tau protein Trusted Source in the brain historically considered to be a hallmark of Alzheimer’s disease — may play a protective role against viral infections before contributing to brain damage later in life.
For this study, Shemesh and his team used various modeling techniques to investigate how HSV-1 might be linked to Alzheimer’s disease.
“Alzheimer’s disease is usually diagnosed by finding clumps of a protein called beta-amyloid outside brain cells and another protein called tau inside the cells,” Shemesh explained. “Tau is found modified and pathogenic in Alzheimer’s disease. Recent Studies suggest that infections might play a role in Alzheimer’s disease, with HSV-1 being a strong suspect.”
“In our study, we detected HSV-1-related proteins in postmortem human brain samples,” he continued. “We found that the viral proteins increase as Alzheimer’s disease worsens and are found in the same areas as the tau, but not with [beta-amyloid]. In experiments using miniature human brain models organoids, we saw that HSV-1 infection increases the amount of tau,” he told us.
Interestingly, Shemesh said, the modified tau seems to reduce the levels of herpes proteins and lower the number of neurons dying after infection, as if the neurons were not infected at all.
“This led us to explore a specific immune response pathway in the brain, the CGAS-sting pathway,” he detailed. “We found that molecules of this pathway are present where HSV-1 and modified tau are found in Alzheimer’s disease.”
“We also discovered that activating this immune pathway boosts tau modification while blocking it stops the tau modification,” Shemesh continued. “These results suggest that tau may be a part of the brain’s immune response in Alzheimer’s disease, and that therapeutic interventions might aim at helping it, not necessarily blocking it.”
Potential for New Alzheimer’s Treatments
Shemesh believes that these findings may one day lead to new treatment options for Alzheimer’s disease:
“The discovery that tau phosphorylation can act as a protective mechanism against HSV-1 infection suggests that enhancing this immune response could help mitigate the impact of viral infections in the brain, which are increasingly being implicated in Alzheimer’s pathology. A promising strategy could be to mimic the beneficial effects of tau phosphorylation without triggering its harmful aggregation, which is associated with Alzheimer’s progression.”
“This approach could help bolster the brain’s innate immune response while avoiding the formation of neurofibrillary tangles that exacerbate the disease,” he continued. “By understanding the specific mechanisms through which tau provides this protection, we can work toward therapeutic interventions that leverage its positive effects while mitigating its detrimental impact on neuronal health.”
“We plan to further explore the mechanisms behind tau’s protective role, investigate other pathogens that might interact with tau (or [beta-amyloid]) in Alzheimer’s, and test potential therapies that can harness or mimic tau’s protective effects,” he added. **Medical News Today is the source of this content.
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