Katharina Buczek
In turn, numerous scientists now believe that this synapse destruction may be at least one contributing factor to the onset of AD– especially since synapse loss has been tied to cognitive decline in AD brains.
As for why female brains are more susceptible to SNO-C3, Lipton and his team believe this is due to the female hormone estrogen. Countless past studies have found estrogen to have a brain-protecting effect under certain conditions.
So, the researchers believe that estrogen protects women from C3 S-nitrosylation during the earlier stages of life. Then, after estrogen levels fall significantly during menopause, the protection is lost.
Experiments using cultured human brain cells also supported this belief, showing that as estrogen levels decrease, SNO-C3 increases. Then, this increase subsequently activates the destruction of neural synapses.
“Why women are more likely to get Alzheimer’s has long been a mystery, but I think our results represent an important piece of the puzzle that mechanistically explains the increased vulnerability of women as they age,” Lipton said.
Now, he and his team are eager to conduct additional experiments centered around de-nitrosylating compounds– or compounds that remove SNO modification– in order to reduce pathology first in animal models of AD and then eventually in human AD brains.
To read the study’s complete findings, which have since been published in Science Advances, visit the link here.
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