Alzheimer’s disease (AD) is a neurodegenerative disorder affecting 26 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. The objective of HERPINAD is to provide a clear understanding of how common HSV1 infection plays a role in the initiation of AD. The hypothesis is that HSV1 infection of peripheral neurons causes inflammation which is relayed to neurons in the brain, resulting in long-term inflammation and neurodegeneration. This neuroinflammation represents the driving force of AD pathology, starting very early in the course of the disease. 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 our new mouse model to study herpesvirusinduced neuroinflammation. Our findings will be of key importance for the design of new therapies that may prevent AD to the current and future generations.