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Agricultural and food sciences
- Laboratory animal medicine
- Veterinary immunology
- Veterinary microbiology
- Veterinary neurology
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.