Under rare conditions, an Alzheimer’s-related protein may have jumped between people, scientists reported this year (SN: 10/17/15, p. 12). If true, that observation, the first of its kind, could recast the way scientists view the disease. “This was a highly unusual finding,” says John Collinge of University College London.
Scientists already had hints that the protein in question, amyloid-beta, behaves like an infectious prion, a misshapen protein that coaxes other proteins to misfold and spread from cell to cell. In a study reported in Nature, Collinge and colleagues found A-beta buildup in four of eight postmortem brains from people who had received growth hormone injections derived from cadavers. Because A-beta buildup is rare in relatively young people — all were between the ages of 36 and 51 — the finding suggests that the buildup might have been seeded by growth hormone contaminated with A-beta.
This result adds to evidence that prions may be behind Alzheimer’s disease as well as other neurodegenerative disorders such as Parkinson’s and Huntington’s. But some scientists caution that it’s too soon to label these disorders as prion diseases. Prion diseases such as mad cow disease, and the related kuru (a disorder spread through ritualistic brain eating) and Creutzfeldt-Jakob disease in humans, evoke fear of contagion. But, as with these established prion diseases, there’s no evidence that Alzheimer’s or other neurodegenerative disorders spread through typical, everyday contact, scientists agree.
Yet thinking of neurodegenerative diseases as prionlike may ultimately reveal new ways to stop or prevent them, scientists say. Removing normal proteins before they are corrupted, for instance, might be one way to block neural destruction.