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Cognitive deficits in experimental autoimmune encephalomyelitis: Neuroinflammation and synaptic degeneration
- Source :
- Neurological Sciences
- Publication Year :
- 2010
- Publisher :
- SPRINGER-VERLAG ITALIA SRL, 2010.
-
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.
- Subjects :
- EAE
Excitotoxicity
GABA interneurons
Microglia
Synaptic alteration
Animals
Brain
Cognition Disorders
Encephalomyelitis, Autoimmune, Experimental
Inflammation
Mice
Nerve Degeneration
Synapses
Encephalomyelitis
Central nervous system
Clinical Neurology
Dermatology
Experimental
medicine
Neuroinflammation
Multiple sclerosis
Experimental autoimmune encephalomyelitis
Neurodegeneration
General Medicine
medicine.disease
Psychiatry and Mental health
medicine.anatomical_structure
Immunology
Settore MED/26 - Neurologia
Synaptopathy
Neurology (clinical)
Psychology
Neuroscience
Autoimmune
Subjects
Details
- Language :
- English
- Database :
- OpenAIRE
- Journal :
- Neurological Sciences
- Accession number :
- edsair.doi.dedup.....f717ef17ad885803aa425c07f0372326