In a new study, researchers found that calcium channel blockers may be effective in treating memory loss, which is a major symptom of Alzheimer’s disease.
They found treating a diseased brain cell with a blocker of the L-type channel reduced the number of calcium ions able to flow into the brain cell.
The research was conducted by a team from the University of Bristol.
Alzheimer’s disease (AD) is the most common cause of dementia but the changes in brain cell function underlying memory loss remains poorly understood.
The researchers used fruit flies to study AD, using a fluorescent molecule that reports the number of calcium ions inside brain cells.
They found that diseased brain cells become overloaded with calcium ions, which at normal levels are important for memory formation.
This overload was due to the overproduction of the gene encoding a channel, known as the L-type channel, which allows calcium ions to flow into the cell from outside.
More of these channels means more calcium ions are able to flow into the cell, disrupting memory formation.
Using a drug to block the L-type channel reversed the effect of disease and reduced the flow of calcium ions to a normal level.
The research team also examined the memory of fruit flies by testing if they could remember which of two odors had previously been paired with an electric shock—similar to Pavlov’s experiments with dogs.
While healthy flies remembered well, the diseased flies, like humans, displayed impaired memory.
However, if the overproduction of L-type channels was corrected in the diseased flies, their brain cells were no longer overloaded with calcium ions and their memory was just as good as healthy flies.
This shows that memory loss is likely due to calcium overload because too many L-type channels are made and, if this is corrected, memory impairment is rescued.
The team says memory loss in Alzheimer’s disease (AD) is a highly distressing and difficult to treat the symptom.
Targeting the early changes in brain cell function—before they begin to degenerate—may be effective in treating memory loss.
In humans suffering from AD, blocking these channels may be beneficial in treating memory impairment.
The findings show that further work should be carried out to determine the mechanism underlying the recovery of memory and whether or not the team’s research will prove effective in humans.
The lead author of the study is Dr. James Hodge, associate professor in neuroscience in the School of Physiology, Pharmacology & Neuroscience.
The study is published in Frontiers in Cellular Neuroscience.
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