Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.02.280321v1?rss=1 Authors: Du, Q., Chang, J., Cheng, G., Zhou, W. Abstract: Dendritic abnormality is the pathological hallmark of Alzheimer's disease (AD), but its underlying mechanism remains elusive. Here we showed that amyloid precursor protein (APP), the precursor of {beta}-amyloid, caused dendritic defects in dendritic arborization neurons of Drosophila accompanied by Golgi outposts (GOPs) disorders. Half of the dendritic APP co-localized with GOPs, impairing their distribution and compartmental organization; in particular, the dynamic behaviors. By analyzing the state of anterograde/retrograde movements, we found that the motor protein dynein and its adapter protein Sunday driver (Syd) mediated APP-induced dynamic alterations of multi-compartment GOPs (mcGOPs) rather than single-compartment GOPs (scGOPs). Moreover, the loss of Syd rescued the defects of dendritic complexity caused by APP. Our findings indicate that APP resident in GOPs disrupts the equilibrium of anterograde/retrograde movements of mcGOPs maintained by dynein/Syd complex, resulting in dendritic abnormalities. This offers new insight into dendritic pathology in AD. Copy rights belong to original authors. Visit the link for more info