Researchers across the nation are chasing answers to one question: Is it possible to transmit Alzheimer’s disease from one person to another?
Some researchers have taken the results of a study featured in the September edition of the journal Nature to say that it’s possible, but one Penn researcher who has studied the same data argues that’s just a misinterpreted result from a too-small study.
“Study another thousand people, then come back to me — another 7,000 people, then come back to me — and tell me what your findings are,” said Dr. John Trojanowski, director of the Alzheimer’s Disease Core Center at the University of Pennsylvania.
Two Cheers for Negative Evidence
For about 20 years until 1985, about 7,700 young Americans with growth problems were injected with pituitary extract containing human growth hormones to stimulate growth. Some of these injections from cadavers also contained prions, researchers later learned. Among the patients in the United States, 29 (0.4 percent) developed Creitzfeldt-Jakob disease, a rare neurodegenerative disease better known as CJD that is caused by a prion infection.
A team of researchers led by Trojanowski, who is also director of the Penn Udall Center for Parkinson’s Research, studied this same cohort as well and found that fifty years later, no one developed instances of Alzheimer’s or Parkinson’s disease.
What Trojanowski and his colleagues were testing is whether persons injected with these proteins were at heightened risk to develop either Alzheimer’s or Parkinson’s diseases.
“Despite the fact that tau, amyloid beta and synuclein were in the pituitary, just as been demonstrated for prions, and were probably co-purified with the growth hormone, just as the prions were…there has been no case of Alzheimer’s or Parkinson’s that emerged in this cohort,” Trojanowski said.
Tau and amyloid beta proteins are found in Alzheimer’s patients; Alpha-synuclein is a protein linked with Parkinson’s disease.
“Negative evidence is always less compelling than positive evidence,” Trojanowski said, “and we had no evidence for Alzheimer’s and Parkinson’s being spread through these daily injections” of pituitary extract.
A Historical Oddity
The study featured in Nature took the additional step of looking into the brains of persons who had received human growth hormone injections. The results of eight autopsies from cadavers found plaque build-up in all but one of the subjects’ brains.
Though Alzheimer’s disease is rare among people of the same of age as those autopsied (36-61 years old), Trojanowski is quick to point out that plaque can begin to accumulate for subjects in their 30s and won’t necessarily lead to Alzheimer’s disease later in life. Furthermore, he adds, the autopsies did not find tangles of tau proteins — twisted protein strands in dead and dying nerve cells — another effect of Alzheimer’s disease.
“This is, I think, insufficient evidence of transmission,” Trojanowski said.
Ultimately, the public needn’t be concerned about being impacted by the effects of human growth hormones obtained from cadavers. Since 1985, clinicians use a synthetic alternative, turning the studied cohort into what Trojanowski calls “a historical oddity.”
“Those people were exposed to something unfortunately that lead to CJD, and that’s terrible, but it’s all over,” he said.
Terms to know:
Prion:
A disease-causing protein that can fold in a way that that can be transmitted to another prion, leading to spread of the disease
Named by University of Pennsylvania alumnus Stanley Pruisner, whose research was awarded the Nobel Prize in Physiology or Medicine in 1997
Creutzfeldt-Jakob disease (CJD):
A rare, fatal disorder caused by misfolding prions in the brain
300 cases are discovered annually in the United States, according to the National Institute of Neurological Disorders and Stroke
Tau:
Proteins that are part of a healthy brain
These proteins can collapse and create tangles, a biomarker of Alzheimer’s disease.
Amyloid beta:
Another protein that can misfold and clump together to form plaques in the human brain
Also a biomarker of Alzheimer’s disease
Alpha synuclein:
Protein that can misfold and develop into Lewy bodies in nerve cells
A biomarker of Parkinson’s disease, dementia with Lewy bodies, and other diseases