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More MS news articles for August 2003

Excitatory amino acids and multiple sclerosis: evidence from cerebrospinal fluid

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12925363&dopt=Abstract

Arch Neurol. 2003 Aug;60(8):1082-8
Sarchielli P, Greco L, Floridi A, Floridi A, Gallai V.
Neuroscience Department, Institute of Clinical and Applied Biochemistry, Policlinico Monteluce, University of Perugia, Via E Dal Pozzo, 06126 Perugia, Italy.

BACKGROUND:

Recent evidence suggests an altered glutamate homeostasis in the brain of patients with multiple sclerosis (MS), as seen in experimental models of MS.

OBJECTIVE:

To test whether the excitotoxic insult contributes to the pathological process in MS by measuring glutamate and aspartate levels in the cerebrospinal fluid of MS patients and control individuals.

PARTICIPANTS:

Twenty-five patients with the relapsing-remitting form of MS during a stable clinical phase, 30 patients with relapsing-remitting MS during relapse, and 25 patients with the secondary progressive form of MS were included in the study.

Data were compared with those of 20 age-matched control subjects without diseases of the central and peripheral nervous systems.

METHODS:

Glutamate and aspartate levels in the cerebrospinal fluid were measured by high-performance liquid chromatography.

RESULTS:

Cerebrospinal fluid glutamate levels were significantly higher in patients assessed during relapse compared with those of the patients with relapsing-remitting MS examined during the stable clinical phase and the controls (P<.001).

The levels of glutamate detected in patients with relapsing-remitting MS during the stable phase who had active lesions were significantly higher than in those without neuroradiological evidence of disease activity (P<.001).

Significantly higher levels of glutamate were found in patients with secondary progressive MS with an increase of 1 or more points on the Expanded Disability Status Scale score compared with stable patients with secondary progressive MS and control subjects (P<.001).

CONCLUSIONS:

Neurotoxic events occur in MS patients, and they can be responsible for oligodendrocyte and neuronal cell death in patients with this demyelinating disease.

The manipulation of glutamate-altered homeostasis or antagonizing glutamate receptor-mediated excitotoxicity may have therapeutic implications in MS patients.