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Old 04-30-2009, 09:03 AM #1
Bearygood Bearygood is offline
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Default Gray Matter Under Attack In Multiple Sclerosis: Protein Could Provoke Immune Attack O

Interesting!

http://www.sciencedaily.com/releases...0430065813.htm

Quote:
It is only a recent discovery that the immune system actually attacks the gray matter in the early stages, along with the myelin sheathing. “
Quote:
In the course of their investigations, they identified Contactin-2 as a new autoantigen – a molecular structure that belongs to the body but which provokes an immune response. This protein is found in the brain and spinal cord, and is present in both the myelin sheathing and in the neurons themselves – which means it exists in the gray matter. "Contactin-2 triggers an immune response in which T-cells and antibodies turn against this molecule,” reports Meinl. “In some ways, this immune response is similar to those that occur in pathogen-induced inflammations.”
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Old 04-30-2009, 03:22 PM #2
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Default YES---MS is not just a demyelinating disease

This is THE definitive study to prove that MS is not just a demyelinating disease.

JackD



Quote:
1: N Engl J Med. 1998 Jan 29;338(5):278-85.

N Engl J Med. 1998 Jan 29;338(5):323-5.

Axonal transection in the lesions of multiple sclerosis.

Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mork S, Bo L.

Department of Neurosciences, Lerner Research Institute, Cleveland Clinic
Foundation, OH 44195, USA.

BACKGROUND: Multiple sclerosis is an inflammatory demyelinating disease of the
central nervous system and is the most common cause of neurologic disability in
young adults. Despite antiinflammatory or immunosuppressive therapy, most
patients have progressive neurologic deterioration that may reflect axonal loss.
We conducted pathological studies of brain tissues to define the changes in
axons in patients with multiple sclerosis.

METHODS: Brain tissue was obtained at
autopsy from 11 patients with multiple sclerosis and 4 subjects without brain
disease. Fourteen active multiple-sclerosis lesions, 33 chronic active lesions,
and samples of normal-appearing white matter were examined for demyelination,
inflammation, and axonal pathologic changes by immunohistochemistry and confocal
microscopy. Axonal transection, identified by the presence of terminal axonal
ovoids, was detected in all 47 lesions and quantified in 18 lesions.

RESULTS:
Transected axons were a consistent feature of the lesions of multiple sclerosis,
and their frequency was related to the degree of inflammation within the lesion.
The number of transected axons per cubic millimeter of tissue averaged 11,236 in
active lesions
, 3138 at the hypocellular edges of chronic active lesions, 875 in
the hypocellular centers of chronic active lesions, and less than 1 in
normal-appearing white matter from the control brains.

CONCLUSIONS: Transected
axons are common in the lesions of multiple sclerosis, and axonal transection
may be the pathologic correlate of the irreversible neurologic impairment in
this disease.

PMID: 9445407 [PubMed - indexed for MEDLINE]
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