New evidence that plaque-forming protein in the brain of patients with Alzheimer's disease is transmissible | Neuroscience



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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 beta. amyloid – which, for example, forms plaques in the brains of patients with Alzheimer's disease. Now, this team reports in the journal Nature that this set of hormones contained this protein and could transmit beta-amyloid pathology to mice. Scientists note, however, that the results of this study do not suggest that Alzheimer's disease is transmissible.

"In the twenty-first century already, a new line of research has emerged that suggests that the proteins of Alzheimer's disease are infectious". , we read in the book Why do not ballerinas have their head on the wheel? (Book Sphere, 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 2012, Stanley Prusiner – a 1997 Nobel laureate in medicine for his discovery of the disease, prions – even suggested that beta-amyloid deposits would be prions, that is, they were infectious and were responsible for Alzheimer's disease. By injecting aggregates of beta-amyloid into the mouse brain, it was found that these deposits increased sometime later and spread to other regions of the brain.

The same year, the team of Martin Hallbeck Linköping, Sweden) revealed that he was able to observe – through colored neurons – that beta-amyloid was transmitted from neuron to neuron as s it was 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 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 CJD. 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 was needed.

The team of John Collinge has now obtained samples of this set of growth hormones. They were badyzed biochemically for beta-amyloid and tau (another protein involved in the formation of cylindrical structures in the neurons of Alzheimer's disease). Results: The presence of both proteins in some samples was confirmed.

Finally, the team asked if the beta-amyloid present in these samples ability to transmit a beta pathology -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. "

" 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 in unmodified mice. because they provide experimental evidence to support the hypothesis that the pathology of beta-amyloid can be transmitted iatrogenic to humans [transmissão acidental através de um tratamento médico ou cirúrgico] ", wrote the scientists in a statement. that these results do not suggest that Alzheimer's disease is contagious or transmissible by blood transfusion.

Precautionary Claim

In the scientific article, they also emphasize: "This experimental confirmation has implications for prevention and treatment. of Alzheimer's disease and should motivate a review of the risk of iatrogenic beta-amyloid transmission through medical and surgical interventions long recognized as presenting a risk of accidental transmission of prions. "

In a commentary on the study also in Nature Tien-Phat Huynh and David Hotzman (both from the University of Washington, USA) study. "These results provide strong evidence that the previously reported pathology of beta-amyloid in people who died of CJD after receiving cadaver growth hormones was caused by the same treatment."

Other scientists, who do not do it. participated in the work, ask for caution 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 It was not examined in this study, therefore the results should be interpreted with "

David Reynolds of Alzheimer's Research UK is also cautious about the link between this study and the transmission of Alzheimer's disease." Alzheimer. "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. guidelines for sterilization and use of surgical equipment, says David Reynolds

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