A large number of neurodegenerative disorders are triggered by the aggregation of misfolded proteins called amyloids. The main pathogenic event in these pro-teinopathies is the accumulation of oligo-mers, soluble assemblies that can disrupt synaptic activity, alter intracellular signaling, and spread to neighboring cells. Thus, preventing the formation of oligo-mers is a common therapeutic strategy for many neurodegenerative disorders. A number of laboratories are focusing on developing specific anti-amyloid agents, but this deliberate approach may benefit only the most prevalent conditions, such as Alzheimer and Parkinson disease. Alternatively, it may be possible to target the conserved structure and patho-biology of amyloids with potentially widespread benefits.
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