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More than three years ago, a group of scientists suggested that a series of cadaver growth hormones used to treat people with Creutzfeld-Jakob Disease (CJD) would be a source of transmission beta-amyloid protein. for example, forms plaques in the brains of patients with Alzheimer's disease. Now, this team announces in the scientific journal Nature that this set of hormones contained this protein and could transmit beta-amyloid pathology to the mice. However, scientists note that the results of this study do not suggest that Alzheimer's disease is transmissible.
"Already in the 21st century, a new line of research has emerged that posits that the proteins of Alzheimer's disease are infectious," reads in the book. Why do not the dancers get their heads? (Sphere Books, 2017) by Filomena Naves and Teresa Firmino. In other words, the hypothesis that beta-amyloid could be infectious and contaminate other proteins, such as with prions (abnormal forms of protein normally produced by mammalian brain), causing spongiform encephalopathies, including CJD in humans. In this disease, prions multiply in the brain and turn into a sponge.
In 2012, Stanley Prusiner – who won the 1997 Nobel Prize for Medicine for the discovery of prions – even suggested that beta-amyloid protein deposits would be prions, that is to say, they were infectious and caused Alzheimer's disease. When aggregates of beta-amyloid were injected into the mouse brain, it was found that these deposits had increased sometime later and had spread to other areas of the brain.
The same year, Martin Hallbeck's team (from Linköping University, Sweden) revealed that he was able to observe – through colored neurons – that the beta amyloid was transmitted from neuron to neuron as an infection. "We have shown that the only diseased cells are those that have received beta-amyloid, which is why only certain areas of the brain get sick, but there is no indication that Alzheimer's disease is contagious between people, "said the scientist at the PUBLIC at the time.
Three years later – in 2015 – the team of John Collinge of University College London announced that he had detected the presence of a beta-amyloid pathology (characteristic of l 39; cerebral amyloid angiopathy and Alzheimer's disease) in the brains of four patients with DCJ. These people had received growth hormone injections of cadavers contaminated with prions. These patients died and, although some showed signs of amyloid cerebral angiopathy, none of them met all the criteria leading to Alzheimer 's disease. At the time, it was thought that they might have developed a beta-amyloid pathology because of this treatment, but further research would be needed.
As such, John Collinge's team obtained samples of this set of growth hormones. They were analyzed biochemically for beta-amyloid and tau (another protein involved in the formation of cylindrical structures in the neurons of Alzheimer's disease). Result: the presence of both proteins in some samples was confirmed.
Finally, the team asked if beta-amyloid in these samples was able to transmit a pathology of beta-amyloid. To this end, samples of these contaminated growth hormones were injected into the brains of genetically modified mice to show the first signs of beta-amyloid accumulation after six months. At approximately 240 days (eight months), beta-amyloid deposits were detected, as well as signs of cerebral amyloid angiopathy. In non-genetically modified mice, these signs were not detected.
"These results demonstrate that the initial group of cadaver growth hormones contains beta-amyloid and can transmit the pathology of beta-amyloid in mice, as well as experimental evidence to support the Hypothesis of a pathology of beta-amyloid, transmitted by the man in an iatrogenic manner [transmissão acidental através de um tratamento médico ou cirúrgico]Scientists have written in a statement about the work.They also suggest that these findings do not suggest that Alzheimer's disease is contagious or transmissible by blood transfusion.
Requested as a precaution
"This experimental confirmation has implications for both the prevention and treatment of Alzheimer's disease and should motivate a review of the risk of iatrogenic beta-amyloid transmission through long-recognized medical and surgical procedures." accidental prions. "
In a comment to the study also in Nature, Tien-Phat Huynh and David Hotzman (both from the University of Washington, USA, which were not part of the paper) emphasize the robustness of the study. "These results provide strong evidence that the previously reported pathology of beta-amyloid in patients who died of CJD after receiving cadaver growth hormones was due to the same treatment."
Other scientists, who did not participate in the work, asked to be cautious about the results. "There is no reason in this study to fear the transmission of Alzheimer's disease in humans," says Tara Spiers-Jones of the University of Edinburgh. And Diane Hanger of King's College London said: "The relevance of these findings for the development or transmission of Alzheimer's disease is still unclear because the pathology of tau n & n Has not been examined in this study, therefore the results should be interpreted with caution. "
For his part, David Reynolds, of Alzheimer's Research UK, is also concerned about linking this study to Alzheimer's transmission. "Although scientifically interesting, this research focused on a small number of people who had a very specific neurosurgical intervention, the latter having taken place in the mid-1980s." However, much has been discovered about prions and new drugs. The guidelines for sterilization and the use of surgical equipment, says David Reynolds.
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