Keywords :
Apolipoprotein E4; Alzheimer Disease/etiology; Alzheimer Disease/genetics; Alzheimer Disease/microbiology; Apolipoprotein E4/genetics; Borrelia burgdorferi; Brain/microbiology; Chlamydophila pneumoniae; Herpesvirus 1, Human; Herpesvirus 6, Human; Herpesvirus 7, Human; Humans; Infections/complications; Infections/microbiology; Porphyromonas gingivalis; Alzheimer Disease; Brain; Infections; Neurology (clinical); Cellular and Molecular Neuroscience
Abstract :
[en] The idea that infectious agents in the brain have a role in the pathogenesis of Alzheimer disease (AD) was proposed nearly 30 years ago. However, this theory failed to gain substantial traction and was largely disregarded by the AD research community for many years. Several recent discoveries have reignited interest in the infectious theory of AD, culminating in a debate on the topic at the Alzheimer's Association International Conference (AAIC) in July 2019. In this Viewpoint article, experts who participated in the AAIC debate weigh up the evidence for and against the infectious theory of AD and suggest avenues for future research and drug development.
Funding text :
T.E.G. is a co-founder and is on the scientific advisory board (SAB) of Lacerta Therapeutics. He is an SAB member for Promis Therapeutics and has served on SABs for Abbvie, Pfizer, Novartis, Roche/Genetic, Bristol Myers Squibb, Eli Lilly and Biogen. He is an inventor on a number of patents relating to Alzheimer disease therapeutics. He receives funding from the NIH, the Facial Pain Research Foundation and the State of Florida. M.T.H. serves as an advisory board member for IFM Therapeutics, Alector and Tiaki. The other authors declare no competing interests.
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