January 8, 2025 — According to a new study in Cell Reports, the research team used advanced techniques to identify 19 HSV-1-related proteins in the brains of people with AD across all stages of the disease. This discovery adds to the growing evidence that infections like HSV-1 might play a role in the development and progression of AD and offer treatment opportunities.

“Our research shows how HSV-1 interacts with the brain and influences the pathologies of Alzheimer’s disease,” says lead researcher Dr. Or Shemesh of the Hebrew University School of Pharmacy. “Early on, the changes in tau may protect brain cells by limiting the virus, but as the disease advances, these same changes could lead to more harm and accelerate neurodegeneration.”

The team’s experiments with human brain organoids derived from stem cells revealed that the HSV-1 infection could increase tau modifications at specific sites linked to Alzheimer’s disease. These modifications seem to help protect brain cells early on by reducing the amount of virus and preventing cell death.

One key finding was the increased activity of a herpesvirus protein called ICP27, which became more prominent as the disease advanced. The protein occupies the same space as tau, but it did not appear near amyloid plaques, another hallmark of the illness. This suggests that HSV-1 may directly affect tau and contribute to the changes seen in Alzheimer’s. The study also highlighted the role of Alzheimer’s pathologies as part of the brain’s natural immune system in this process, focusing on a pathway called cGAS-STING, which influences tau changes.

While more research is needed to fully understand these processes, these findings open the door to innovative ways to slow or stop the progression of this devastating disease.

The research paper titled “Anti-Herpetic Tau Preserves Neurons vis the cGAS-STING-TBK1 Pathway in Alzheimer’s Disease” is now available in Cell Reports and can be accessed here.

(DOI: 10.1016/j.celrep.2024.115109)