Brain Cell Activity Increases Levels Of Key Ingredient In Alzheimer's Plaques
Washington University School of Medicine in St. Louis
Increased communication between brain cells increases levels of amyloid beta, the key ingredient in Alzheimer's brain plaques, scientists at Washington University School of Medicine in St. Louis have found.
Through a series of these experiments, researchers linked increased amyloid beta levels to the release of synaptic vesicles, small packets containing chemical messengers known as neurotransmitters. The primary way nerve cells send messages to each other is to release the vesicles waiting at the synapse, a structure where the arms of two nerve cells almost touch. The neurotransmitters cross the synapse and bind to receptors on the surface of the receiving nerve cell. Normal brain physiology produces amyloid beta and naturally clears it from the brain, so they conducted a series of follow-up experiments to try to get a sense for whether increased synaptic vesicle release was affecting amyloid beta production or clearance.
"It's probably not clearance, and the effect on production is probably pretty small," they say. "Instead, it appears that synaptic activity is regulating the amount of amyloid beta that gets released from inside brain cells, where amyloid beta is produced. We're going to follow up with studies of whether particular neurotransmitters can be linked to changes in amyloid beta levels."
Washington University School of Medicine in St. Louis
Increased communication between brain cells increases levels of amyloid beta, the key ingredient in Alzheimer's brain plaques, scientists at Washington University School of Medicine in St. Louis have found.
Through a series of these experiments, researchers linked increased amyloid beta levels to the release of synaptic vesicles, small packets containing chemical messengers known as neurotransmitters. The primary way nerve cells send messages to each other is to release the vesicles waiting at the synapse, a structure where the arms of two nerve cells almost touch. The neurotransmitters cross the synapse and bind to receptors on the surface of the receiving nerve cell. Normal brain physiology produces amyloid beta and naturally clears it from the brain, so they conducted a series of follow-up experiments to try to get a sense for whether increased synaptic vesicle release was affecting amyloid beta production or clearance.
"It's probably not clearance, and the effect on production is probably pretty small," they say. "Instead, it appears that synaptic activity is regulating the amount of amyloid beta that gets released from inside brain cells, where amyloid beta is produced. We're going to follow up with studies of whether particular neurotransmitters can be linked to changes in amyloid beta levels."
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