Cognitive deficits in experimental autoimmune encephalomyelitis: Neuroinflammation and synaptic degeneration

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

Research output: Contribution to journalArticle

42 Citations (Scopus)

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.

Original languageEnglish
JournalNeurological Sciences
Volume31
Issue numberSUPPL. 2
DOIs
Publication statusPublished - Nov 2010

Fingerprint

Autoimmune Experimental Encephalomyelitis
Multiple Sclerosis
Microglia
Neurobehavioral Manifestations
Synaptic Transmission
Cognition
Glutamic Acid
Central Nervous System
Learning
Lymphocytes
Cytokines
T-Lymphocytes
Antigens

Keywords

  • EAE
  • Excitotoxicity
  • GABA interneurons
  • Microglia
  • Synaptic alteration

ASJC Scopus subject areas

  • Clinical Neurology
  • Psychiatry and Mental health
  • Dermatology

Cite this

Cognitive deficits in experimental autoimmune encephalomyelitis : Neuroinflammation and synaptic degeneration. / Mandolesi, G.; Grasselli, G.; Musumeci, G.; Centonze, Diego.

In: Neurological Sciences, Vol. 31, No. SUPPL. 2, 11.2010.

Research output: Contribution to journalArticle

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