Researchers have discovered a genetic mutation associated with this typical motor neuron disease or amyotrophic lateral sclerosis, which has a pathological effect similar to certain genetic mutations have shown in previous studies. Ultimately, researchers hope that understanding what causes motor neuron disease (MND) will lead to new ways of treatment.

MDN is a progressive neurodegenerative disease that attacks the upper and lower motor neurons. The degeneration of motor neurons causes weakness and atrophy of muscles, causing increasing loss of mobility in the limbs, difficulty speaking, swallowing and breathing.

The new research, published today in the journal Proceedings of the National Academy of Sciences and conducted by researchers from Imperial College London, provides strong additional evidence that genetics is a disease caused by the protein reconstituted in motor neurons, cells that help control muscle movement.

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An international survey of scientists from New Zealand and Denmark revealed exactly how the superbug Staphylococcus aureus escapes the body’s immune defenses key.

Maurice Wilkins Centre scientists led by Professor John Fraser, University of Auckland and a team of scientists led by Professor Gregers Anderson of the University of Aarhus, Denmark, described how a protein from S. Staphylococcus interferes with the human immune system. Their results were published in the journal Proceedings of the National Academy of Sciences USA (PNAS).

In New Zealand, like many other countries, S. aureus is the most common cause of nosocomial infection. It also causes severe outbreaks in the community where antibiotic resistant strains such as MRSA is proving very difficult to treat.

Professor Fraser, associate director of the Maurice Wilkins Centre, says the study, the culmination of six years, focuses on a small protein called superbug SSL7 (protein Staphylococcal superantigens and 7). The team has shown that this protein binds to immunoglobulin A (IgA), an antibody of special pleading in your gut and lung. The protein also binds complement C5 SSL7 a series of proteins that “complement” the work of antibodies to destroy bacteria.

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