A step of progress was reported this week in developing better understanding of the molecular processes underlying Alzheimer’s Disease. For some time it has been known that beta-amyloid protein shows up in excessive quantities in the brains of Alzheimer’s Disease patients and that this protein causes synaptic damage to neurons. But the mechanism by which damage was inflicted was unknown. In the new research it was observed that beta-amyloid protein multimers create excessive production of nitric oxide. This free-radical substance was shown to attack a mitochondrial protein Drp1 in cultured nerve cells through a process known as S-nitrosylation. This in turn led to activation of enzymatic activity that induces mitochondrial fragmentation. The reaction damages neuron synapses leading to nerve cell death and eventually to loss of brain function. It is thought that one avenue of therapy for Alzheimer’s Disease that could come out of this understanding could be blockage of S-nitrosylation. Or better yet, figure out how to prevent the buildup of beta-amyloid protein in the first place,
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