UPO confirms with research that herpes simplex virus type 1 increases the risk of developing Alzheimer’s disease.

In a press release sent by the university, they note that this discovery was recently published in a journal. Alzheimer’s disease research and therapy. Herpes simplex virus 1 (HSV-1) is a human pathogen that has a high prevalence in the population and the ability to establish itself in cells of the nervous system. The source of HSV-1 infection, acquired in most cases during childhood, is in the epithelial cells of the oral/nasal mucosa, from where the virus is transported to the neurons of the trigeminal ganglia and remains there in a latent state throughout life.

External factors such as stress, According to the UPR, persistent inflammation or, among other things, immunosuppression may make it easier for this virus to access the brain during aging, a condition that naturally increases the vulnerability of the immune system and the permeability of the blood-brain barrier.

University Professor of Physiology Pablo de Olavide and lead author of the study Jose Luis Cantero, explained that “studies in cellular and animal models have shown that recurrent reactivation of HSV-1 increases brain pathology in Alzheimer’s disease. However, data in humans are very sparse and were obtained in the clinical stages of the disease when brain damage is very obvious.”

A study in which, in addition to Cantero, a researcher from Laboratory of Functional Neuroscience UPR Mercedes Atienza and researchers from the Center for Molecular Biology of Severo Ochoa, Maria Jesús Bullido and Isabel Sastre, demonstrated in asymptomatic older adults that the extent of HSV-1 infection is specifically related to beta-amyloid plaques, which appear decades before the first symptoms of Alzheimer’s disease appear. .

Likewise, studies have confirmed that the relationship between HSV-1 and amyloid-beta load in the brain is particularly evident in cases where the virus is carried by herpes simplex virus-1. APOE4 genetic variant, is considered the most important genetic risk factor for Alzheimer’s disease and is present in approximately 25% of the population. These results suggest that herpes simplex-1 viral load may be a risk factor for the development of beta-amyloid plaques, which are considered the earliest neuropathological lesion of Alzheimer’s disease, “for which there is no evidence in older adults,” the study said. Professor of Molecular Biology at the Autonomous University of Madrid and co-author of the study Maria Jesús Bullido.

Elevated levels of herpes simplex-1 may not only contribute to an increased beta-amyloid load in the brain, but also increase levels of peripheral inflammation, which may contribute to the development of the disease. “It’s not that herpes simplex virus 1 causes Alzheimer’s disease; This is probably another factor that contributes to the development of the disease.”– said Professor Cantero.

Finally, UPO notes that a significant number of epidemiological and experimental studies support the infection hypothesis of Alzheimer’s disease, which posits that chronic bacterial and/or viral infections may contribute to the development of the disease in various ways. Pathogenesis of Alzheimer’s disease, This is a possible risk factor that should be considered when identifying new preventive and therapeutic strategies for a disease that is currently untreatable.