Alzheimer's disease is the most common cause of dementia, and a leading cause of disability in high age. There are currently no disease-modifying treatments available.
A recent breakthrough in the understanding of Alzheimer's disease pathogenesis is the finding that the amyloid beta peptide, the main constituent of the plaques accumulating in the brains of individuals with Alzheimer's disease, is a potent antimicrobial peptide and an important part of the innate immune system within the brain. Persistent infections might trigger amyloid beta accumulation and subsequent neurodegeneration.
In 2015 we could confirm that herpes simplex infection give an increased risk of later Alzheimer's disease development, using large prospective population-based materials and biobank samples. Our continuing research aims at understanding immunological, genetic and environmental factors contributing to an increased risk of HSV1-associated Alzheimer's disease, and, in a pilot clinical drug trial, to investigate whether antiviral drug treatment might have beneficial effects on disease processes.