Cognitive deficits in experimental autoimmune encephalomyelitis: neuroinflammation and synaptic degeneration.

Neurological Sciences : Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
Georgia MandolesiDiego Centonze

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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Citations

Mar 19, 2013·Journal of Molecular Neuroscience : MN·Hung HsuchouWeihong Pan
Oct 8, 2013·Prostaglandins, Leukotrienes, and Essential Fatty Acids·Sara Palumbo, Francesca Bosetti
Jul 31, 2013·Neuromolecular Medicine·Francesco MoriDiego Centonze
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