Abstract
Sickness in mammals can lead to cognition deficits, although the underlying mechanisms remain elusive. In a recent Nature Medicine article, Garré et al. (2017) report that sickness-induced cortical dendritic spine loss and impaired memory formation is mediated by CX3CR1+ monocyte-derived TNF-α.
Copyright © 2017 Elsevier Inc. All rights reserved.
MeSH terms
-
Animals
-
CX3C Chemokine Receptor 1
-
Dendritic Spines / physiology*
-
Humans
-
Memory
-
Mental Disorders / etiology
-
Mental Disorders / immunology*
-
Mental Disorders / psychology
-
Mice
-
Monocytes / physiology*
-
Monocytes / virology
-
Motor Neurons / physiology*
-
Motor Neurons / virology
-
Nerve Net*
-
Neuronal Plasticity*
-
Poly I-C / immunology
-
Receptors, Chemokine / metabolism
-
Tumor Necrosis Factor-alpha / metabolism
-
Virus Diseases / complications
-
Virus Diseases / immunology*
-
Virus Diseases / psychology
Substances
-
CX3C Chemokine Receptor 1
-
Cx3cr1 protein, mouse
-
Receptors, Chemokine
-
Tumor Necrosis Factor-alpha
-
Poly I-C