Is the Alzheimer’s protein contagious?

Sep 16, 2015


By Emily Underwood

Beginning in 1958, roughly 30,000 people worldwide—mostly children—received injections of human growth hormone extracted from the pituitary glands of human cadavers to treat their short stature. The procedure was halted in 1985, when researchers found that a small percentage of recipients had received contaminated injections and were developing Creutzfeldt-Jakob disease (CJD), a fatal neurodegenerative condition caused by misfolded proteins called prions.

Now, a new study of the brains of eight deceased people who contracted CJD from such injections suggests that the injections may also have spread amyloid-β, the neuron-clogging protein that is a hallmark of Alzheimer’s disease. The study is the first evidence in humans that amyloid-β might be transmissible through medical procedures such as brain surgery—according to the researchers. Skeptics, however, note that the CJD prion itself often triggers unusual amyloid deposits; epidemiological studies, they say, find no connection between the injections and increased risk of developing Alzheimer’s disease.

Aside from CJD and the related mad cow disease, kuru is perhaps the most famous prion disease. Endemic to Papua New Guinea and now essentially eradicated, kuru is transmitted through the ritual consumption of human brain tissue at funerals. Increasingly, however, scientists are recognizing that a number of other neurodegenerative diseases, including Alzheimer’s, Huntington disease, and Parkinson’s disease, also involve aberrant proteins that act like “seeds” in the brain. They convert otherwise normal proteins into fibers that “break, form more seeds, break, and form more seeds,” says John Collinge, a neuropathologist at University College London and lead author of the new study.

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2 comments on “Is the Alzheimer’s protein contagious?

  • The real problem is not just that annoying skeptics keep debunking potentially lucrative r&d white elephants but that Alzheimers seems to be strongly lifestyle related, similar to many cases of diabetes.

    Lifestyle changes don’t have any obvious ROI opportunities involving patent rights in genetics or pharmaceuticals. There are no gene tech tests to apply or pharmaceutical targets. Some people might be genetically slightly more or less at risk, modified by lifestyle, but If varying lifestyle factors make all the difference then it almost doesn’t matter exactly what are the processes leading to amyloid plaque accumulation over 6 decades. There are probably multiple dependencies anyway, as seems to be the case with all the emerging NCD epidemics.

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