Synaptic plasticity in multiple sclerosis and in experimental autoimmune encephalomyelitis

Robert Nisticò, Francesco Mori, Marco Feligioni, Ferdinando Nicoletti, Diego Centonze

Research output: Contribution to journalArticlepeer-review


Approximately half of all patients with multiple sclerosis (MS) experience cognitive dysfunction, including learning and memory impairment. Recent studies suggest that hippocampal pathology is involved, although the mechanisms underlying these deficits remain poorly understood. Evidence obtained from a mouse model of MS, the experimental autoimmune encephalomyelitis (EAE), suggests that in the hippocampus of EAE mice long-term potentiation (LTP) is favoured over long-term depression in response to repetitive synaptic activation, through a mechanism dependent on enhanced IL-1β released from infiltrating lymphocytes or activated microglia. Facilitated LTP during an immune-mediated attack might underlie functional recovery, but also cognitive deficits and excitotoxic neurodegeneration. Having identified that pro-inflammatory cytokines such as IL-1β can influence synaptic function and integrity in early MS, it is hoped that new treatments targeted towards preventing synaptic pathology can be developed.

Original languageEnglish
Article number20130162
JournalPhilosophical transactions of the Royal Society of London. Series B: Biological sciences
Issue number1633
Publication statusPublished - Jan 5 2014


  • Experimental autoimmune encephalomyelitis
  • Hippocampus
  • Interleukin-1β
  • Long-term potentiation
  • Multiple sclerosis
  • Synaptic plasticity

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)


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