Early dementia symptoms in five adults The human growth hormone they received as children decades ago may now be stopped with medical treatment, a new study suggests.
The study, published Monday in the journal Nature Medicine, provides the first reported evidence of clinically acquired Alzheimer's disease in the living population. In these cases, patients' early dementia symptoms may be the result of a possible transfer of amyloid beta protein, a key component of Alzheimer's disease. Builds up plaques in the brain.
Abnormal formation of amyloid beta protein Amyloid beta contamination in the brain is associated with Alzheimer's disease and the new study suggests that it may have a link to the early dementia symptoms experienced by the patients in the study. The study results do not suggest that Alzheimer's disease is infectious or spread like viral or bacterial infections, but they do raise new questions about Alzheimer's and other degenerative diseases.
“I must emphasize that these are very rare cases, and most of them are related to medical procedures that are no longer used,” John Collinge, the study's lead author and director of the London Institute of Brion Diseases, said in a news release. Explanation.
All five adults had growth hormone deficiency as children and the pituitary growth hormones were produced in a specific way. The Pituitary gland Located at the base of the brain, and Human growth hormoneOr HGH, a natural hormone the gland produces and releases, which promotes growth in children.
Between 1959 and 1985, at least 1,848 of these patients in the United Kingdom were treated with human growth hormone obtained from the pituitary gland of a cadaver, according to the study. At that time, this treatment was also used in other parts of the world. including the United States. The therapeutic approach was discontinued after one case A rare brain disorder called Creutzfeldt-Jakob disease were found to be related The Administration of contaminated human growth hormone from corpses.
New study suggests repeated exposures, for many years, Treatments with cadaver-derived HGH contaminated with prions associated with Creutzfeldt-Jakob disease and amyloid beta seeds may propagate Alzheimer's disease. Prions are Proteins that can act as transmissible agents Neurodegenerative diseases.
In their study, the researchers wrote that Alzheimer's disease may, in some circumstances, be contagious, similar to conditions called “”.Prion diseases” — a family of rare progressive neurodegenerative disorders associated with prion proteins, including Creutzfeldt-Jakob disease or CJD. Although Alzheimer's is not a prion disease, some are A separate study Two proteins that are hallmarks of Alzheimer's disease — amyloid beta and tau — behave like prions.
“What's happening in Alzheimer's disease looks very similar in many respects to what's happening in human prion diseases like CJD,” Koling said at the news conference. “This raises implications for therapeutic approaches to Alzheimer's disease.”
In 2015, researchers previously described “Possible evidence” That Transfection of amyloid beta protein The development of a corpse is possible from the hormone to the recipient and then In 2018They studied this in lab mice.
“We now provide evidence that Alzheimer's disease spreads under certain conditions,” researchers from University College London and the National Hospital for Neurology and Neurosurgery in the United Kingdom wrote in their study. Although they add that this type of spread is “rare,” there is no suggestion that amyloid beta spreads between people in everyday activities or in modern routine medical care.
“After human growth hormones fell out of use in the 1980s due to concerns about the spread of Creutzfeldt-Jakob disease, strict procedures were put in place to reduce cross-contamination. But in light of these findings, the researchers suggest that clinical practices should be reconsidered to ensure that rare cases of Alzheimer's disease transmission do not occur in the future,” said Dr Susan Kohlhaus, executive director of research and partnerships at Alzheimer's Research UK, about the new study in a written statement distributed by the UK-based Center for Science Media.
“This study suggests that in very rare circumstances Alzheimer's disease can be transmitted between humans via human growth hormone from deceased donors. It should be emphasized that this treatment is no longer used today and has been replaced with synthetic growth hormone,” Kohlhaas said in the statement. “It is also important to emphasize that this is the only recorded case of Alzheimer's spreading between humans.”
Dr., who was not involved in the new study. Richard Isaacson said in an email that he had suspected for a while that Alzheimer's disease might have some transmissibility similar to prion diseases, but previous research he had seen could not prove it.
“Compared to previous work, there must be something different about how HGH may have affected the recipients in this study,” said Isaacson, director of research at the Institute for Neurodegenerative Diseases in Florida.
He added that since this type of human growth hormone therapy is not in clinical practice, “the public has nothing to fear,” but the study emphasizes the importance of sterilizing and sterilizing instruments between surgeries.
While there is no suggestion that amyloid beta can be spread between individuals in everyday activities, its recognition “emphasizes the need to reconsider measures to prevent accidental transmissions through other medical and surgical procedures,” the researchers wrote in the study.
“I'm interested in how these results may inform potential therapeutic targets and strategies in the future,” Isaacson said of Alzheimer's disease.
Researchers studied eight cases in which a person had a history of treatment with human growth hormone obtained from a cadaver's pituitary gland. They were all considered children. Five patients were still alive at the time of the study and were in their 50s. The other three died at the ages of 57, 54 and 47.
Five patients had symptoms consistent with early onset dementia and three of those five had been diagnosed with Alzheimer's before the study, the researchers found. Four patients started experiencing symptoms between the ages of 48 and 49. The remaining patient had onset of symptoms at age 55.
“We found that it is possible that amyloid-beta pathology spreads and contributes to the development of Alzheimer's disease,” said Dr. Kargi Banerjee, the study's first author and researcher. University College London Institute of Prion Diseasessaid in a message liberation
“The transmission occurred following treatment with the now-obsolete growth hormone, and repeated treatments with the contaminated material over the years,” Banerjee said. “There is no indication that Alzheimer's disease can be acquired from close contact or during routine care.”
The new study, said Dr. James Calvin, director of the Comprehensive Center for Brain Health at UHealth, University of Miami Health System, is the first he has heard about Alzheimer's disease spreading in humans.
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“The cases were all very young in onset, which raises a suspicion of extraneous factors. In general, early onset is linked to genetic mutations, but since this has not been detected, the most common cause would be cadaveric growth hormone therapy. Further investigation is needed,” Calvin, who was not involved in the study, said in an email.
“I would say at this point, there is nothing we need to do in clinical practice, but it certainly helps us ask new scientific questions. Proteins involved in brain disease, such as the prion protein in Creutzfeldt-Jakob disease and bovine spongiform encephalopathy, are transmissible,” he said. “Additionally, other proteins involved in diseases such as alpha-synuclein in Parkinson's disease and Lewy body dementia share some of these properties, but do not appear to be transmissible. The science of amyloid and tau proteins in Alzheimer's disease may need to be reexamined.
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