SnapShot: Neuronal dysfunction in inflammation

Matthias Kneussel; Manuel A Friese

doi:10.1016/j.neuron.2021.03.005

SnapShot: Neuronal dysfunction in inflammation

Neuron. 2021 May 19;109(10):1754-1754.e1. doi: 10.1016/j.neuron.2021.03.005.

Authors

Matthias Kneussel¹, Manuel A Friese²

Affiliations

¹ Institute of Molecular Neurogenetics, Center for Molecular Neurobiology Hamburg (ZMNH), University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
² Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology Hamburg (ZMNH), University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.

PMID: 34015268
DOI: 10.1016/j.neuron.2021.03.005

Abstract

Neuronal function relies on tightly controlled cytoskeleton transport with adaptive cargo trafficking as prerequisite for synaptic transmission. During inflammation in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), axonal transport efficiency declines, followed by neurodegeneration. Furthermore, neuroinflammation causes an imbalance between excitatory and inhibitory transmission, triggering synaptic dysfunction and loss. Recent data suggest that neuronal transport and synaptic deficits during neuroinflammation are functionally interconnected. To view this SnapShot, open or download the PDF.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Cytokines / metabolism
Encephalomyelitis, Autoimmune, Experimental / immunology
Encephalomyelitis, Autoimmune, Experimental / physiopathology*
Humans
Multiple Sclerosis / immunology
Multiple Sclerosis / physiopathology*
Neurons / immunology
Neurons / physiology*
Synaptic Transmission

Substances

Cytokines