Alzheimer’s

It is a serious mistake according to the latest study on Alzheimer’s

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To this day, Alzheimer’s disease continues to be one of the greatest challenges in medicine to understand why it occurs, to lead to better treatments. And although pharmacology is advancing in leaps and bounds to try to stop it, science makes it increasingly clear to us that lifestyle is our best weapon to prevent the disease. And we not only talk about the diet either physical exercisebut also of how the brain is ‘trained’ with writing or reading. Some activities that we are losing. New evidence. A new study published in the prestigious magazine Neurology has pointed out that having “cognitive enrichment” throughout life can reduce the risk of developing Alzheimer’s by 38% and delay the onset of the disease up to five years. Although here the question is how the brain can be enriched to avoid this devastating disease. A protective shield. The study is based on a small sample of 1939 peoplewith an average age of 80 years and with 75% women, who did not have any type of dementia at the beginning of the experiment. From here they began to follow them for eight years with different annual evaluations to determine the degree of dementia they had. But what exactly is “cognitive enrichment”? The team of researchers measured the exposure of these individuals to intellectually stimulating environments throughout their lives, which include such everyday and accessible habits as reading, writing, learning new languages, visiting museums or libraries, and having educational resources at home from childhood. The results. Once all the data was analyzed and cross-referenced, it was possible to see that the people who had the greatest cognitive enrichment showed an incidence of Alzheimer’s of 21%. This is a figure that increases as less intellectual and cultural activity is seen, until reaching an incidence of 34% in those patients who are in the 10% range of cognitive enrichment. Overall, the group with greater stimulation had a 38% lower risk of Alzheimer’s and a 36% lower risk of mild cognitive impairment. Delaying the disease. Beyond the risk percentages, the most important thing is the delay in the onset of the disease. Here the study found that people with a highly stimulated mind delayed the onset of Alzheimer’s in about five yearsmanifesting on average at 94 years of age compared to 88 years of age in the group with less stimulation. In the case of mild cognitive impairment, the “delay” achieved was even greater when the disease debuted at age 78 to age 85. What is it due to? One of the most fascinating aspects of the work comes from analyzing different corpses to see what was happening in their own brains depending on the lifestyle they lived when they were alive. And here it was seen that cognitive enrichment did not prevent amyloid plaques from forming, which is one of the causes of Alzheimer’s. What was seen here is that people who had kept their minds active with writing or reading showed much slower cognitive decline and better memory and thinking ability, even when their brains already showed the physical damage associated with dementia. It is as if the brain, having been trained and nurtured for decades, had built other pathways to continue functioning efficiently even though the main pathways began to collapse due to the ‘junk’ in the brain generated by the disease. There are nuances. In this case we have focused on an observational study based, in part, on the memory of the patients’ own experiences, such as what they did fifty years ago. This shows an important association, but it is not a direct coincidence or indisputable by other studies. However, the findings do not fall on deaf ears, but rather They add to a mountain of previous evidence which suggests that prior enrichment reduces the pathologies associated with Alzheimer’s. This makes science point to the recommendation of dedicate at least one hour a day to hobbies and reading can protect our brain. Technology against us. It is a reality that today some activities such as handwriting have declined in favor of writing on a tablet or computer to take notes or write emails. This is also added to the fact that audiobooks are beginning to have a lot of weight in our daily lives, which means that we train our brain less and less to put on and read a good book. In this way, keeping the brain busy with activities such as crossword puzzles, sudoku or any type of activity can be essential to stop diseases as devastating as this one. Images | Thought Catalog In Xataka | Alzheimer’s no longer seems irreversible: science allows brains with advanced damage to recover for the first time in animals

The new strategy against Alzheimer’s is not to attack, but to ‘reprogram’ the brain to clean itself

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Alzheimer’s can be resemble a great fortress with a large number of defenses that makes it very difficult for us. One of its most formidable defenses is blood brain barriera biological wall that protects the brain from harmful substances, but, ironically, also prevents the entry of most drugs. In Alzheimer’s patients, this barrier not only blocks help, but also becomes an accomplice to the disease. But we have already found a way to access and attack this pathology. The investigation. A team of scientists has been able to develop a radically new strategy to treat Alzheimer’s. Instead of trying to force entry into the brain, they have created smart nanocapsules that “reprogram” the barrier itself to do its job again: actively cleaning up toxic waste. Something that they have already tested in mice, and they have given spectacular results: a reduction of almost 45% of the amyloid load in just two hours and a cognitive recovery that was maintained for six months. The problem. In order to understand this advance, we must know exactly how ‘access’ to our brain works. The blood-brain barrier (BBB) ​​functions as an incredibly strict customs checkpoint. Like any border, it must have an entry and exit gate and in this case it is the LRP1 receiver. In the case of a healthy brain, LRP1 will be responsible for capturing beta-amyloid proteins and transporting them out of the brain for elimination. But in the case of a brain that is already old, and more markedly in Alzheimer’s, the amount of these LRP1 receptors is reduced, causing beta-amyloid to end up accumulating in our neurons, causing this disease to begin to show signs of presence. The discovery. In this case, the research team discovered that the fate of the LRP1 receptor depends on how it interacts with the molecules that bind to it. This is where the concept of “greedy,” or total bonding strength, comes into play. Very strong union. If a molecule clings too tightly to LRP1 (as beta-amyloid aggregates do in Alzheimer’s), the receptor activates an emergency pathway that sends it directly to be destroyed in the cellular “dumping ground” that is the lysosomes. This makes the problem even worse, as it eliminates the few exit doors left in the brain to take out the ‘garbage’. Moderate union. Or average greed. If the binding is “just right,” the receptor activates a non-destructive express transport pathway (the PACSIN2 pathway). This pathway creates a kind of tubular tunnel that transports cargo through the barrier quickly and safely, preserving the LRP1 receptor so it can continue working. In fact, this pathway even promotes the expression of more LRP1 receptors, which is what interests us most in this situation. The result. Based on this principle, the researchers designed nanocapsules called “polymersomes” (A₄₀-POs). They are tiny spheres decorated with a very specific number of “keys” (angiopep-2 ligands) on their surface. The number of these keys was calculated to achieve that perfect “medium greed”, with the aim of achieving the result similar to that of a moderate union. Results. When they administered these nanocapsules to model mice with advanced Alzheimer’s, the effects were surprising. A massive brain cleanse was achieved in just two hours, causing beta-amyloid protein levels in the mice’s brains to be reduced by 45%. In order to confirm that the protein was not just moving from place to place, its blood levels were measured. The result was an 8-fold increase, which shows that the blood-brain barrier was expelling the ‘waste’. The tests. In order to see the result in practice, behavioral tests such as the Morris water maze were carried out. Here treated Alzheimer’s mice showed significant improvement in spatial learning and memory. In this case, their performance became comparable to healthy mice without the disease. Most strikingly, these cognitive benefits persisted for up to six months after a single course of treatment, suggesting a long-term restorative effect. More than a drug. This work represents a paradigm shift. Most therapeutic strategies for Alzheimer’s treat the blood-brain barrier as an obstacle to overcome. This new approach treats it as a dysfunctional biological system that can be repaired by adding more exit doors for the organism to maintain this homeostasis. By using these nanocapsules with the “perfect keychain”, not only is the existing beta-amyloid removed, but the brain’s natural cleaning mechanism is reactivated. The treatment was able to restore levels of LRP1 and the beneficial transport pathway (PACSIN2) while reducing the destructive pathway. In essence, nanocapsules are not the drug itself, but a tool to reprogram the biology of the brain so that it heals itself. Although the results have been obtained in mouse models and the path to human trials is long and complex, this research opens a completely new and hopeful therapeutic avenue. The idea of ​​”repairing the barrier instead of just breaking it down” could be the key not only to Alzheimer’s, but also to other neurodegenerative diseases where transport and brain clearance play a key role. Images | Bhautik Patel In Xataka | We have a new “theory of everything” to understand Alzheimer’s. Its key is in some small granules

The body warns of Alzheimer’s long before the brain. The track is in the intestine

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Keep ‘healthy’ The bacteria we have in the intestine It is more important than we can think. During the last decade there are many voices that have arisen pointing to the relationship between our microbiota and other parts of our body. Now, a study has given light on the amazing connection that exists between digestive and metabolic health and the risk of developing diseases neurodegenerative as Alzheimer’s either Parkinson. A study that has used data of all kinds. Research, published in Science Advances, Not only identifies specific disorders that increase the risk of these diseases, but also demonstrates that these signals can be detected up to 15 years before neurological diagnosis, opening a new and promising via for Early detection and prevention. The work, which analyzed the clinical, genetic and proteomic data of hundreds of thousands of biobancos such as the UK Biobank, Finngen and Sail, is the most extensive of its kind and reinforces the importance of called intestine-corebro axisthe complex communication network that connects our digestive system with the central nervous. Digestive disorders and Alzheimer’s. The researchers analyzed the association of 155 digestive, endocrine, metabolic and nutritional disorders with the future risk of Alzheimer and Parkinson. The results are revealing. For Alzheimer’s, it was found that previous diagnoses of the following conditions significantly increased the risk: Gastritis and duodenitis Esophageal reflux disease (esophagitis) Diabetes (all types) Vitamin D deficiency Electrolyte disorders and acid-base balance Functional intestinal disorders (such as irritable intestine syndrome) There are also warning signs for Parkinson. A disease that is also neurodegenerative and is iconicly characterized with a constant tremor, among many other signs. In this case, the pathologies that could be an alert sign to generate this disease were: Dyspepsia (indigestion) Diabetes (dependent and independent of insulin) Functional intestinal disorders The importance of being a stratified study. This means that the data were divided into windows from 1 to 5, 5 to 10 and 10 to 15 years before diagnosis. This is something really important, since researchers could confirm the theory that the increase in risk is not something that happens just after the appearance of the first neurological symptoms, but it is a process that is created over more than a decade. For example, a diagnosis of non -insulin -dependent diabetes between 10 and 15 years before was associated with a 71% greater risk of developing Alzheimer’s. The importance of an early diagnosis. And it is that diagnosing a neurodegenerative disease so in advance is the best asset we have to avoid its most unwanted effects. Right now Alzheimer is an incurable disease, but There are drugs that stop the disease. From here lies the importance of having an early diagnosis, since the sooner the timely treatment begins, the more difficult it will be to progress to the worst stages. It also has protection functions. Curiously, it has been seen that a hemorrhoid diagnosis was associated with a lower risk of Alzheimer’s. The authors speculate that this could be due to a survival bias: the serious conditions that are sometimes associated with hemorrhoids could have a higher mortality rate, which would reduce the probability that these patients live enough to be diagnosed with Alzheimer’s. Genetics or lifestyle? One of the most counterintuitive findings in the study has to do with genetics. The researchers calculated the polygenic risk scores (PRS), which is a measure of genetic predisposition to a disease, and compared them. They discovered that patients who developed Alzheimer’s or Parkinson and also had one of these digestive or metabolic disorders, on average, had a lower genetic risk score than those who developed the neurological disease in isolation. Inheritance does not matter so much. These results can translate into that the person with intestinal comorbidity, environmental and lifestyle factors They play a much more decisive role in the development of Alzheimer’s or Parkinson’s than the genetic inheritance itself. It is the evidence that we needed to reinforce the idea that the disease is not only in our genetic material, but that the environment and our decisions can intervene in its development. Towards a multimodal predictive model. The true qualitative leap of the study is the creation of a multimodal prediction model. Instead of based on a single type of data, scientists combined four pillars of information: clinical, genetic, proteomic data (with the analysis of 1,463 biomarkers) and demographic. The result was a model with a predictive capacity much higher than that of any individual paradigm. For Alzheimer’s, the combined model reached a 0.90 precision (AUC), a very high level for this type of predictions. It is interesting to note that the model that excluded clinical data, but maintained genetics, proteomics and demography, obtained almost identical precision (0.89), which suggests that blood biomarkers already capture much of the biological information that underlies clinical diagnoses. A diagnosis based on an analytical. Among the most influential biomarkers were found GLIAL FIBRARRARARY ACID PREIIN (GFAP) and the light chain neurofilament (NFL), both known as indicators of neuronal damage, which validates the biological robustness of the model. This approach demonstrates that the integration of different “omics” (genomic, proteomic) with clinical data is the way to follow for truly early and personalized detection, long before cognitive symptoms or irreversible motors appear. The team has even developed an interactive web platform so that other researchers can explore the results, promoting transparency and reproducibility. Images | Weermeijer Robina Julien Tromeur In Xataka | We have a new “theory of all” to understand Alzheimer’s. Your key is in small granules

Scientists have a new very powerful tool to fight Alzheimer’s and Parkinson: quantum computers

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To solve most of the problems that scientists expect to be able to address in the future with Quantum computers capable of amending their own mistakes, such as optimization, those in the field of cryptography or artificial intelligenceit will be necessary have several million cubits. It can even, that hundreds of millions of cubits. The most advanced quantum processor currently IBM has itand it has just over a thousand cubits, so it is evident that many technological challenges remain that it is necessary to solve. The interesting thing is that there is no single way to go through this path. Organizations that are investigating in the field of quantum computing work in several different cubits technologiesand each of them is in a different degree of development. IBM, Intel and Google are some of the big companies that have opted for superconductor cubits, but also do so smaller ones, such as Atlantic Quantum, IQM, Anyon Systems, Rigetti Computing or Bleximo. In fact, if we stick to the number of companies that are working on this type of quantum bits it is reasonable to conclude that this is the technology that has greater support and greater investment, so, in some way, it is the one that goes in the lead. This strategy is probably what will help us to have more cubits, but it is also more prone to make mistakes than ion traps cubits, which are one of the alternatives to superconductors. In addition, these last cubits are characterized by working at a temperature of about 20 millikelvin, which are approximately -273 degrees Celsius, with the purpose of operating with the greater degree of isolation of the possible environment. Ion traps are given great proteins Ion traps are currently the main alternative to superconductor cubits. This is the technology in which they are working, among other companies, Ionq and Honeywell, and is characterized by using ionized atoms, and, therefore, with a non -neutral global electric charge. This property allows them to be isolated and confined inside an electromagnetic field, although this is only the starting point. From here Ionq acts on the quantum state of its cubits with ion traps cooling them to reduce the level of computational noise and uses lasers just then to operate with them. However, it does not use a single laser; Use one for each ionand also a global laser that acts on all of them simultaneously. Honeywell also uses ionized and laser atoms, but the procedure used to establish the intertwining between two ions and act on them with a laser is different from that used by Ionq. For scientists it is crucial to understand the folding of proteins that triggers Alzheimer’s or Parkinson Parkinson Precisely a team of researchers from this last company and the German emerging company specialized in quantum quantum computing To do something amazing: Solve protein folding problems with up to 12 amino acids. To carry it out they designed a quantum optimization method that seeks to find the optimal configuration of protein folding. Expressed in this way it seems complex, and it is, but the really important thing, and with what is worth it, it is that these quantum computers thanks to the appropriate algorithm are able to help scientists Understand the protein folding mechanism that triggers diseases such as Alzheimer’s or the Parkinson. And understand this phenomenon well is the first step towards the elaboration of effective treatment. This result is very promising, but there is still a lot of work to do so that quantum computers help us in front of these diseases. On the one hand, folding models must evolve to be more reliable and realistic. And, in addition, the classic algorithm that is responsible for refining the results delivered by the quantum algorithm should be more precise. Even so, the work of these researchers is an exceptionally promising starting point. Image | Ionq More information | Arxiv In Xataka | Quantum computers threaten encryption technologies. This is the reason why we do not have to panic

We have been detecting a relationship between Herpes and Alzheimer’s years. Now we are discovering that treating one helps with the other

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A few years ago the scientists detected A strange coincidencea relationship between herpes virus and a neurodegenerative and noncommissible disease: Alzheimer’s. What at the time seemed a spurious and casual relationship, it seems more and more proven and proven. Adding tests. Now a new study He has obtained evidence of this relationship. However, perhaps the most important fact that we can extract from the new analysis has to do with vaccines against infection. According to the study, antiviral treatments against herpes are related to a 17% lower risk of suffering from Alzheimer’s, suggesting that treatment against this virus can protect us against the appearance of this form of dementia. HSV-1. In study he linked again the infection by the Herpes simplex virus Type 1 (HSV-1) with the appearance of Alzheimer’s disease, a form of dementia that is characterized by accumulation in the brain of beta-amyloid plates. Today we do not have a clear idea of ​​how this relationship occurs “(Some) studies have indicated that inflammatory alterations in the brain caused by HSV infection are central to the development of (the disease),” Explain the team Resposable study. “It is pointed out that peptides (beta-amyloids (Aβ)) are deposited in response to HSV infection and protect host cells (…). Consistently, they threw antimicrobial properties against several pathogens, including HSV-1,” they detail. 344,628 matches. In his study, the team He turned to 344,628 participants with Alzheimer who were paired with two participants without diagnosis but with similar characteristics. They observed that among people with Alzheimer’s 0.44% had been previously diagnosed with HSV-1, while only 0.25% of the control group had the same previous diagnosis. The analysis indicates that, taking into account other relevant factors, the probability of finding a previous HSV-1 diagnosis was 80% higher among people with Alzheimer’s than in people without the disease. The details of the study were published In an article In the magazine BMJ Open. Not only HSV-1. The study focused on a variant of the herpes virus but also paid attention to other pathogens of the “family”, such as the HSV-2, Varicela Zoster, or Citomegalovirus. They found a relationship between two of them (HSV-2 and Vicela Zoster) and a greater risk of Alzheimer’s. Understanding the causes. New studies will still be necessary that Explain biochemical mechanisms that explain this type of relationship between infectious processes and noncommunicable diseases. Only in this way can we establish the underlying causal relationships and, hopefully, to find more effective treatments in the fight against disorders as serious as cancer and Alzheimer’s. “Although there is a lot of research ahead to find out the reasons and mechanisms that lead from infection to a process of dementia that manifests many years later, the accumulation of the evidence suggests that the management of these infections, with treatments that are effective for all herpes, or with vaccines such as herpes zoster, is an interesting tool to reduce the risk or delay dementia” explained to SMC María Jesús Bullido Gómez-Heres, head of the Research Group Pathogenic mechanisms of Alzheimer’s disease, who was not involved in the study. Not so non -transmissible diseases. This is not the only example of a noncommissible disease to which we have found a surprising relationship with past infections. A recent example We find it in colorectal cancer and its possible link with infections caused by bacteria Escherichia coli. In Xataka | We are getting closer to ahead of the arrival of Alzheimer’s. Knowing it can reassure us, but maybe too much Image | Matteo Vistocco / CDC/DR. Erskine Palmer

Alzheimer’s starts long before its symptoms. And we have discovered one of its first mechanisms

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We generally associate Alzheimer’s disease with memory loss since this is probably its most visible symptom. However, it is still what we do not know about the biological processes that unleash these symptoms. Piece by piece, we are solving this immense puzzle. New mechanism. A team in which researchers from the Severo Ochoa Molecular Biology Center (CBM-CSIC-UAM) participate He has discovered A mechanism linked to the early development of Alzheimer’s disease. The key component of this mechanism is in a protein called SFRP1. Astrocytes and SFRP1. As described by the team responsible for the finding, in the origin of the mechanism are brain cells called astrocytes. Astrocytes They are glial cells (A type of nerve cell) that for a while we thought were “assistants” of neurons but whose relevance we are seeing grow. In a mice -based model, the new study has shown that these cells could play an important role in the appearance of Alzheimer’s through an “excessive” production of the SFRP1 protein. This protein is one of the compounds involved in the regulation of communication between different cells during development, but in later stages of life its excess may imply risks. A “jam” in the brain. As the equipment continues, the accumulation of the SFRP1 protein in the adult brain is associated with chronic inflammatory processes associated with aging, and also to Alzheimer’s own disease. The problem arises when this excess blocks the activity of the adam10 enzyme, which plays a key role in maintaining the proper functioning of neuronal connections. “This blockage generates an imbalance that deteriorates synaptic plasticity, an essential cell mechanism to form and consolidate memories that allows neurons to regulate their connectivity in response to different stimuli,” They explain in a press release. Long -term synaptic potentiation. The accumulation of the SFRP1 protein would thus be interfering with a process called LTP or long -term synaptic potentiation. This is a “fundamental” process for learning and memory, the team stands out. A vital process in brain plasticity, that is, that allows the neuronal connections that are most frequently used to be reinforced, something indispensable when consolidating new memories. The details of the study have been published In an article In the magazine Cell Reports. A possible trigger. The fight against Alzheimer’s is a fight against the clock. The appearance of its most easily noticeable effects is associated with lesions already irreversible in the brain, so the only remaining route of action is to delay the advance of the disease. The techniques focused on detecting the internal signs of the disease, mainly the accumulation of amyloid plaques in the brain can allow us to advance ourselves to the appearance of the external symptoms of the disease. Now, the new study Open a road To get into stages still prior to the disease. “The increase of SFRP1 in early stages seems to act as an active engine of pathology, not as a simple companion of other degenerative processes,” Explain in the press release Guadalupe Pereyra, co -author of the study. Beyond rodents. Like any study in mice, extrapolating its conclusions can be complicated, so studies that validate what you have learned and the degree to which it is applicable to the development of the disease in humans will be needed. Converting what has learned into new therapeutic pathways will not be simple either, but this type of advance can help us in different ways. First, because understanding the disease and its mechanisms is essential in order to find a future cure; and second, since in the fight against their symptoms, Early detection It is a very important advantage. In Xataka | If the question is how to hunt the Alzheimer Image | CSIC

We are getting closer to ahead of the arrival of Alzheimer’s. Knowing it can reassure us, but maybe too much

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Get ahead of the arrival of degenerative diseases such as Alzheimer’s is today a chimera, but achieving it would be key when looking for treatments that manage to go beyond containing symptoms and are able to reverse the disease. What is already in our hand is to estimate our risk of suffering. The question is to what extent is a good idea. Pros and cons. This type of evidence that allows us to know our chances of suffering from Alzheimer’s impact on our psychological well -being and our motivation. A new study He has investigated In these effects and has observed that, although this knowledge does not have an effect on our emotional stress can reduce our motivation to maintain a healthy life. Even among people with a high risk of suffering from this disorder. Win the career to the disease. Get ahead of Alzheimer’s arrival It is key For professionals who treat it: the sooner the diagnosis is the greater the margin of maneuver to design the ideal therapeutic strategy that allows to slow down the appearance of symptoms and their progressive worsening. It also helps patients and their environment adapt to the arrival of the disease, psychologically but also more practical. Count plates. Although we do not know the mechanisms that operate after Alzheimer’s, we know that beta-amyloid plaques play a fundamental role. These clusters that are formed in the brain appear in people with this disease and are therefore an important diagnostic tool. The scanners Positron emission tomography offer a non -invasive technique that allows you to detect these clusters in the brain. From the identification of these clusters it is possible to estimate the risk that the disease begins to unleash a patient and allows health personnel and affected people to take the necessary preventive measures. 199 participants. The new study had 199 participantsall healthy adults who would go through this process to determine the presence or absence of plates in the brain. Before completing the scanner, the group completed surveys to find symptoms of anxiety, depression, memory and motivation problems; Surveys that repeated six months after the test. The details of the study were published In an article In the magazine Alzheimer’s & Dementia. Lights and shadows. As explained by the team responsible for the study, participants who did not present plaques experienced “emotional improvements”: lower depression, anxiety and even less memory problems. However, the team also observed a lower degree of motivation when taking measures to improve their lifestyle to make it healthier. Among the participants there were also cases in which plaques were detected. They also did not see an increase in depressive symptoms a memory problems, but their anxiety level was reduced. The problem is that, as in the case of the first group, its motivation to introduce changes in their day to day was also reduced. “The findings suggest that revealing the presence of amyloids does not negatively affect the participants, and simply knowing the results seems to decrease the negative feelings globally,” explained in a press release Schnaider Beeri, Ocautora of the study. The role of the psychological. Physiological diseases can affect our mental well -being, but our psychology can also play a determining role when facing body diseases. Motivation when introducing changes in our life is, in this sense, of difficult importance to estimate. In Xataka | If the question is how to hunt the Alzheimer Image | Daria Obymaha

Finding quick and reliable tests for Alzheimer’s is a key mission for science. And we have a new candidate

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Ahead of Alzheimer’s. It is a simple but difficult objective to achieve since the symptoms of this disease tend to appear when the disorder is advanced and has already caused important damage to our brain. A difficult objective but what It can help us treat the disease With greater efficacy, managing to delay the appearance of some of its symptoms such as cognitive deterioration. Maybe one day helps us cure it. In the blood. A group of researchers has tested a new blood test aimed at the early detection of Alzheimer’s disease. The test is based on a biomarker present in the blood, P-TAU217, which shows changes long before the appearance of symptoms in people with the disease. The study showed precision when detecting the disease greater than 90%. These results also did not depend on the age or gender of the participants, either on the existence of comorbidities or whether the test was carried out by specialists or primary care personnel. This marker can be measured with simple and cheap tools and the process is automatic, which can facilitate detection in various circumstances, democratizing the diagnosis of the disease. “This is an important step to bring simple blood tests for Alzheimer’s disease to health systems around the world,” said the team responsible for the essay in a press release. P-TAU217. Detection methods based on the P-TAU217 compound They are not exactly new. These types of tools are already implemented in the United States and it is expected that they will soon reach the rest of the world, says the team itself. The new method seeks to offer a simpler alternative to the available tools. The new study analyzed the precision of this New Test in the conditions in which it would be used, not only in specialized clinics but also in primary care. In three countries. The essay was carried out from 1,767 participants with cognitive symptoms distributed in three countries: Spain, Italy and Sweden. The details of the study were published In an article In the magazine Nature Medicine. The New Test included two cut points. One of them served to interpret the negative results: from this threshold the test rules out the presence of the disease. The second of the cut points serves to find the positive ones: this threshold shows the presence of the disease. This leaves, between one cut and another, a “gray zone” in which the results are inconcuing, however the use of a test with a single threshold slightly reduced the accuracy of the diagnostic tool. Above 90%. The study showed that the test achieved an accuracy between 92% and 94% when used in its two cuts mode. However, this precision fell to levels between 83% and 87% when only a cutting point was used and applied to more advanced ages. “When the method was tested in patient sides, the precision was between 92% and 94%,” NOëlle Warmenhoven explainedfirst signer of the study. “This is promising since this method will probably become one of the most used in clinical practice around the world.” In Xataka | We have a new “theory of all” to understand Alzheimer’s. Your key is in small granules Image | Kaboomps.com

Terry Pratchett was diagnosed with Alzheimer’s in 2007. They have found signs of the disease in their 90s books

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In 2007, Terry Pratchett approached Rob Wilkins, his assistant, and told him that the ‘s’ of his keyboard had disappeared. He was laughing. I thought it was a joke, an innocent. “What the hell have you done with her?” He asked. But the ‘S’ was still in the same usual place: on the keyboard. After a few months of testing, the writer knew that the only place where the ‘S’ was disappeared was his head. Postterio cortical atrophy sufferedA, a neurodegenerative disorder typically related to Alzheimer’s, which causes problems to see, to process information, to read, speak and write. He died in 2015 In a small town west of Salisbury. When does dementia begin? That basically is The question asked Thom Wilcockson and his team from the University of Laughborough. Pratchett’s case was very interesting because posterior cortical atrophy has an impact on the use of language and this man wrote a lot. So Wilcockson’s team He examined 33 Books of World Disco (29 published before 2007 and four later) to see if there was any point where the first symptoms of the disease could be identified. And it seems that. Among the first books and the last, the researchers discovered a significant decrease of number of nouns, verbs and adjectives. In addition, they found that the number of phrases increased (something that, according to researchers, fits a tendency towards simpler language). The funny thing is that the turning point was not 2007, but 1998. In that year, Pratchett published ‘The country of the end of the world‘And it is the work in which the change in trend begins to become evident. “This demonstrates a long preclinical period of dementia and the subtle deficiencies that are not always detected with traditional cognitive evidence,” Wilcockson explained. It is not the first time that the equipment uses this type of analysis. They have done it with Iris Murdoch (who also died of Alzheimer’s) and with Agatha Christie (we suspect he suffered). However, not everyone is sane with researchers. Not because they believe they are wrong, but because there are many more factors to consider. In New Scientistfor example, Rob Wilkins explained that in recent years Terry began to have a much more intense “professional life” and that prevented reviewing novels as thoroughly as previously. Be that as it may, the investigation is fascinating. Especially now, at a time when we write (and do audios) much more often than ever. Algorithms like these could dive in our emails, our WhatsApp conversations and in our social networks to identify signs of problems many years before they become evident. Image | Solarisgirl | David Skinner In Xataka | Mundodisco technology

We knew that smell and memory are closely related. And that unlocks an advantage: detect the Alzheimer’s

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Alzheimer’s disease may be difficult to detect. The symptoms of this disorder usually become evident only after the progress of this dementia, which is a huge problem. And, in the absence of a definitive cure, our ability to stop the impact of the disease depends largely on early detection. Smell. One of the clues we have when detecting Alzheimer’s in its early stages is through smell. A study conducted by researchers from the University of Chicago analyzed the impact of the disease on our sensory capacity and detected that there is a rapid loss of smell when making us greater could predict with some accuracy The advent of Alzheimer’s disease. Smell of Magdalena. The relationship between memory and smell is very narrow. We know that the evocative capacity of smells It did not go unnoticedbut in recent decades science He has been confirmed This unique connection. The reason for this close relationship can be anatomical. The olfactory bulb is the region of the brain that processes in the first instance the smells and then send the signal to other areas of the brain. This signal crosses key areas of the limbic system, areas linked to emotions and memory. “The olfactory signals reach the limbic system very quickly,” Explain to The Harvard Gazette Venkatesh Murthy, head of the university’s cell and molecular biology department. 515 participants. The study of the University of Chicago had 515 participants, advanced adults, registered in the memory and aging project of the Rush University. These participants were examined annually, exams that test their cognitive abilities to detect signs of dementia. These tests also studied their ability to identify odors, in addition to other health -related parameters. More than memory loss. The team thus found a new link between smell and memory: a rapid loss of olfactory capacity prior to any cognitive loss could predict the arrival of various symptoms associated with Alzheimer’s. These symptoms included a lower volume of gray matter in the areas of the brain linked to smell and memory, cognitive loss and a greater risk of dementia. They also found a relationship between this olfactory loss and the presence of the APOE-E4 gene, a genetic variant considered risk factor in the advent of Alzheimer’s. The details of the study were published In an article In the magazine Alzheimers & Dementia. “This study provides another clue on how a rapid loss of the meaning of smell is a very good indicator of what will end structurally in specific regions of the brain,” ” explained in a press release Jayant M. Pinto, co -author of the study. Get ahead of the disease. Alzheimer’s is an incurable disease for now, but there are different treatments that allow us to delay the development of its symptoms. For that, we must get ahead of the disease as much as we can. Something difficult in a disorder that only shows its consequences once the disease is advanced. “If we could identify their 40, 50 or 60 people with greater risk, we could potentially have enough information to aim them in clinical trials and develop better medications,” also added in a press release Rachel Pacyna, work caoautora. Own initiative. The fact that the change in our smell is rapid and before the arrival of cognitive deterioration opens an important window, putting the patient itself in warning. And it is that most of the ways we have to detect the appearance of dementia is through external evaluations, for example when family members detect memory problems or In language. The loss of smell is something that, in principle, It can be striking to the patient himself and put it on guard or encourage him to seek medical advice. When the smell of the Magdalena stops bringing us memories, perhaps what we are playing is not only the evocation of a memory. In Xataka | We have a new “theory of all” to understand Alzheimer’s. Your key is in small granules Image | Cottonbro Studio

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