Evaluation of the effects of Herpes simplex glycoprotein B on complement system and cytokines in in vitro models of Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disorder that causes memory loss and dementia, and is characterized by a decline in cognitive functions. Brain infections, especially induced by Herpes simplex virus type-1 (HSV-1), are suggested to play a key role in the pathogenesis of AD. Within the scope of this study, two different AD models [Tau model and amyloid beta (Aβ)] were created in the SH-SY5Y cell line and HSV glycoprotein B (gB) was applied to the cell line and on the generated AD models. Study groups (n = 3) were designed as: 1. control; 2. HSV-gB group; 3. retinoic acid (RA) and brain derived neurotrophic factor induced (BDNF) Alzheimer's model (AD), 4. RA and BDNF induced alzheimer's model + HSV-gB (ADH), 5. amyloid beta 1-42 peptide induced Alzheimer's model (Aβ) and 6. amyloid beta 1-42 peptide induced Alzheimer's model + HSV-gB (AβH). Levels of complement proteins and cytokines were determined comparatively. In addition, specific markers of AD (hyperphosphorylated Tau proteins, Aβ 1-40 peptide and amyloid precursor protein) were measured in all groups. HSV-gB administration was found to increase Aβ and hyperphosphorylated Tau levels, similar to AD models. In addition, our data confirmed that immune system and chronic inflammation might have a crucial roles in AD development and that HSV-1 infection might also be an underlying factor of AD.