Reversing Effect Of Cell-Traversing Protein May Be Key To Slowing Parkinson’s
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Science has helped in the curing and cessation of many diseases and deformities in our time, and I can only hope in wide-eyed naivete that all of the world’s ailments will one day be extricated from humanity’s timeline. I care, of course, for the millions in misery at this very moment, but mostly, it’s in hopes that Seth MacFarlane might shoot for some original jokes on Family Guy once in a while.
(Michael J. Fox cutaway gag.)
Virginia Lee, a neurobiologist from the University of Pennsylvania in Philadelphia, led a team in researching cellular travel of Parkinson’s disease. Published in Science, the study involved injecting the brains of mice with a misfolded synthetic version of the a-synuclein protein, which had already been shown to spread between neighboring cells, sometimes causing cellular death. Previous research also indicated that Parkinson’s might be spread from neuron to neuron via rogue protein. The injected mice almost certainly proved the causal relationship between protein and spread of disease, disproving previous beliefs that the disease spontaneously arises in the cells.
When the mice were injected, the clumps of protein called Lewy bodies, telltale signs of Parkinson’s, quickly began to appear. They were injected in the areas of their brain rich in dopamine, and the death of those dopamine neurons soon occurred. Nerve cells near the injection also began growing Lewy bodies, a sign of the protein transference. Within six months, the mice were suffering with a deterioration of coordination, grip strength, and balance, a smaller scale of what happens to humans affected by the disease.
There is still no evidence proving how Lewy bodies form in the first place, but researchers hope this breakthrough will lead to treatments of existing cases, rather than offer any preventative solutions just yet. Clinical trials of a-synuclein antibodies may be on the way relatively soon.
