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Published in: Neurological Sciences 2/2010

01-11-2010

Cognitive deficits in experimental autoimmune encephalomyelitis: neuroinflammation and synaptic degeneration

Authors: G. Mandolesi, G. Grasselli, G. Musumeci, Diego Centonze

Published in: Neurological Sciences | Special Issue 2/2010

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Abstract

Multiple sclerosis (MS) is characterized by auto-reactive T cells that respond to central nervous system (CNS)-based antigens and affect motor, sensory as well as behavioral and cognitive functions. Cognitive deficits are now considered an early manifestation of the disease in MS patients. However, the pathophysiology responsible for the cognitive symptoms in MS remains unclear. Increasing evidence from a mouse model of MS, the experimental autoimmune encephalomyelitis (EAE), suggests a correlation between the synaptopathy induced by microglia activation in the early phase of the disease and cognitive dysfunction. In particular, EAE causes deficits in hippocampal-dependent learning and memory that are associated with early microglial activation, synaptic loss and neurodegeneration. Interestingly, inflammatory cytokines released from infiltrating lymphocytes or activated microglia are able to alter synaptic transmission. Increased glutamate-mediated transmission and loss of GABAergic inputs were observed in EAE. They may thus underlie cognitive dysfunction in this model and in MS.
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Metadata
Title
Cognitive deficits in experimental autoimmune encephalomyelitis: neuroinflammation and synaptic degeneration
Authors
G. Mandolesi
G. Grasselli
G. Musumeci
Diego Centonze
Publication date
01-11-2010
Publisher
Springer Milan
Published in
Neurological Sciences / Issue Special Issue 2/2010
Print ISSN: 1590-1874
Electronic ISSN: 1590-3478
DOI
https://doi.org/10.1007/s10072-010-0369-3

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