JNeurosci: Highlights From the October 26 Issue
Check out these newsworthy studies from the October 26, 2016, issue of JNeurosci. Media interested in obtaining the full text of the studies should contact media@sfn.org.
High levels of uric acid in the blood can accompany obesity, hypertension, and metabolic disorders, and have been linked to cognitive and memory deficits. In a new study in rats, researchers find a diet high in uric acid triggers inflammation in the hippocampus, an area of the brain critical for learning and memory. Blocking a specific protein pathway protects against inflammation in the hippocampus and cognitive dysfunction. The findings shed light on the mechanism linking uric acid to cognitive deficits and offer a potential strategy for preventing them.
Corresponding author: Xiaobo Cen, xbcen@scu.edu.cn
In response to a traumatic nerve injury, the immune cells of the central nervous system — microglia — may present a double-edged sword: While they respond quickly to clean up damaged tissue, they also secrete an excess of pro-inflammatory chemicals that can damage neurons further. In a new study in mice, researchers identify a specific signaling pathway in microglia that induces inflammation in the spinal cord and exacerbates neuropathic pain. However, previous studies have found that activation of this pathway is actually protective against Alzheimer’s disease.
Corresponding author: Hiroshi Kiyama, kiyama@med.nagoya-u.ac.jp
By shuttling electrically charged atoms, or ions, in and out of cells, ion channels generate the electrical signals neurons use to communicate. Oxidants alter a specific type of potassium channel, impairing its ability to conduct electrical current, and researchers have previously found a buildup of these aberrant channels in mouse models of neurodegenerative diseases. In a new study in mice, researchers demonstrate that potassium channel oxidation causes cellular and cognitive deficits after a traumatic brain injury (TBI). They also find dasatinib — an FDA-approved drug to treat leukemia — reduces cellular and cognitive deficits caused by channel oxidation after TBI.
Corresponding author: Federico Sesti, sestife@rwjms.rutgers.edu
is published by the 黑料社, an organization of nearly 38,000 basic scientists and clinicians who study the brain and nervous system.
