THE ESSENTIAL
- American scientists have identified forms of proteins linked to the herpes virus in the brains of adults affected by Alzheimer’s disease.
- HSV-1 protein expression increases with the severity of neurodegenerative pathology and colocalizes strongly with phosphorylated tau protein.
- Phosphorylation (a biochemical reaction) of tau protein after infection initially reduces the viral protein and stimulates cell viability, before damaging the brain.
We know: beta-amyloid and tau proteins, naturally present in the body, are implicated in the brain lesions detected in Alzheimer’s disease. “The beta-amyloid protein accumulates outside neurons, forming plaques called amyloid plaques or senile plaques, which are toxic to neurons. The tau protein, which normally participates in the constitution of the skeleton of cells, is modified and , by disorganizing the structure of neurons, it produces neurofibrillary degeneration leading to the death of neurons. indicates Health Insurance. However, emerging evidence suggests a potential link between Alzheimer’s disease and pathogens, such as herpes simplex virus 1 (HSV-1).
Alzheimer’s: proteins linked to the herpes virus in the brains of patients
Thus, as part of a study, researchers from the University of Pittsburgh (United States) wanted to look into the question. “Our research, which uses metagenomics, mass spectrometry, western blotting and uncoupling expansion pathology, detects proteins associated with HSV-1 in brain samples from people with Alzheimer’s disease,” they wrote. Based on their analysis, published in the journal Cell Reportsthe team identified forms of proteins related to the herpes virus, with higher amounts of viral proteins colocalized “with tangles of phosphorylated tau” in regions of the brain particularly vulnerable to Alzheimer’s disease at all stages of the pathology.
“The protein may initially act as part of the brain’s immune defense”
Another observation: the tau protein could, initially, protect the brain from the herpes virus by reducing the expression of these proteins and by significantly reducing post-infection neuronal death from 64% to 7%. However, it then contributes to brain damage. “Our study challenges the conventional view of tau as solely harmful, showing that it may initially act as part of the brain’s immune defense. These findings highlight the complex interplay between infections, immune responses and neurodegeneration, providing a new perspective and potential new targets for therapeutic development”, said lead author Or Shemesh, author of the work.
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