A new paper claims to have solved a long-outstanding mystery in neuroscience – how, exactly, do the cells of people with Huntington’s disease produce damaging amyloid proteins from other proteins in a game of maladaptive Lego?
Sign up for our email newsletter for the latest science newsclaims to have solved a long-outstanding mystery in neuroscience – how, exactly, do the cells of people with Huntington’s disease produce damaging amyloid proteins from other proteins in a game of maladaptive Lego?
After some painstaking work, they came up with a surprisingly simple explanation for where amyloids come from.Until now, the overall picture was relatively clear. People with Huntington’s Disease have a genetic mutation that encodes for a protein, Huntington, that contains far too many of the amino acid glutamine, a common building block for proteins.
Using DAmFRET, which features a “direct intracellular reporter,” the researchers concluded that the nucleus was remarkably simple – a tiny, four-stranded shape – a quirk within a single protein molecule. But once formed, this nucleus kicks off the formation of amyloid fibers, which accumulate to form plaques.
. “That event ignites the chain reaction for amyloids that kill cells and may provide critical insight into how amyloids cause disease.”The new paper points to a potential medical strategy – polyQ molecules don’t form nuclei when crowded together with other proteins. They need space to develop the structure, and a treatment may work by somehow getting in the way.
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