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Cell-surface sugar defects may trigger nerve damage in multiple sclerosis patients
September 21, 2007Defects on cell-surface sugars may promote the short-term inflammation and long-term neurodegeneration that occurs in the central nervous system of multiple sclerosis patients, according to University of California, Irvine researchers.
The findings also suggest that a dietary supplement similar to glucosamine may be useful as an oral therapy to correct these defects and to treat both the short-term and the long-term symptoms of the disease. Study results appear on the online version of the Journal of Biological Chemistry.
"The findings raise the possibility that these may both be treated by metabolic therapy," said Dr. Michael Demetriou, an assistant professor of neurology, and microbiology and molecular genetics. "This is particularly important, as therapies are not currently available to treat neurodegeneration in MS."
In tests on mice, Demetriou found that genetic deficiencies in a process called protein glycosylation led to a spontaneous disease very similar to MS, including paralysis associated with inflammatory damage to the protective myelin coating on nerve cells and degeneration of axons and neurons. Protein glycosylation refers to the addition of specific sugars to proteins; virtually all cell-surface and secreted proteins have complex sugars attached to them.
MS is a two-stage disease, with initial attacks of inflammatory demyelination, which damages myelin, followed approximately 10 years later by a slow, progressive neurdegenerative phase marked by loss of axons and nerve cells.
The irreversible damage to the central nervous system induced by neurodegeneration in MS leads to long term disability, including paralysis, incoordination, dementia and pain, and is not targeted by currently available therapies.
Demetriou's findings provide the first genetic model of MS in which both inflammatory demyelination and neurodegeneration arise from defects in a single biological pathway.
In previous studies, Demetriou found that the dietary supplement N-acetylglucosamine (GlcNAc), which is similar but more effective than the widely available glucosamine, corrected defects in protein glycosylation in cells and inhibited inflammatory demyelination in mice. The new study opens the possibility that metabolic therapy with GlcNAc may also prevent neurodegeneration. Studies in humans are required to assess the potential of this therapy in MS.
University of California - Irvine
In tests on mice, Demetriou found that genetic deficiencies in a process called protein glycosylation led to a spontaneous disease very similar to MS, including paralysis associated with inflammatory damage to the protective myelin coating on nerve cells and degeneration of axons and neurons. Protein glycosylation refers to the addition of specific sugars to proteins; virtually all cell-surface and secreted proteins have complex sugars attached to them.
MS is a two-stage disease, with initial attacks of inflammatory demyelination, which damages myelin, followed approximately 10 years later by a slow, progressive neurdegenerative phase marked by loss of axons and nerve cells.
The irreversible damage to the central nervous system induced by neurodegeneration in MS leads to long term disability, including paralysis, incoordination, dementia and pain, and is not targeted by currently available therapies.
Demetriou's findings provide the first genetic model of MS in which both inflammatory demyelination and neurodegeneration arise from defects in a single biological pathway.
In previous studies, Demetriou found that the dietary supplement N-acetylglucosamine (GlcNAc), which is similar but more effective than the widely available glucosamine, corrected defects in protein glycosylation in cells and inhibited inflammatory demyelination in mice. The new study opens the possibility that metabolic therapy with GlcNAc may also prevent neurodegeneration. Studies in humans are required to assess the potential of this therapy in MS.
University of California - Irvine
Neurodegeneration News and Current Neurodegeneration Events RSSRhode Island Hospital study finds link between obesity, type 2 diabetes and neurodegeneration
New research from Rhode Island Hospital found that obesity and Type 2 Diabetes Mellitus (T2DM) can contribute to mild neurodegeneration with features common with Alzheimer's disease (AD) - the first study to show that obesity can cause neurodegeneration.
Study finds B-vitamin deficiency may cause vascular cognitive impairment
A deficiency of B-vitamins may cause vascular cognitive impairment, according to a new study. Researchers at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts University used an experimental model to examine the metabolic, cognitive, and microvascular effects of dietary B-vitamin deficiency.
MIT zeroes in on Alzheimer's structures
MIT engineers report a new approach to identifying protein structures key to Alzheimer's disease, an important step toward the development of new drugs that could prevent such structures from forming.
Lou Gehrig's protein found throughout brain, suggesting effects beyond motor neurons
Two years ago researchers at the University of Pennsylvania School of Medicine discovered that misfolded proteins called TDP-43 accumulated in the motor areas of the brains of patients with amyotropic lateral sclerosis (ALS), or Lou Gehrig's disease.
Genetics of ALS progression
An upcoming paper from Drs. Hidenori Ichijo and Hideki Nishitoh (The University of Tokyo) and colleagues lends new and valuable insight into the genetics of ALS.
'Intrabody' can mop up mutant protein in Huntington's disease model
Scientists have created a tool for mopping up the clumps of mutant protein that drive neurodegeneration in Huntington's disease. Emory University researchers engineered a virus to make an intracellular antibody or "intrabody" against huntingtin, the protein whose mutant forms poison the brain cells of people with Huntington's.
RNA Toxicity Contributes to Neurodegenerative Disease, University of Pennsylvania Scientists Say
Expanding on prior research performed at the University of Pennsylvania, Penn biologists have determined that faulty RNA, the blueprint that creates mutated, toxic proteins, contributes to a family of neurodegenerative disorders in humans.
Researchers uncover mechanism of action of antibiotic able to reduce neuronal cell death in brain
Virginia Commonwealth University researchers have discovered how an antibiotic works to modulate the activity of a neurotransmitter that regulates brain functions, which eventually could lead to therapies to treat Alzheimer's disease, Huntington's disease, epilepsy, stroke, dementia and malignant gliomas.
'Rotten eggs' in the blood
Hydrogen sulphide (H2S) is a gas most commonly associated with the smell of stink bombs, sewage and rotten eggs, but a team of researchers from the Peninsula Medical School in the South West of England and King's College London have now identified a role for this gas in regulating blood pressure, according to research published today in the leading science journal "Circulation".
Investigators unveil new drug discovery tool for Alzheimer's disease
An article published in the April issue of the Journal of Alzheimer's Disease presents a detailed characterization of a new drug discovery tool for Alzheimer's disease.
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