Lastly, we address PrP shedding in samples of patients affected by neurodegenerative diseases including CJD and AD, and demonstrate that sPrP, in the presence of proteopathic aggregates, is redistributed from an originally nondescript and diffuse to a plaque-associated pattern, thus warranting further studies on the proposed role of sPrP in blocking and sequestering extracellular toxic oligomers into potentially less harmful deposits. The gene discussed is PRNP; the disease is Alzheimer disease.