Rare reports of potential Alzheimer’s disease transmission found in patients receiving treatment that was stopped

According to a new study, five persons who had early-onset dementia symptoms may have been treated with human growth hormone decades ago as children, although the treatment is currently terminated.

The research, which was released on Monday in the journal Nature Medicine, offers the first proof of Alzheimer’s disease that has been medically acquired in a living individual. In these instances, amyloid beta protein transmission—a major factor in Alzheimer’s disease when it forms plaques in the brain—may have contributed to the patients’ early-onset dementia symptoms.

The new study indicates that amyloid beta contamination may be related to the early dementia symptoms that the study participants experienced. Alzheimer’s disease is linked to abnormal accumulation of the protein amyloid beta in the brain. The study’s conclusions raise fresh concerns about Alzheimer’s and other degenerative diseases, but they do not imply that the illness can be communicative or spread like bacterial or viral infections, for example.

John Collinge, the study’s lead author and director of the University College London Institute of Prion Diseases, stated in a news conference that “I should emphasize these are very rare occurrences, and the majority of this relates to medical procedures that are no longer used.”

Rare reports of potential Alzheimer's disease transmission found in patients receiving treatment that was stopped

Each of the five individuals suffered from a growth hormone shortage as youngsters and were given specially manufactured pituitary growth hormones derived from cadavers. The pituitary gland is situated at the base of the brain. It naturally produces and releases human growth hormone, or HGH, which aids in a child’s growth.

According to the report, these patients were among the at least 1,848 persons in the UK who had treatment with human growth hormone extracted from the pituitary gland of a cadaver between 1959 and 1985. At the time, the United States and other countries throughout the world also adopted this technique. After incidences of Creutzfeldt-Jakob disease, a rare brain illness, were linked to the use of tainted human growth hormone from cadavers, the treatment strategy was abandoned.

According to a recent study, Alzheimer’s disease may be spread through repeated exposure over a period of years to cadaver-derived HGH treatments tainted by amyloid beta seeds and prions linked to Creutzfeldt-Jakob disease. Proteins known as prions have the ability to spread neurodegenerative illnesses.

According to the study’s findings, Alzheimer’s disease may occasionally be transmissible in a manner akin to “prion diseases,” a group of uncommon, progressive neurodegenerative illnesses linked to prion proteins that includes CJD (Creutzfeldt-Jakob disease). Despite the fact that Alzheimer’s is not a prion disease, some independent research indicates that tau and amyloid beta, two proteins that are characteristic of the illness, behave like prions.

During the news briefing, Collinge stated, “It appears that what’s happening in Alzheimer’s disease is very similar to what happens in the human prion diseases like CJD.” “It does raise questions regarding Alzheimer’s disease treatment strategies.”

“The general public is not in danger.”

Researchers first reported “possible evidence” in 2015 that it was possible to transfer amyloid beta protein from a cadaver’s growth hormone to a receiver. In 2018, they investigated this in laboratory animals.

In their study, the researchers from University College London and the National Hospital for Neurology and Neurosurgery in the United Kingdom stated, “We now provide evidence that Alzheimer’s disease is also transmissible in certain circumstances.” However, they also note that this kind of transmission is “rare” and that neither routine medical care nor daily activities appear to be potential sources of amyloid beta transfer.

Strict protocols were implemented to reduce cross-contamination when human growth hormones were phased out in the 1980s due to worries about the spread of Creutzfeldt-Jakob disease. In a written statement about the new study released by the UK-based Science Media Centre, Dr Susan Kohlhaas, executive director of research and partnerships at Alzheimer’s Research UK, stated that “researchers recommend that medical procedures should be reviewed in light of these findings to ensure that rare cases of Alzheimer’s transmission like this do not happen in the future.”

This study raises the possibility that, in extremely rare cases, human growth hormone from deceased donors could spread Alzheimer’s disease amongst people. Kohlhaas stated in the statement, “It must be emphasized that this treatment is no longer used today and has been replaced with synthetic growth hormone.” “It is imperative to emphasize that this represents the sole documented case of Alzheimer’s disease transmission amongst individuals.”

In an email, Dr. Richard Isaacson, who was not involved in the new study, stated that while previous research he has seen has not been able to establish it, he has long hypothesized that Alzheimer’s disease may have some transmissibility comparable to prion illnesses.

“It’s difficult to say, but compared to previous research, there must be a difference in how HGH may have infected recipients in this study,” stated Isaacson, director of research at the Institute for Neurodegenerative Diseases in Florida.

Although the study stresses the significance of sterilizing and decontaminating instruments in between surgeries, he continued, saying that “the public has nothing to fear” because this form of human growth hormone treatment is no longer used in clinical practice.

Researchers noted in the study that “its recognition emphasizes the need to review measures to prevent accidental transmissions via other medical and surgical procedures,” even though there is no evidence that amyloid beta can be spread between people during daily activities.

Regarding Alzheimer’s disease, Isaacson added, “I’m also intrigued by how these results may inform potential therapeutic targets and strategies in the future.”

“Proposing novel scientific inquiries”

The study looked at eight cases where the patient had previously received treatment using human growth hormone that was extracted from the pituitary gland of a deceased person. They had all been treated like kids. Five of the patients were in their 50s and still alive at the end of the research. The ages of the three other deceased were 47, 54, and 57.

Three of the five patients had received an Alzheimer’s disease diagnosis prior to the study, and the researchers discovered that five of them had symptoms that were compatible with early-onset dementia. Between the ages of 48 and 49, symptoms began to appear in four of the patients. At the age of 55, the last patient began experiencing symptoms.

First author of the study and researcher at the University College London Institute of Prion Diseases, Dr. Gargi Banerjee, stated in a news release that “we have found that it is possible for amyloid-beta pathology to be transmitted and contribute to the development of Alzheimer’s disease.”

“This transmission involved repeated treatments with contaminated material, often over several years, and occurred following treatment with a now-outdated form of growth hormone,” Banerjee added. “There is no evidence that routine caregiving or close contact can result in the acquisition of Alzheimer’s disease.”

Dr James Galvin, the director of UHealth, the University of Miami Health System, has never heard of human transmission of Alzheimer’s disease before, until this latest study.

The fact that all of the instances had very young onsets raises the possibility that there are unrelated variables at play. Early onset is usually associated with genetic abnormalities; however, since these were not discovered, the most plausible common cause would be the use of growth hormone therapy in cadavers. Galvin, who was not involved with the study, stated in an email that more research was necessary.

In terms of clinical practice, I would say that nothing more needs to be done at this time, but there is definitely need for further research into this. He stated that brain disease-causing proteins are transmissible. Examples of these proteins include the prion protein in bovine spongiform encephalopathy and Creutzfeldt-Jakob disease. Furthermore, some of these characteristics are shared by other disease-causing proteins, such as alpha-synuclein in Parkinson’s disease and Lewy body dementia, but they do not seem to be transmissible. There may be a need to review the evidence surrounding the roles of the proteins tau and amyloid in Alzheimer’s.

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