- New research shows that errors in how it attaches can cause damaged brain structure, poor motor skills, hyperactivity and learning difficulties in mice.
New research from The Johns Hopkins University suggests that a molecule commonly found “decorating” brain cells in higher animals, including humans, may affect brain structure. The study showed that small changes made in how sialic acid attaches to cell surfaces can cause damaged brain structure, poor motor skills, hyperactivity and learning difficulties in mice. The findings suggest that sialic acid plays a significant role in how brain cells communicate, possibly shedding light on the underlying causes of certain brain disorders.
A summary of the research appears in the July 2015 issue of The FASEB Journal.
“Sialic acid is part of the molecular language that cells use to communicate among themselves,” says Ronald Schnaar, Ph.D., a professor of pharmacology and neuroscience at the Johns Hopkins University School of Medicine. “As we learn that language, we can use the knowledge to better understand disease and perhaps thoughtfully intervene.”
To make their discovery, Schnaar and colleagues mutated mouse genes responsible for sialic acid attachment and then compared the brain structure, motor functions, activity and learning in the deficient mice to those of normal mice. They found that the mice with altered sialic acid attachment had significant neurological problems when compared to the normal mice.
“The molecular codes that control the human brain are as yet poorly worked out,” says Gerald Weissmann, M.D., editor-in-chief of The FASEB Journal. “This report shows how small molecules, such as sialic acid, direct cell communication to profoundly affect behavior. With this information, researchers have new ways to work out the mechanisms that determine hyperactivity and other brain disorders.”
Other authors of the report include Seung-Wan Yoo, Mary Motari and Jillian Prendergast of the Johns Hopkins University School of Medicine; Keiichiro Susuki of Baylor College of Medicine; Andrea Mountney of the Walter Reed Army Institute of Research; and Andres Hurtado of the Hugo W. Moser Research Institute.
This work was supported by grants from the National Institute of Neurological Disorders and Stroke (NS037096, NS057338) and the National Multiple Sclerosis Society.
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