Inflammation plays a role in learning and memory loss that can result from brain Injury or disease, and researchers now have evidence that neurons may be suffering from too much gas and too little food.
Mir et al., 2014 - Cytokine-induced GAPDH sulfhydration affects PSD95 degradation and memory.
They've found that the inflammation-mediator interleukin 1β, or IL-1β, prompts production of the short-lived gas hydrogen sulfide, impacting the brain cells' ability to use food and glucose, and ultimately resulting in the destruction of synapses, where the cells connect so information can be stored and memories made.
"So just think about this. If this protein is being chewed up, then neuron-to-neuron communication is disrupted," says Dr. Nilkantha Sen, neuroscientist at the Medical College of Georgia at Georgia Regents University. "If it continues to happen in your brain or in my brain, our memory will be shut down."
Sen, corresponding author of the study in the journal Molecular Cell, is referencing damage to the protein PSD95, which is essential to the framework of the synapses that connect brain cells and which gets modified by the gas hydrogen sulfide.
Loss of PSD95 already is implicated in dementia as well as depression, anxiety disorders, and addiction. IL-1β signaling in the brain plays a critical role in learning and memory however, the rapid accumulation that follows injury appears to have the opposite effect.