Researchers at Northwestern University have discovered a molecular mechanism -- a tiny protein attacking nerve cells -- that could explain why the brain damage in early Alzheimers disease results in memory loss and not other symptoms such as loss of balance or tremors.
The research team, led by William L. Klein, professor of neurobiology and physiology, found that toxic proteins, called "amyloid ß-derived diffusible ligands" (ADDLs, pronounced "addles"), from the brain tissue of individuals with Alzheimers disease specifically attack and disrupt synapses, the nerve cell sites responsible for information processing and memory formation.
These results, which show that only particular neurons and synapses are targeted by the neurotoxins, were published Nov. 10 in the Journal of Neuroscience. An understanding of how ADDLs disrupt synapses without killing neurons could lead to the development of new therapeutic drugs capable of reversing memory loss in patients who are treated early, in addition to preventing or delaying the disease. "Memory starts at synapses, so it was probable that Alzheimers disease would be a synapse failure," said Klein. "Our work, which shows that ADDLs bind with great specificity to synapses, is the first demonstration of that.
Megan Fellman | EurekAlert!
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