Prions, known for their role in causing diseases such as “mad cow,” are similar to viruses in that they are not alive, yet are able to replicate themselves through the assistance of a host. Specifically, abnormal (disease-causing) prions multiply by corrupting normal prions in the body.
Scientists transferred prions from brain cells to other cells.
In the Scripps study, scientists transferred prions from brain cells to other cells. Some prions successfully “adapted” and quickly overran other prions. However, when transferred back to brain cells, the prions that had adapted were unable to compete, and the prions still suited for brain cells became dominant again.
Scripps’ Charles Weissmann explained, “On the face of it, you have exactly the same process of mutation and adaptive change in prions as you see in viruses. This means that this pattern of Darwinian evolution appears to be universally active.”
Are the prions “evolving”? We echo Weissmann in that, “on the surface,” it would be fair to consider the prion population in the experiment to be “evolving”—in the sense of “changing” based on a selective process. However, we note, first, that even the simplest single-celled life-forms are astoundingly complex compared to prions, and, second, the way the prions are “adapting” is by corrupting other prions more rapidly—which does not sound like a constructive equivalent of the information-adding mutations Darwinists need evolution to produce. Thus, even if we assume that no minority of “adapted” prions was in the experimental population to begin with, prion evolution offers a poor analogy to Darwin’s eons-long process.
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