Summary: Researchers discovered a connection between Alzheimer’s disease and herpes simplex virus-1 ( HSV-1 ), suggesting viral infections may contribute to neurodegeneration. The study discovered that tau protein, which is usually associated with Alzheimer’s, may initially guard against the virus but later only increase damage.
HSV-1 popular proteins were observed near beta strands in Alzheimer ‘s-affected mind areas, pointing to a complicated relationship between disease, immune response, and aging. These results could lead to the development of therapies that target viral proteins or alter immune responses in an effort to slow Alzheimer’s growth.
Important Information:
- HSV-1 and Tau: HSV-1 disease influences tau protein degrees, first protecting neurons but afterwards contributing to destruction.
- Alzheimer’s Link: Viral proteins co-localize with beta tangles in brain areas susceptible to Alzheimer’s.
- Medical Possible: Targeting viral protein or fine-tuning the immune response may tell Alzheimer’s solutions.
Origin: University of Pittsburgh
Researchers at the University of Pittsburgh found a surprising connection between herpes simplex virus-1 ( HSV-1 ), which suggests that viral infections may be a factor in Alzheimer’s disease.
The research results are published now in , Cell Reports.
The study also revealed how alpha protein, which is frequently thought to be dangerous in Alzheimer’s, may immediately protect the head from the virus but eventually cause brain damage. These results could lead to novel solutions for treating brain and immune responses to infections.
” Our analyze challenges the conventional view of tau as entirely dangerous, showing that it may first work as part of the body’s immune security”, said senior author Or Shemesh, Ph. Assistant professor in the Pitt Department of Ophthalmology.
” These findings emphasize the complex interplay between infections, immune responses and neurodegeneration, offering a fresh perspective and potential new targets for therapeutic development”.
The researchers found HSV-1-related protein forms in Alzheimer’s brain samples, with more viral proteins co-localized with tangles of phosphorylated tau, one of the hallmarks of Alzheimer’s disease pathology, in brain regions that are particularly vulnerable to Alzheimer’s across disease stages.
Further research on Petri dish miniature models of human brains suggested that HSV-1 infection might regulate brain tau protein levels and regulate its function, a protective mechanism that appeared to lower the post-infection death of human neurons.
Shemesh and his colleagues intend to look into these questions in upcoming research even though the precise mechanisms by which HSV-1 influences the tau protein and contributes to Alzheimer’s disease are not yet known.
They want to find out whether other neurodegenerative diseases, such as Parkinson’s disease and ALS, have similar mechanisms that could be used to target viral proteins or modify the brain’s immune response.  ,
Other authors of the study are Vanesa Hyde, Chaoming Zhou, M. D., Juan Fernandez, Krishnashis Chatterjee, Ph. D., Pururav Ramakrishna, Amanda Lin, Gregory Fisher, Ph. D., Orhan Tunç Çeliker, Jill Caldwell, and LeonardoD’Aiuto, Ph. D., all of Pitt, Omer Bender, Ph. D., and Daniel Bar, Ph. D., both of Tel Aviv University, and Peter Joseph Sauer and Jose Lugo-Martinez, Ph. D., both of Carnegie Mellon University.
About this Alzheimer’s disease research news
Author: Anastasia Gorelova
Source: University of Pittsburgh
Contact: Anastasia Gorelova – University of Pittsburgh
Image: The image is credited to Neuroscience News
Original Research: Open access.
” Anti-Herpetic Tau Preserves Neurons vis the cGAS-STING-TBK1 Pathway in Alzheimer’s Disease” by Or Shemesh et al. Cell Reports
Abstract
Anti-Herpetic Tau Preserves Neurons vis the cGAS-STING-TBK1 Pathway in Alzheimer’s Disease
Alzheimer’s disease ( AD ) diagnosis relies on the presence of extracellular β-amyloid ( Aβ ) and intracellular hyperphosphorylated tau (p-tau ).
Emerging evidence points to a potential link between infectious agents and AD pathologies, with herpes simplex virus 1 ( HSV-1 ) being a prime example.
Our investigation, using metagenomics, mass spectrometry, western blotting, and decrowding expansion pathology, detects HSV-1-associated proteins in human brain samples.
ICP27, a herpesvirus protein, significantly increases with AD severity and colocalizes with p-tau but not with A. Modeling in human brain organoids shows that HSV-1 infection elevates tau phosphorylation.
Notably, p-tau reduces ICP27 expression and markedly decreases post-infection neuronal death from 64 % to 7 %.
This modeling prompts investigation into the cGAS-STING-TBK1 pathway products, nuclear factor ( NF ) -κB and IRF-3, which colocalizes with ICP27 and p-tau in AD.
Furthermore, experimental activation of STING enhances tau phosphorylation, while TBK1 inhibition prevents it.
Together, these findings suggest that tau phosphorylation acts as an innate immune response in AD, driven by cGAS-STING.
