Document Type


Publication Date

Spring 5-30-2019


This review will focus on the interaction of herpes simplex virus type 1 (HSV-1) and its causative role in pathogenesis of Alzheimer’s disease (AD) noting specifically, the epidemiological relevance of addressing this problem, as well as the molecular pathways associated. HSV-1 reactivation tends to be one of the primary causative events that is responsible for many of the pathologies associated with AD, such as: amyloid beta (Aβ) accumulation caused by malfunctioning cleavage of amyloid precursor protein (APP) as well as tau hyperphosphorylation. HSV-1 reactivation is a primary causative event in downstream dysfunction and is also shown to be directed by the c-Jun N-terminal kinase (JNK) stress pathway; however, the glycogen synthase kinase type-3 (GSK-3) pathway is most important for Aβ accumulation and is also associated with tau hyperphosphorylation: the two proteins responsible for AD. The purpose of discussing these molecular pathways associated with the connection between HSV-1 and AD is to prove that proactive treatment is a necessity, while also advocating for a more detailed understanding of the causative affects of HSV-1 on AD. This review is important to increase awareness of the association between this highly prevalent virus and an extremely debilitating disease, with the goal of increased understanding and treatment for both HSV-1 and Alzheimer’s disease.