The gap between amyloid pathology and cognition.

Abstract

Nrf2 is a transcription factor critical for protecting the brain against oxidative stress and is decreased in Alzheimer's disease (AD) patients, making it a potential therapeutic target. The Curran lab previously identified a novel regulator, WDR23. Now, in a new study by Liu et al., they demonstrate that knocking out WDR23 in the 3xTg-AD mouse improves spatial working memory, interestingly, while increasing a measure of AD-like pathology. Their work brings up several interesting new questions and adds to a growing body of literature that highlights how the relationship between cognition and amyloid pathology is not as clearcut as once thought.