Rogue Proteins Found in MS Brains

Could multiple sclerosis be caused by a “rogue protein” that attacks the central nervous system?

That’s the hypothesis of a research team from the University of Surrey, Guildford, UK and researchers at the University of Texas Houston Medical School’s Mitchell Center for Alzheimer’s Disease and Related Brain Disorders.

Working with the Antibody Discovery Laboratory / PrioCam in Houston, TX, the researchers created antibodies that confirmed that certain proteins normally associated with Alzheimer’s disease and Parkinson’s disease also appeared in lesions and plaques of MS patients. They used brain tissue and cerebrospinal fluid from MS patients collected at autopsies and stored at the UK Multiple Sclerosis Tissue Bank.

They concluded that these “rogue proteins” associated with other degenerative neurological diseases may trigger MS. The proteins included Amyloid beta, tau protein, and amyloid precursor protein.

“Our research indicates that rogue proteins share a common structure and may share similar pathogenic mechanisms,” said senior author Monique David, “this study consistently and reproducibly links the presence of abnormally shaped proteins to multiple sclerosis.”

The researchers hypothesized that oligoclonal antibodies consistently found in MS patients are stimulated by toxic soluble oligomers and are secreted through the T-cell-independent B-cell immune response.

The study was published online Dec. 2, 2014 in Frontiers in Neurology.

The work shows for the first time that protein aggregates detected by anti-oligomer specific antibodies are associated with MS, researchers Monique Antoinette David of the University of Texas and Mourad Tayebi of the University of Surrey wrote in the journal article.

The researchers concede that “the pathogenic relevance of thes MS associated soluble oligomers to disease process remains to be investigated.” But they said “this study sets the ground for further investigating this relationship.”

The study was funded by the George and Cynthia Mitchell Foundation.