Alzheimer’s disease is a progressive neurodegenerative disorder characterized by behavior changes, memory loss, and cognitive decline. One of the pathological hallmarks of Alzheimer’s disease is amyloid-beta plaque formation in the brain. Findings from a new study suggest that herpes simplex virus I infection contributes to the formation of amyloid-beta plaques.
Amyloid-beta is a toxic 42-amino acid peptide that aggregates and forms plaques in the brain with age. Some evidence suggests amyloid-beta plaques are causative agents in Alzheimer’s disease.
Herpes simplex virus I causes oral herpes, commonly known as cold sores. After the herpes simplex virus I enters the body, it remains there for life and can lead to recurrent outbreaks. Large quantities of herpes simplex virus I are commonly found in the autopsied brains of people who had Alzheimer’s disease.
The authors of the study exposed cultured human-induced neural stem cells to herpes simplex I virus for three days. They found that the infection induced an Alzheimer’s disease-like condition in the mice that shared common features of Alzheimer’s, including neuroinflammation, changes in glial cells, and the formation of amyloid-beta plaques.
These findings suggest that viral infection plays a key role in Alzheimer’s disease pathology and can inform future research on therapeutic strategies to mitigate the disease’s effects.