Nisticò R, Mori F, Feligioni M, Nicoletti F, Centonze D. Synaptic plasticity in multiple sclerosis and in experimental autoimmune encephalomyelitis.Philos Trans R Soc Lond B Biol Sci. 2013 ;369(1633):20130162. doi: 10.1098/rstb.2013.0162. Print 2014.
Approximately half of all people 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.
The Hippocampus (looks like a sea horse) is a site in the brain where memories are formed and can be affected in MS. Promoting plasticity will help overcome disability associated with MS