Salvador Dalí could never have imagined that one day his work would feature in such a prominent place for an artist of his stature. He could not have thought this in his wildest dreams, and he did have some pretty wild dreams. The image takes inspiration from 3 of his famous paintings, the first being "Dream caused by the flight of a bee around a pomegranate a second before awakening". Well, there are no pomegranates here but we do have a tiger leaping out of the sky and clamping its jaw around a neuron. Pretty cool and not quite as confusing as the pomegranate, fish, tiger, tiger, gun sequence from the original painting. The melting clock in the foreground is of course from Dalí's "The persistence of memory", its presence here probably a sad reflection that Huntington's disease can affect many people early in their lives. And finally the trees in the background come from "The three sphinxes of bikini". They are meant to symbolise the mushroom cloud of an atomic bomb in the original painting and so here gives another hint to the deadly nature of the disease. Not really much fun here after all.
I like that Nature Chem Bio does give you a little peak into what the authors were smoking when they made the image. The tiger apparently is meant to show the "difference in proteostasis mechanisms" which determines the "longevity of a neuron". Hence why our tiger is trying to eat that giant neuron.
No tigers were harmed during the making of this cover
The Paper: Proteostasis of polyglutamine varies among neurons and predicts neurodegeneration
Found at: Nature Chemical Biology, 2013, 9, 586-592
The paper is a study on the huntingtin toxin, a protein that causes Huntington's disease. The level of glutamine residues in the toxin can vary and it is this variation that leads to the protein misfolding and causing the disease. The larger polyglutamine regions were important as they also reduced the lifetime of the toxin. It was found that different neurons cleared the huntingtin toxin at different rates, with cortical neurons acting quicker than striatal neurons and thus living longer. They concluded that the biological pathways and in particular the Nrf2 pathway, responsible for protein degradation would be good targets for therapeutics for treating misfolded protein diseases. So maybe some good news in the end.
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