Could Alzheimer’s Disease Be Transmissible?
New research on a rare, transmissible degenerative brain disease has provided scientists with insight into whether Alzheimer’s could possibly be spread from person to person.
A study published this week in Nature involved eight patients with Creutzfeldt-Jakob disease (CJD), a rare, degenerative—and ultimately fatal—brain disease. CJD is caused by an abnormal type of protein called prions that enter the body through certain medical procedures involving the eyes or brain. These proteins replicate inside the brain and prompt a misfolding of normal proteins. Some prior research on mice has shown that a similar misfolding of proteins also occurs in Alzheimer’s disease.
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The researchers examined the autopsies of eight patients with CJD, aged 36 to 51, who had all received injection of human growth hormone from cadavers in childhood. They found that four of them had moderate to severe amount of gray matter and vascular amyloids plaques in their brains. Both gray matter and amyloid plaques are hallmarks of Alzheimer’s disease. The researchers did not find a genetic mutation associated with early-onset Alzheimer’s disease in these individuals. Additionally, they didn’t observe an accumulation of tau proteins, which are another indicator of Alzheimer’s disease.
The researchers concluded that while these patients hadn’t yet developed symptoms of Alzheimer’s disease, they most likely would have later in life. The findings, they say, suggest the human growth hormone the patients received in childhood contained the “seeds” of amyloid plaques, in addition to prions.
Only about 200 people worldwide develop CJD each year. Other prion diseases include mad cow and kuru disease. These diseases can be transmitted through grafts of dura (the tissue that covers the brain), corneal transplantation and poorly sterilized electrodes implanted in the brain, as well as injection of contaminated pituitary growth hormone from the pituitary glands of infected cadavers. The U.S. health care system stopped the use of cadaver human growth hormone in 1985.
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The authors of the study stress that more work is needed to explore the link between prions and amyloid plaques. But some Alzheimer’s disease researchers worry the study could send the wrong message to the public.
Dr. John Trojanowski, a professor of geriatric medicine and gerontology at the University of Pennsylvania, told Scientific American that the study will “generate more confused thinking and stoke unreasonable concerns by the public about the infectivity of Alzheimer’s, which I think does not help the field of prion and AD research.”
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