Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016053 (fibromyalgia)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Membrane Lipid Replacement is the use of functional oral supplements containing cell membrane glycerolphospholipids and antioxidants to safely replace damaged membrane lipids that accumulate during aging and in various chronic and acute diseases. Most if not all clinical conditions and aging are characterized by membrane phospholipid oxidative damage, resulting in loss of membrane and cellular function. Clinical trials have shown the benefits of Membrane Lipid Replacement supplements in replenishing damaged membrane lipids and restoring mitochondrial function, resulting in reductions in fatigue in aged subjects and patients with a variety of clinical diagnoses. Recent observations have indicated that Membrane Lipid Replacement can be a useful natural supplement strategy in a variety of conditions: chronic fatigue, such as found in many diseases and disorders; fatiguing illnesses (fibromyalgia and chronic fatigue syndrome); chronic infections (Lyme disease and mycoplasmal infections); cardiovascular diseases; obesity, metabolic syndrome and diabetes; neurodegenerative diseases (Alzheimer's disease); neurobehavioral diseases (autism spectrum disorders); fertility diseases; chemical contamination (Gulf War illnesses); and cancers (breast, colorectal and other cancers). Membrane Lipid Replacement provides general membrane nutritional support during aging and illness to improve membrane function and overall health without risk of adverse effects.
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PMID:Clinical Uses of Membrane Lipid Replacement Supplements in Restoring Membrane Function and Reducing Fatigue in Chronic Diseases and Cancer. 3230 76

Multiple sclerosis is a progressive autoimmune disorder of the myelin sheath and is the most common inflammatory disease of young adults. Up to 65% of multiple sclerosis patients have cognitive impairments such as memory loss and difficulty in understanding and maintaining attention and concentration. Many pharmacological interventions have been used to reverse motor impairments in multiple sclerosis patients; however, none of these drugs improve cognitive function. Melatonin can diffuse through the blood-brain barrier and has well-known antioxidant and anti-inflammatory properties with almost no side effects; it is, therefore, a promising neuroprotective supplement for many neurological diseases, such as multiple sclerosis, Alzheimer's disease, Parkinson's disease, ischemic stroke, and fibromyalgia. However, only some researches have assessed the effect of melatonin on cognitive dysfunction in multiple sclerosis. Here, we evaluated the effects of melatonin supplementation on memory defects induced by cuprizone in a mouse model of multiple sclerosis. Cuprizone (400 mg/kg) and melatonin (80 mg/kg) were administered to SWR/J mice daily for 5 weeks. Open field, tail-flick, and novel object recognition behavioral tests were performed. Also, expression of cAMP-response element-binding protein, synaptophysin, and postsynaptic density protein 95 were measured in the prefrontal cortex. Melatonin significantly improved the memory defects induced by cuprizone toxicity by up-regulating cAMP-response element-binding protein and by increasing expression of the synapse-associated synaptophysin and postsynaptic density protein 95 genes in the prefrontal cortex. These results indicate that melatonin may provide protective effects against memory impairments associated with multiple sclerosis.
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PMID:Melatonin improves memory defects in a mouse model of multiple sclerosis by up-regulating cAMP-response element-binding protein and synapse-associated proteins in the prefrontal cortex. 3270 87


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