2024-02-07 18:00:00
SPECIAL OFFER: -10€ EXTRA discount on your subscription to National Geographic magazine with the code: SANVALENTIN10 Only 100 coupons!
This Valentine’s Day, give away National Geographic magazine with an EXTRA €10 discount with the coupon SANVALENTIN10. Only 100 coupons!
Alzheimer’s is the most common type of dementia, and is caused by the premature death of neurons. This deterioration of brain tissue is accompanied by memory loss, difficulty thinking, erratic behavior and disorientation. Currently, there are various hypotheses about the mechanisms behind the onset of Alzheimer’swhich can act alone or together.
Video: The effects of sugar on your brain
One of the most accepted theories, although not without great controversy, is the amyloid beta theorywhich states that the accumulation of this protein in the form of plaques damages neurons and can cause their death, triggering the symptoms of Alzheimer’s.
Although the cause is not clear, plaques or accumulations of beta amyloid are observed in sick people, as well as fibers of another protein called hyperphosphorylated Tau, so the relationship is possible.
Shutterstock
Alzheimer’s disease, aggregates of amyloid plaques.
Alzheimer’s is not contagious. However, a study presented in the journal Nature has provided evidence suggesting that it could have been transmitted to a small group of patients through medical treatment carried out more than 40 years ago. The treatment consisted of the injection of growth hormone from the pituitary of cadavers. Over the years, more than 1,800 child patients with some type of malformation or brain cancer They were treated in this way as a complement to radiotherapy, chemotherapy or other therapies.
A hormonal treatment would have caused early Alzheimer’s in five patients
Now, 40 years later, at least 5 of these patients have developed early dementia (between 35 and 55 years old). The authors conclude that this type of transmission – called iatrogenic – would shed light on the intricate mechanisms that cause the disease. According to the authors, a prion mechanism could follow. At the moment other experts urge caution, since these are isolated cases and require more evidence to demonstrate their validity. But, to understand the reason for this controversy, it is best to start at the base. And what better way to do it than talking about origami.
A special origami
Origami is the Japanese art of folding paper into recognizable shapes.. By making certain folds in a specific order, the sheets of paper come to life as small animals, objects or simple geometric shapes. Most of us have, at some point, created a small airplane to throw around the room, but few reach the level of the great masters of this art.
Applying basic rules of geometry, topology and mathematics, The most skilled origami practitioners can create realistic animals, dresses, or even fantasy landscapes that marvel and amaze anyone who sees them. Now, even if you don’t believe it, right now and without knowing it you are practicing origami much more complex than that of any master.
Maya Wei-haas
Origamist and physicist Robert J. Lang created this crane from a single square piece of paper.
And our cells are masters of their own origami. Cellular origami has different rules and materials than humans since, instead of paper, cells use the long chains of amino acids that form proteins as elements. Constantly, the hundreds of thousands of proteins that are being produced simultaneously need to be folded in very specific ways to function correctly.
The only rule of cellular origami is to get it the protein is as stable as possible with the materials with which it is made so that it can fulfill its function. In human origami, the punishment for following the steps when folding the paper is a figure different from the original, but In cellular origami, the punishment can be much more severe.
When origami goes wrong
Most proteins that have some failure in their folding can be easily eliminated by other specialized proteins called chaperonas. Once eliminated, the amino acids that form them can be used again for other processes and create correct proteins from their remains.
However, some incorrect foldings form structures that are not so easy to eliminate. Misfolded proteins can accumulate in the cell and occupy a space that is often limited, which can be a big problem. Or worse yet, A special folding can transform very specific proteins into infectious prions.
John Collinge has spent much of his life studying prions, proteins that are as terrifying as they are fascinating. Prion proteins are present in many cells, but especially in brain tissue. Although its function is not completely clearit has been observed that They can be bonded to metals. Now, misfolding of this protein can produce a infectious prion with a structure different from its natural form.
This new form, instead of becoming inactive, has the ability to take a well-formed prion protein and ‘infect’ it with its misfolding. In this way, they can be transmitted through the nervous tissue, transforming healthy proteins into malignant ones. The transformation slowly causes the deterioration and death of neurons, which triggers certain diseases, such as Creutzfeldt–Jakob in humans.
The revolutionary technique to diagnose Alzheimer’s with a blood test
One of the most famous cases involving prions occurred in the late 1980s, where bovine spongiform encephalopathy – or mad cow disease– caused havoc among stabled cattle. These animals were fed feed containing meat meal and remains of bones from other animals to increase their protein intake.
The problem occurred because some of those feed was contaminated with infectious prions from sick animals, so the cattle disaster was served. Finally, By consuming that contaminated meat, some people also developed Creutzfeldt–Jakob.
Stalled cattle consuming hay
The controversy of prions and Alzheimer’s
In the Collinge laboratory they have been studying prion diseases and their methods of transmission for years. Therefore, due to the complexity of the disorder, They believe that Alzheimer’s could, in some cases, have prion-like behavior, only through amyloid beta proteins.
According to their study, the injections that contained traces of amyloid beta proteins They could be transmitted to children and favored the creation of senile plaques at an early age. For them, the 5 cases are further proof of the prion nature of Alzheimer’s.
But this hypothesis does not convince many experts. According to comments in your X account (formerly Twitter) David Pérez, head of the Neurology Service Hospital 12 Octubre and Hospital La Luz, These extraordinary conclusions also require extraordinary evidence. As indicated, The study has major limitations. The first is that the patients received other aggressive treatments that could induce beta amyloid formationso that could be the cause of the dementia.
Furthermore, the clinical picture presented by the patients, although similar to Alzheimer’s disease, had certain atypical components, so It cannot be assured that it is this, if not another disease with similar characteristics. Finally, it points to the paradox that exists with the same 1800 patients and another disease.
Why aren’t there more cases?
The authors of the study published a previous article in which they detected 80 cases of prion disease in those 1800 patients. Prion diseases are very rare in people, so it is unlikely that they were present in the elderly corpses that were used to obtain growth hormone. Still, despite its rarity, 80 patients were diagnosed with this rare disease.
Amyloid beta protein plaqueshowever, are present in at least a third of people over 80 years of age, and only 5 cases have been reported. For this reason, David Pérez calls for caution, since if they were prion in nature, it is most likely that the number of cases would be much higher.
Without a doubt, these types of debates and controversies in the world of neurology help to specify what paths can be taken to find out the mechanisms of this complex and multifactorial disease. What is clear is that Alzheimer’s is not contagious, and that more research is needed to find out how it works and, thus, delay the symptoms as much as possible.
#transmission #Alzheimers #sparks #controversy #among #neurologists