NDLI: Cdk5 is a New Rapid Synaptic Homeostasis Regulator Capable of Initiating the Early Alzheimer-Like Pathology.

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Cdk5 is a New Rapid Synaptic Homeostasis Regulator Capable of Initiating the Early Alzheimer-Like Pathology.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sheng, Yanghui Zhang, Lei Su, Susan C. Tsai, Li-Huei Julius Zhu, J.
Description	Country affiliation: Moldova Author Affiliation: Sheng Y ( Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA Undergraduate Class of 2011, Yuanpei Honors College, Peking University, Beijing 100871, China Current address: Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD); Zhang L ( Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.); Su SC ( Picower Institute for Learning and Memory and Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.); Tsai LH ( Picower Institute for Learning and Memory and Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.); Julius Zhu J ( Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.)
Abstract	Cyclin-dependent kinase 5 (Cdk5) is a serine/threonine kinase implicated in synaptic plasticity, behavior, and cognition, yet its synaptic function remains poorly understood. Here, we report that physiological Cdk5 signaling in rat hippocampal CA1 neurons regulates homeostatic synaptic transmission using an unexpectedly rapid mechanism that is different from all known slow homeostatic regulators, such as beta amyloid (Aß) and activity-regulated cytoskeleton-associated protein (Arc, aka Arg3.1). Interestingly, overproduction of the potent Cdk5 activator p25 reduces synapse density, and dynamically regulates synaptic size by suppressing or enhancing Aß/Arc production. Moreover, chronic overproduction of p25, seen in Alzheimer's patients, induces initially concurrent reduction in synapse density and increase in synaptic size characteristic of the early Alzheimer-like pathology, and later persistent synapse elimination in intact brains. These results identify Cdk5 as the regulator of a novel rapid form of homeostasis at central synapses and p25 as the first molecule capable of initiating the early Alzheimer's synaptic pathology.
File Format	HTM / HTML
ISSN	10473211
e-ISSN	14602199
Journal	Cerebral Cortex
Issue Number	7
Volume Number	26
Language	English
Publisher	Oxford University Press
Publisher Date	2016-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Neuroscience Discipline Neurology
Content Type	Text
Resource Type	Article
Subject	Cognitive Neuroscience Cellular and Molecular Neuroscience

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