Hormonal treatment may have caused early Alzheimer’s disease in five patients
Beginning in 1959, thousands of children began receiving growth hormone treatment, which by then They were extracted from the pituitary glands of corpses.. It was not until 1985 that this process was stopped when it was discovered that injected drugs were transmitting proteins that cause fatal Creutzfeldt-Jakob disease to patients.
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Building on this context, a team of neurologists at University College London has spent the last decade investigating other possible side effects resulting from this disease. outdated treatment. So, in 2015 they published a study in the journal Nature in which they suggested a possible link between injections of cadaver-derived hormones and the accumulation of beta-amyloid, a known precursor protein for Alzheimer’s disease, in the brain.
Although the hypothesis caused controversy in the scientific community, especially because it was based on medical practices that are no longer usedA team led by a neurologist continued to explore this correlation: now, in their latest study, scientists have provided evidence that 5 out of 8 patients who received this treatment because the children later developed behavioral signs early onset dementia.
No, Alzheimer’s disease is not contagious.
A study published by the team in 2015 was wave of misinformation around Alzheimer’s disease. The results were so misinterpreted that voices were heard claiming that if the disease could supposedly be transmitted from the tissues of a corpse to the human body – somehow iatrogenic, that is, due to harmful consequences resulting from unintentional medical errors – then it was a contagious disease. But Nothing could be further from reality: Actually, none of the research suggests this idea.
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However, the paper in question shows the process of research carried out with postmortem brains of four people who at this time received growth hormones. They were found beta amyloid accumulationswhich are usually associated with a condition called cerebral amyloid angiopathy (AAS), which, in turn, may be a precursor to the development of Alzheimer’s disease.
Later, in 2018, a review of the analyzes led to examine batches of hormones employees over these nearly three decades, and, more importantly, John Collinge’s team discovered that training contains beta-amyloid proteins. With this evidence, the treatment was applied to the mice, causing CAA as expected by the researchers. The milestone strengthened the team’s proposal that Alzheimer’s disease, although not spread by contact, can be transmitted.
Five cases of early Alzheimer’s disease
In their latest review, based on all previous results, the researchers found that 5 out of 8 people who received hormonal treatment in childhood but did not develop Creutzfeldt-Jakob disease presented Behavior in Alzheimer’s disease early onset between 38 and 55 years of age.
This neurodegenerative disease is usually It is caused by genetic variantsfor example, being a carrier of the 2nd allele of apolipoprotein ε4, but neurologists did not find these characteristics in 3 out of 5 patients who presented signs, so they assume that Alzheimer’s disease would be transmitted through biological material extracted at that time from infected corpses.
On the contrary, they did not have to wait long. the voices that color the results presented by Collinge and his team: On the one hand, dementia experts from the University of Edinburgh argue that it is difficult to convincingly confirm the hypothesis because the study sample (8 patients) is too small. Moreover, representatives of the German Center for Neurodegenerative Diseases in Göttingen note that people may have developed dementia regardless of hormonal treatment.
In any case, the possibility of “transmissible” iatrogenic Alzheimer’s disease does not currently pose a threat, since the hormone therapy believed to be causing these cases no longer exists. With this in mind, there is no doubt that the study, although not conclusive, opens the door to further exploration of the role played by amyloid beta protein in the development of Alzheimer’s disease, which accounts for 60% to 70% of dementia cases worldwide.