Protect Against Protein Aggregation
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Alzheimer's disease now strikes more than one in 30 Americans, and about half the population that lives past 85 acquires Alzheimer's. Approximately one million Americans have Parkinson's disease, including three out of every 100 people over age 60. Aging is the most important risk factor for both of these diseases.
The new study-conducted in a C. elegans model, a roundworm that expresses a protein whose aggregation appears to cause Alzheimer's disease-showed that toxicity from protein aggregation is "drastically reduced" when aging is slowed by modulating the insulin growth factor (IGF) signaling pathway.
Moreover, the researchers found two novel independent activities promoting this cellular survival. The first protective mechanism disassembles and cuts up protein aggregates. Surprisingly, the second protective mechanism enables the formation of larger aggregates from smaller ones that appear to be more toxic.

"Now, we want to use this mechanistic information to discover the macromolecular basis for these activities and to discover small molecules that will delay the aging program and thus delay the onset of proteotoxicity associated with these diseases by modulating aggregation and disaggregation activities," Kelly states. "The hope is that, by manipulating the protective mechanism inherent in cells, we can find a single entity-a single drug-that would be useful for a variety of neurodegenerative diseases where protein aggregation leads to neurodegeneration."