Is Alzheimer's disease linked to Herpes simplex virus type 1 infection? A mini‐review of the molecular correlation and the possible disease connections

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease in the world. Several pathological pathways and genetic alterations have been linked to AD; however, the definitive cause of the disease remains unknown. Recently, an increasing body of evidence suggests that neurodegenerative diseases, including AD, might be triggered by microbial infections. Herpes simplex virus type 1 (HSV1) has been found in brain samples from dead AD patients. At some point of in their lifetime, every person comes into contact with HSV1, but when this enters the brain, it remains latent. However, it was observed that when a person becomes old, and there is a decline in their immunity, the latent HSV1 virus becomes reactivated. The reactivated virus then causes damage to the neural cell DNA and disrupts the DNA repair system, leading to AD. The present review would provide a clear understanding of how HSV1 influences DNA damage, and causes plaque formation and phosphorylation of tau protein, which in turn leads to AD, by inducing the production of interferons that would facilitate the production of specific humoral immunity, which could lead to neurodegeneration.

Molecular Mechanisms of Astaxanthin as a Potential Neurotherapeutic Agent

“…In recent decades, the prevalence of AD has risen significantly [ 35 , 36 ]. It may have a huge effect and obstacles on the well-being and the ability to lead a healthy life by the affected patients [ 37 , 38 ]. The excessive accumulation of β-amyloid protein (Aβ) in the cerebral cortex and hippocampus is one of AD’s main features [ 39 ].…”

Herpes simplex virus reactivation and the relationship with Alzheimer's disease: A countering view

“…At an elemental level, though, this conclusion is at odds with the finding that HSV blocks caspase‐dependent pathways to apoptosis, so as to ensure that the infected cells maximize viral progeny. This tenet in virology undermines the hypothesis that HSV actively contributes to the hallmark characteristic of AD – neuronal cell death – yet the theory of viral etiopathogenesis in AD is gaining traction and many authors, including Bahbah et al ., have attempted to describe the molecular mechanisms of this process . This commentary not only challenges the concept of a viral etiology in AD with longitudinal evidence showing that high HSV avidity reduces conversion from adult mild cognitive impairment to AD, but also proposes that viral reactivation is a compensatory reaction to other causal exposures in AD pathophysiology.…”