Alzheimer’s Researchers Build Mock Protein That Might Help Them Understand Disease

Alzheimer’s Researchers Build Mock Protein That Might Help Them Understand Disease
Researchers at the University of Sussex in England have built a protein closely resembling amyloid-β, except for the fact that it is not capable of aggregating. The new protein, described in a report titled, "A critical role for the self-assembly of Amyloid-β1-42 in neurodegeneration," published in the journal of Scientific Reports, will allow researchers to understand the details of how amyloid-β misfolds and accumulates — triggering processes toxic to nerve cells. Studies in lab dishes and animals suggest that once that the amyloid protein starts clumping together in what scientists refer to as oligomeric forms of the protein, neurodegeneration will soon follow. Despite enormous research efforts, scientists have, however, not been able to figure out exactly how a misbehaving protein can kill neurons. Studies of the aggregation mechanisms turned out to be more difficult than expected, and the lack of a suitable control protein made interpretation of results difficult. Up to now, researchers have used proteins folded in a different way, amyloid-β from a rat (that doesn’t aggregate), or simply omitted the protein to construct a control experiment, but such solutions are far from optimal in that they can’t take into account structural features of amyloid-β that might contribute to cell toxicity. The newly developed protein does not form oligomers (aggregates containing just a few protein molecules) or any other types of protein clumps. In contrast to normal human amyloid-β, the new factor did not disrupt processes within synapses connecting neurons, nor di
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