Display options
Cite
Barry R, Payton M, Groome N. Characterization of myelin basic protein catabolism products in the cerebrospinal fluid from multiple sclerosis, stroke and head injury patients. Neurochem Int. 1991;18(2):291-300doi: 10.1016/0197-0186(91)90197-l.
Barry, R., Payton, M., & Groome, N. (1991). Characterization of myelin basic protein catabolism products in the cerebrospinal fluid from multiple sclerosis, stroke and head injury patients. Neurochemistry international, 18(2), 291-300. https://doi.org/10.1016/0197-0186(91)90197-l
Barry, R, et al. "Characterization of myelin basic protein catabolism products in the cerebrospinal fluid from multiple sclerosis, stroke and head injury patients." Neurochemistry international vol. 18,2 (1991): 291-300. doi: https://doi.org/10.1016/0197-0186(91)90197-l
Barry R, Payton M, Groome N. Characterization of myelin basic protein catabolism products in the cerebrospinal fluid from multiple sclerosis, stroke and head injury patients. Neurochem Int. 1991;18(2):291-300. doi: 10.1016/0197-0186(91)90197-l. PMID: 20504705.
Copy Download .nbib Format: NLM
Share it on

Neurochem Int. 1991;18(2):291-300. doi: 10.1016/0197-0186(91)90197-l.

Characterization of myelin basic protein catabolism products in the cerebrospinal fluid from multiple sclerosis, stroke and head injury patients.

Neurochemistry international

R Barry, M Payton, N Groome

Affiliations

  1. School of Biological and Molecular Sciences, Oxford Polytechnic, Gipsy Lane, Headington OX3 OBP, U.K.

PMID: 20504705 DOI: 10.1016/0197-0186(91)90197-l

Abstract

Polyclonal antisera were raised to thirteen synthetic peptides corresponding to different regions of the human myelin basic protein molecule. These were used with a radioligand of human myelin basic protein to establish region-specific assays for the detection of myelin basic protein catabolism products in spinal fluid. The limits of detection for the various assays ranged from 0.2 to 2.5 ng/ml human myelin basic protein. These assays were used to search for evidence of myelin basic protein-like immunoreactivity in spinal fluids from multiple sclerosis, stroke and head injury patients. Generally, those assays specific for regions in the centre of the molecule measured the largest amounts of material and this was true for all the samples regardless of aetiology. It would appear from the results of this preliminary study that any disease specific pattern of peptides is superimposed on to a strong general background pattern. The simultaneous detection in individual spinal fluid samples of material cross-reactive with anti-peptide antibodies raised to multiple different regions of myelin basic protein is strong evidence that the material is in fact derived from myelin basic protein. The region-specific antisera described in this study should prove valuable reagents for the continued study of myelin basic protein catabolism.

Publication Types