Project

Peripheral HSV1 infection and neuroinflammation as potential trigger mechanisms of Alzheimer’s disease

Code
G057623N
Duration
01 January 2023 → 31 December 2026
Funding
Research Foundation - Flanders (FWO)
Promotor-spokesperson
Research disciplines
  • Medical and health sciences
    • Inflammation
    • Virology
    • Neurosciences not elsewhere classified
Keywords
peripheral viral infection Neuroinflammation Alzheimer's disease
 
Project description

Alzheimer’s disease (AD) is a neurodegenerative disorder affecting 50 million people worldwide. To date, there is no cure and current therapies are not effective in delaying progression. Thus, there is an urgent need to change the way of looking at the disease and to rethink possible therapies. Herpes simplex virus type 1 (HSV1) has recently received growing attention for its role in AD. HSV1 infects the mouth and invades peripheral sensory nerves. The virus remains inactive in sensory neurons but when a person is stressed, it can reactivate and return to the mouth, resulting in cold sores. Occasionally, the virus spreads from peripheral neurons to the brain after reactivation. In this project, we aim to provide a clear understanding of how common HSV1 infection plays a role in the initiation of AD. Based on exciting recent data of the promoter, we will examine how peripheral HSV1 infection may trigger a rapid neuroinflammatory response in the absence of viral infection in the brain. Next, we will determine whether peripheral HSV1 reactivations may cause the accumulation of neuroinflammatory episodes and the initiation of AD pathologies in the brain. The paradigm shift will focus on the peripheral nervous system and will be away from the current thinking that the brain is directly infected by HSV1. This work will be performed using the new mouse model developed by the promoter to study herpesvirus-induced neuroinflammation. This research may lead to targeted preventions.