An ECSIT‐centric view of Alzheimer's disease (Comment on DOI 10.1002/bies.201100193)

Characterization, molecular cloning, and expression analysis of Ecsit in the spinyhead croaker, Collichthys lucidus

“…In 2011, West et al (2011) reported that Ecsit could interact with TRAF6 in mitochondria, which led to ubiquitination and enrichment at the mitochondrial periphery, thus increasing the generation of mitochondrial and cellular reactive oxygen species, and contributing to the bactericidal activity of mouse macrophages. Based on our understanding of mitochondrial and immune functions, some researchers have suggested that Ecsit may be used as a biomarker for future therapies to halt or prevent inflammation, oxidative stress, and neurodegenerative disorders related to mitochondrial dysfunctions (Milward et al, 2007;Mattson, 2012;Soler-López et al, 2012).…”

ECSIT prevents Alzheimer’s disease pathology by regulating neuronal mitochondrial ROS and mitophagy

“…In this study, we demonstrate that dysregulation of the mitochondrial protein ECSIT is associated with the development of AD and contributes to the development of AD-like pathology in animal models. An analysis of reported and predicted ECSIT interactions with redox and mitochondrial proteins encoded by AD susceptibility genes led to the hypothesis that ECSIT might be an interaction hub for many of these proteins, including PSEN1, and could thus play an important role in the etiology of AD 28, 29, 62, 63 . A role for mitochondrial dysfunction and mitochondrial ROS in AD had been suggested based on multiple studies, leading to the “mitochondrial cascade hypothesis” 4–7, 11, 33, 64 .…”