Source: University of Alabama
Summary: Researchers have found that a dietary supplement can induce a biochemical alteration in brain proteins and dampen the brain’s hyperexcitability.
Seizure disorder or epilepsy is the 4th most common neurological disorder and observed in people of all ages. Seizures is associated with brain’s pathological hyperexcitability. It is unfortunate that there are limited treatments available to treat this brain’s hyperexcitability. However, researchers from University of Alabama, Birmingham, have found that a dietary supplement glucosamine can induce a biochemical alteration in brain proteins and dampen the brain’s pathological hyperexcitability in rat and mouse models. These findings open a door for novel therapeutic targets for treating seizure disorders. The findings were published in The Journal of Neuroscience.
Proteins work consistently in the living cells, and their activities are regulated in a rapid manner in response to changing conditions. Generally, addition and removal of the phosphoryl group to a protein is considered to be a well-known regulator for many proteins. It is estimated that there are almost 230,000 phosphorylation sites in human proteins. But another less-known regulation is by addition or removal of N-acetylglucosamine to proteins, that is usually controlled by glucose (primary fuel for neurons). Earlier it was found that brain cells had the second-highest amounts of proteins with N-acetylglucosamine, or O-GlcNAcylation, in the body. Therefore it is observed that acute increases in protein O-GlcNAcylation caused long-term synaptic depression, a reduction in neuronal synaptic strength, in the hippocampus of the brain.
Researchers said, “Our findings support the conclusion that protein O-GlcNAcylation is a regulator of neuronal excitability, and it represents a promising target for further research on seizure disorder therapeutics.”
More Information: Luke T. Stewart et al, “Acute Increases in Protein O-GlcNAcylation Dampen Epileptiform Activity in Hippocampus”, The Journal of Neuroscience (2017). DOI: 10.1523/JNEUROSCI.0173-16.2017