Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental allergic encephalomyelitis (EAE) is widely considered as an animal model of multiple sclerosis (MS). Damage to the bulbospinal serotonergic (5-HT) neurons occurs in the early paralytic stages of EAE in rats with the severity of neurologic signs corresponding to spinal serotonergic depletion. Neurologic recovery of EAE rats is associated with reestablishment of spinal 5-HT transmission possibly through sprouting of undamaged axons and nerve terminals. Damage to the bulbospinal serotonergic fibers also occurs in patients with MS (as reflected by reduced lumbar CSF 5-HIAA levels) and may contribute to several manifestations of the disease including autonomic dysregulation, sensory symptoms (i.e., paresthesias, pain) and motor symptoms (weakness, spasticity, clonus). Spinal serotonergic neuronal sprouting with regeneration of 5-HT nerve terminals may also occur in the early stages of MS and may be associated with spontaneous remission of MS symptoms following an acute relapse. Sprouting of serotonergic neurons may also explain the disparity in MS between the extent of demyelinating plaques and clinical signs of the disease. The chronic course of MS may be associated with progressive axonal degenerative changes with reduction of serotonergic nerve terminals and loss of their sprouting capability. It is proposed that the beneficial effects of treatment with AC pulsed electromagnetic fields on the symptoms and course of the disease in patients with chronic progressive MS may be related in part to renewed sprouting of serotonergic neurons.
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PMID:Serotonergic neuronal sprouting as a potential mechanism of recovery in multiple sclerosis. 1068 Nov 22

The aim of this study was to investigate the role of monoamine neurotransmitters on the severity of experimental autoimmune encephalomyelitis (EAE) in obese mice. EAE was induced in mice with normal diets (ND-EAE) and obese mice with high-fat diets (HFD-EAE) through the immune response to myelin oligodendrocyte glycoprotein (MOG) (35-55). The levels of dopamine (DA), serotonin (5-HT) and their metabolites in different anatomical brain regions were measured by high-performance liquid chromatography. The plasma and tissue NADPH oxidase and matrix metalloproteinases (MMP)-9 activities were analyzed by fluorescence spectrophotometry. The cumulative disease index and disease peaks were significantly higher in HFD-EAE compared with those in ND-EAE. Significantly higher 5-HT levels and lower 5-HT turnovers 5-hydroxyindole acetic acid ((5-HIAA)/5-HT) were found in the brains of HFD-EAE mice compared with those found in the HFD-CON and ND-EAE mice brains. Moreover, increased DA levels were observed in the caudate nucleus of the HFD-EAE mice compared with the control and ND-EAE mice. The NADPH oxidase and MMP-9 activities in the plasma and tissues were significantly higher in both the ND-EAE and HFD-EAE groups than in their respective controls. The cytokine levels in the plasma, tissues, and cultured splenocytes were found to be significantly altered in EAE mice compared with control mice. Moreover, HFD-EAE mice exhibited significantly higher MMP-9 activity and lower IL-4 levels than ND-EAE mice and were significantly correlated with brain 5-HT levels. In conclusion, the increased 5-HT levels in the brain significantly correlated with MMP-9 activity and IL-4 levels play an important role in the exacerbation of disease severity in HFD-EAE mice.
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PMID:Increased levels of brain serotonin correlated with MMP-9 activity and IL-4 levels resulted in severe experimental autoimmune encephalomyelitis (EAE) in obese mice. 2682 May 99