Typically characterized as poisonous, corrosive, and smelling of rotten eggs, hydrogen sulfide’s reputation may soon get a facelift.
In a new study, researchers found that the foul-smelling gas may help protect aging brain cells against Alzheimer’s disease.
The finding opens doors to the development of new drugs to combat neurodegenerative disease.
The research was conducted by a team at John Hopkins Medicine and the University of Exeter.
The human body naturally creates small amounts of hydrogen sulfide to help regulate functions across the body from cell metabolism to dilating blood vessels.
The rapidly burgeoning field of gasotransmission shows that gases are major cellular messenger molecules, with particular importance in the brain.
Previous studies using a new method have shown that sulfhydration levels in the brain decrease with age, a trend that is amplified in patients with Alzheimer’s disease.
In the study, the team used the same method and confirmed a decrease in sulfhydration in the AD brain.
They studied mice genetically engineered to mimic human Alzheimer’s disease. They injected the mice with a hydrogen sulfide-carrying compound that slowly releases hydrogen sulfide while traveling throughout the body.
The researchers then tested the mice for changes in memory and motor function over a 12-week period.
They found that hydrogen sulfide improved cognitive and motor function by 50% compared with mice that did not receive the injections.
Treated mice were able to better remember the locations of platform exits and appeared more physically active than their untreated counterparts with simulated Alzheimer’s disease.
The results showed that the behavioral outcomes of Alzheimer’s disease could be reversed by introducing hydrogen sulfide, but the researchers wanted to investigate how the brain chemically reacted to the gaseous molecule.
A series of biochemical experiments revealed a change to a common enzyme, called glycogen synthase β (GSK3β).
researchers observed that in the absence of hydrogen sulfide, GSK3β is over-attracted to another protein in the brain, called Tau.
When GSK3β interacts with Tau, Tau changes into a form that tangles and clumps inside nerve cells. As Tau clumps grow, the tangled proteins block communication between nerves, eventually causing them to die.
This leads to the deterioration and eventual loss of cognition, memory, and motor function that is characteristic of Alzheimer’s disease.
The team says understanding the cascade of events is important to designing therapies that can block this interaction like natural hydrogen sulfide is able to do.
They plan to continue studying how sulfur groups interact with GSK3β and other proteins involved in the pathogenesis of Alzheimer’s disease in other cell and organ systems.
One author of the study is Bindu Paul, M.Sc., Ph.D., Faculty Research Instructor in neuroscience.
The study is published in The Proceedings of the National Academies of Science.
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