Exploring the Role of HSV-1 in the Pathogenesis of Alzheimer’s Disease

Alzheimer’s Disease (AD) is the most common neurodegenerative disorder, characterized by excessive amyloid beta(Aβ) plaque and tau protein tangles in the brain. While the exact cause of AD remains unclear, recent research implicates viral vectors, particularly Herpes Simplex Virus 1 (HSV-1), in its progression. This review investigates how HSV-1 infection can contribute to the development and transmission of AD through viral mechanisms, including pathological amyloid beta and tau protein deposition. A systematic review of 30 peer reviewed articles from the past 10 years was conducted, focusing on HSV-1’s influence in AD, using databases such as PubMed and Google Scholar with keywords ‘HSV-1,’ ‘AD,’ ‘amyloid beta,’ and ‘tau protein.’ Findings indicate HSV-1 contributes to AD pathology, evidenced by HSV-1 DNA in AD patients’ brain. A meta-analysis revealed HSV-1 infection is associated with an increased risk of AD, with a pooled odds ratio (OR) of 1.40. These observations suggest HSV-1 promotes Aβ and hyperphosphorylated tau protein accumulation via viral effects like neuroinflammation. This review supports the hypothesis that HSV-1 plays a significant role in AD development, offering new insights into disease progression. Targeting HSV-1 and its pathways may offer novel therapeutic strategies for preventing AD. Further research is needed to examine HSV-1’s long-term effects on neurons and develop interventions that mitigate its impact on AD. Understanding the role of HSV-1 in transmitting AD could pave the way for future research investigating novel therapeutic and preventive strategies that target the viral interactions that lead to Alzheimer’s pathology.