Bad Ac-etylated Tau

Jane C Hettinger; John R Cirrito

doi:10.1016/j.neuron.2016.04.008

Bad Ac-etylated Tau

Neuron. 2016 Apr 20;90(2):205-6. doi: 10.1016/j.neuron.2016.04.008.

Authors

Jane C Hettinger¹, John R Cirrito²

Affiliations

¹ Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
² Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: cirritoj@neuro.wustl.edu.

PMID: 27100190
DOI: 10.1016/j.neuron.2016.04.008

Abstract

By using a tau construct with two mimicked acetylation sites as identified in AD brains, Tracy et al. (2016) found that acetylated tau promotes synaptic dysfunction through disruption of postsynaptic KIBRA signaling pathways, actin dynamics, and AMPA receptor trafficking.

Keywords: Alzheimer’s disease; KIBRA; acetylation; post-translational modification; tau; tauopathy.

Publication types

Comment

MeSH terms

Alzheimer Disease*
Brain
Humans
Receptors, AMPA
Signal Transduction
tau Proteins*

Substances

Receptors, AMPA
tau Proteins