brain

The man who failed to transform Siri and the brain of the AI ​​strategy ends his stage

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Apple has communicated that John Giannandrea, one of the most influential executives in its AI strategy in recent years, will begin a retirement process that will culminate in 2026. The company explains that the executive will leave his position as senior vice president of Machine Learning and AI Strategy, although he will continue to collaborate as an advisor in the coming months. This announcement comes months after a realignment of responsibilities related to Apple Intelligence and Siri. Giannandrea landed at Apple in 2018 as one of its most notable signings, with the task of strengthening the AI ​​strategy and giving Siri a new direction. His team was in charge of areas such as Apple Foundation Models, the internal search engine and machine learning research, technical pieces on which Apple has built much of its recent strategy. He also took on responsibility for guiding the evolution of Siri and coordinating AI projects that affected multiple teams in the company. A project that began with ambition and ended in postponements. Apple Intelligence was born as a profound renewal of the user experience, but the advances were not at the expected pace. The Information detailed that the demo shown at WWDC 2024 did not fully reflect the advanced capabilities that Apple had suggested, and that many of those features were not implemented at the time of the presentation. The pressure increased when the company confirmed that the new Siri with personalized functions would be delayed until 2026. What was supposed to be the new turning point ended up becoming a chain of postponements. Internal war in Cupertino over the direction of AI. Tensions between the AI/ML group and the software team were long-standing, according to The Information. While the area led by Giannandrea opted for a more cautious advance focused on privacy, Craig Federighi defended a more pragmatic approach aimed at tangible results. The clash of priorities became evident when some engineers began referring to the AI/ML team as “AIMLess,” a sign of the accumulated unrest. The situation led to a March 2025 twist that placed Federighi and Mike Rockwell at the forefront of Siri’s new direction. A loss of influence that had been brewing. According to Bloomberg, Tim Cook’s trust in Giannandrea suffered after the numerous delays in the development of the Apple Intelligence functions promised during WWDC 2024. In a meeting with his team, the manager admitted that the delays were “ugly” and acknowledged the shame and anger that this situation had generated among the staff. After the change in leadership in 2025, a good part of his functions began to be left in the hands of other managers, while he maintained other tasks in research into AI and robotics technologies. This shift in operational focus serves as a backdrop to the announcement that he will become an advisor before retiring in 2026. The landing of Amar Subramanya and the new architecture of power. Apple has hired Amar Subramanya as vice president of AI after his time as corporate vice president of AI at Microsoft and 16 years at Google, where he was responsible for engineering the Gemini assistant. According to the official note, Subramanya will take charge of key areas such as Apple Foundation Models, machine learning research and AI Safety and Evaluation teams. He will report directly to Craig Federighi, thus reinforcing his weight in the artificial intelligence strategy. The rest of the organization linked to this area will be under the supervision of Sabih Khan and Eddy Cue, a cast that seeks to align responsibilities with their respective departments. Giannandrea’s retirement and the arrival of new managers mark a turning point for Apple in its artificial intelligence strategy. The company now relies on a more defined structure, with Craig Federighi at the center of the project and Amar Subramanya leading key research areas and foundational models. The challenge will be to convert this reorganization into visible improvements for users and regain competitiveness in a market that evolves at high speed. Images | Apple In Xataka | Huawei has a patent with which to manufacture 2nm chips. The only problem is that it’s just a patent.

We are discovering how the brain “hacks” us to make us hungry. And it is a key step in the race towards losing weight.

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Right now, treatments to lose weight are the order of the day, with a clear protagonist like Ozempic. The problem is that beyond the aesthetic effects that are achieved, there are many doubts about both the side effects as well as all the effects it has on the body. But little by little science you understand much better how they achieve their effectwhich seems like a real miracle for many. What we knew. In general, these treatments They are ‘copies’ of GLP-1 which is a hormone that we produce normally in our body and makes us have the feeling of satiety. The moment we increase it exogenously we have a greater feeling of satiety that allows patients to lose weight (although with a risk of bouncing when treatment is stopped). But beyond this effect, the action it could have directly on the brain was something that had only been explored in animals. Now, a new study published in Nature has crossed this frontier thanks to Casey Halpern’s team, which has taken advantage of a “unique opportunity” to observe, for the first time in humans, the impact of Mounjaro (tirzepatide) directly into the reward center of the brain. Why it is important. The discovery of how the brain can ‘hack’ our body to eat much less opens many doors for us in the field of pharmacology to be able to continue working on definitive treatment. against obesitybecause we are seeing that it is something in high demand by many people who find it necessary to have this help (although it is not a miracle) to be able to reduce their weight. And we even see how in the United States purchasing is becoming more and more accessible. And we say that it is a miracle, because Ozempic or Mounjaro does part of the work, but we must not leave aside the change in eating habits to adjust the diet and be able to maintain it after stopping the treatment. The problem is that there are people who after stopping the treatment continue eating normally, and logically they see that there was no miracle involved. How it was done. The study focused on a 60-year-old woman with treatment-resistant obesity and type 2 diabetes. This patient was already taking Mounjaro for diabetes, and coincidentally, she was participating in another trial to treat dysregulated eating. This coincidence allowed the researchers to do something unprecedented: use the electrodes, already implanted in its nucleus accumbens (NAc)for hear brain activity while the drug took effect. And this brain nucleus is really important as it is the center of pleasure in humans and reward, that is, it is the point that can be modulated to restrict food consumption. The sign of craving. Those cravings we have for eating a little chocolate, a greasy pizza or a hamburger are something we all have because it is what gives us pleasure. In this case it was seen that the signal changed over the months, specifically the delta-theta frequency band. In the first months of treatments with Mounjaro, the patient had no desire for food in that sense of craving. Something that corresponded to a null signal in this nucleus, so it could be said that the medication was silencing this ‘noise’ that is generated in the pleasure center. The problem is that in the fifth to seventh months, despite being on the maximum dose of medication, the patient again had severe concern about food. And here again the signal in the nucleus had spiked to match that of those people who had no treatment. An advantage for the future. The most important finding here is that the change in the brain preceded the behavior. That is, before having a relapse this signal was increasing as if it were a warning signal. That is, a future where a sensor can detect this brain signature and alert the patient or doctor that the effectiveness of the drug is decreasing, before that the person will feel the cravings again in an uncontrolled way. Much ahead. This is a study with a single person, and it has many limitations and its conclusions logically cannot condition the clinical activity of the use of these medications. What it is useful for (and a lot) is to understand that the brain has a lot to do with this weight loss as if it were a real button to control eating habits. Perhaps silencing this brain nucleus in a very specific and sustained way may be the ‘holy grail’ that weight loss science seeks to control these cravings that can ruin a diet imposed by specialists. Although there is still a lot to investigate and it is only a first door for other medications that can complement Ozempic or Mounjaro, which has given great results. Images | Shawn Day Victoria Shes In Xataka | This is the great hope of the competition to replace Ozempic. Your weapon: banish needles with a pill

That a teenager begins to ‘hate’ his parents is something that is in his brain, and science has already found the pattern

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If you’re a parent of a teenager, you know: their world revolves around their friends. If you were one of them, you surely remember: parents’ opinion took a backseat. And although it seems that it is a sign of the rebellion that we see normal at this age, the reality is that the guilt is literally found in the brain. The culprit. But when asked what causes this indolence among adolescents? The answer comes from the magnetic resonance imaging that has been applied to the brains of some adolescents. And research shows that, during adolescence, the brain not only changes its interest, but also reconfigures your reward circuits so that the voices of strangers are more gratifying than the voice of one’s own mother. And this is something that explains the fact that adolescents give much more importance to a friend than to their own closest family, and even go so far as to prioritize them above anything else. Although in the end he has a good excuse in his brain systems. The study. To find this out, the researchers didn’t have the teens listen to scolding. They used a more cunning methodology by gathering 46 children and adolescents between 7 and 16 years old who were exposed to listening to recordings of nonsense words such as teebudie-shawlt. The important thing about this investigation was that these meaningless words were spoken by two voices: that of their own mother and that of two women unknown to them. In this way, when the recording was played, the activity of their brains began to be analyzed through functional magnetic resonance imaging (fMRI) to see the parts of the brain that were lighting up with each of the voices that were playing. The results. In the youngest children between seven and twelve years old, their mother’s voice caused a party at the reward centers of the brain, specifically in the nucleus accumbens (NAc) and the ventromedial prefrontal cortex (vmPFC). The interesting thing here is that this activity was much greater than what was felt when hearing the voices of the strangers and it is logical because the mother is the center of her social universe that causes her greater happiness. But things change completely in adolescents between 13 and 16 years old, where these same reward and social evaluation regions showed significantly greater activity for unfamiliar voices than for their own mother’s. In this way, the age that we can consider as a border between them paying attention to their mother and when they are going to completely ignore what they are told will be around 13.5 years. Because. In this case we are not talking about adolescents rejecting their parents, since in a behavioral test they were able to identify mothers’ voices in an almost perfect way. The change is precisely in the valuation of that voice. This neurobiological turn is considered an adaptive process essential for maturity. The teenage brain is being “refreshed” for a new mission: leaving the nest. To prepare for independence, the brain must begin to find new social connections more rewarding. You have to tune in with your companions, future allies and partners. The bibliography. This finding fits with previous models that were made to identify the differentiated stages in social and brain development, where the affective focus passes from the mother to friends and finally to romantic relationships. Recent reviews reaffirm that the reward system in adolescence is especially sensitive to novel social stimuli, and that the maturation of frontostriatal connections modulates these changes. A previous work by the same group had already shown that in childhood the maternal voice has a privileged response in the mesolimbic circuit and the current study extends and completes that model by showing how this pattern is reversed in adolescence. In this way, every time we see a teenager who literally tells his mother that he doesn’t even want to hear her, but spends all day talking to his friends, we already know why: his brain has changed so that he likes it more. Images | Sebastien Mouilleau Amir Hosseini In Xataka | If the question is where to find the time to play sports or learn languages, you have the answer on your mobile

From 27 to 36 years old the brain reaches its peak, then everything is downhill

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Concentration is a key skill in our daily lives, influencing how we learn, work, and perform important tasks. Without concentration, errors follow one another and the execution time multiplies. Recent studies have sought to determine at what point in our lives we reach the higher level of care and mental efficiency, a fact that may be very surprising to those who believe that young people are the most concentrated by nature. This information is also important to know what happens after that stage and how we can maintain or improve our ability to concentrate with appropriate exercises and habits. The zenith of concentration A meta-analysis A comprehensive study of 139 studies conducted by researchers from different departments at Hangzhou Normal University found that you can never be as focused as you are between the ages of 27 and 36. According to researchers, attention and memory capacity draws a Gaussian bell marking its peak between 27 and 36 years of age. During this age group, the brain achieves its greatest efficiency in sustained attention and executive skills, surpassing even those of young people as young as 20. From the age of 36, cognitive abilities related to concentration begin to deteriorate little by little, affecting processing speed and working memory. This decline is natural, but progressive, which does not imply that this capacity is lost drastically in a short period of time, the brain simply needs more care and strategies to maintain its optimal performance over time. Train body and mind Although concentration declines as maturity is reached, studies carried out at the Autonomous University of Madrid have revealed physical changes in the cerebral cortex after a cognitive training program based on memory and attention tests. The participants showed an increase in cortical thickness in regions linked to concentration control, suggesting that, with adapted exercises, the brain can develop and strengthen these abilities at any age. Maintain a mental exercise routinepromoting mindfulness and controlling distractions are key to prolonging states of concentration. Constant practice of tasks that require attention and organization techniques They are tools that help keep the brain active and alert. Furthermore, there is scientific evidence about the impact of regular physical exercise in cognitive processes, including attention and concentration, thanks to the increase in cerebral blood flow and the activation of brain regions involved in these functions. The scientific literature agrees that moderate physical activity and enriched environments promote neurogenesis and improve concentration markers. Habits that improve concentration To strengthen concentration and prevent the brain from wandering easily, it is essential to train the mind with specific exercises and adopt effective habits. According the statements By Estanislao Bachrach, a molecular biologist specialized in the relationship between the brain and human behavior, one of the most recommended exercises is daily meditation, which helps reduce stress and improve memory. The excess of distracting elements, such as cell phones or environmental noise, makes it difficult to achieve a state of attention and concentration sustained over time. multitasking He’s not a great ally either. to maintain focus, since with each task change the brain must relocate to the new task, something that takes it out of this “flow” state which Mihály Csíkszentmihályi talked about in his book ‘Flow‘. Finally, motivation plays a crucial role: when a task does not interest us or we feel anxious, nervous or overwhelmed, concentrating becomes more difficult. In Xataka | How to regain the concentration that social networks and multitasking have taken from us Image | Unsplash (Jonathan Borba)

is that they “hack” your brain so that you eat even more

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The consumption of ultra-processed foods For many, it is an ideal option in the case of not having time to cook or simply because it is something they don’t like to do. The problem is that science recently issued an alert what points to the risk that exists between the consumption of ultra-processed foods and structural changes in the brain that cause us to eat even more. As if it were a true ‘vicious circle’ from which it is very difficult to escape. The study. Using data extracted from brain scans Of almost 30,000 middle-aged participants, the team of scientists has seen the relationship between the consumption of ultra-processed foods and markers of adiposity, inflammation, or metabolism. But what interests us in this case, above all, are the modifications in brain structure. For this they used the data from UK Biobankmaking the average intake of ultra-processed foods among those studied 46% of the energy consumed in an entire day. But what was also interesting is that the scans measured cortical thickness, the integrity of the white matter and the microstructure of deep areas related to feeding. Changes in the brain. High consumption of ultra-processed foods was associated with changes in brain regions that play an important role in controlling appetite and the reward effectespecially the nucleus accumbens, hypothalamus, putamen and amygdala. The fact that it alters nucleus accumbens It is related to the reduction of neurons and an increase in extracellular space that is compatible with the processes associated with overeating and food addiction. But in addition, the study found that part of these changes were mediated by systemic inflammation and metabolic imbalances. An addictive loop. Although part of the effect involves increased adiposity and inflammation, the analysis suggests direct mechanisms on brain areas that regulate compulsive eating behaviors. Specifically, the brain changes associated with the consumption of ultra-processed foods could reinforce patterns of seeking out and excessive consumption of these same products, creating a loop that perpetuates eating the same thing. This fits quite well within clinical theories about the addictive nature of some processes and their ability to “hijack” brain circuits, reward. These circuits are what generate the pleasure that opens the door for us to have an addiction to the ‘stimulus’ that presses that pleasure button that we have in the brain. There are exceptions. Obviously, not all ultra-processed foods are the same. The research clearly differentiates between processed foods. There are some that are clearly positive, such as frozen vegetables, but others are negative, these being those that have industrial addictives and chemically modified compounds. Specifically, it has been seen how the harmful effects are strongly linked to additives such as emulsifiers, artificial sweeteners and other compounds that promote the intestinal inflammation that we hate so much, impacting the brain directly. And we already know that attacking the microbiota of our intestine has consequences that are increasingly important. Public health. The conclusions of the study reinforce the growing consensus in the scientific literature on the impact of ultra-processed foods on health. The accumulated evidence points to the importance of reducing its consumption and moving towards stricter regulations on the composition and also the advertising that is being done. The authors of the study point to the need to reduce the intake of ultra-processed foods and strengthen standards within the industry to improve the health of all citizens. Something that also has an impact on them having less contact with the doctor and that can liberalize services. Reprogramming brains. Faced with the question of whether ‘ultraprocessing’ reprograms our brain, there is still a long way to go to analyze the different pathways that exist. But clearly we are facing a first step in understanding food addiction. Images | Kobby Mendez Shelley Evans In Xataka | When it comes to meat, science knows there’s something better than protein shakes: lean pork

There are foods that literally hijack your brain.

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A potato chip crunches, the salty flavor mixes with the sweetness of the soda, and the brain asks for more. It’s not a coincidence. What seems like a simple craving is actually a programmed reaction: a dopamine rush as powerful as that caused by some drugs. More and more scientists argue that certain foods are hooking us. A new approach? For a long time, obesity and eating disorders were seen as simple matters of will. However, advances in neuroscience are changing that perception. Psychiatrist Claire Wilcox explains thatlittle by little, scientists agree on something surprising: some foods activate the brain almost the same as drugs like nicotine or alcohol. “Eating certain products—cookies, soft drinks, industrial pastries— activates the brain’s reward centersgenerating a feeling of immediate well-being. And the more we repeat that stimulus, the more we need it,” he details. The problem is that, unlike tobacco or alcohol, we cannot stop eating. What happens in our head? addictions They share three brain systems clue: The reward system, which releases dopamine when something gives us pleasure. The stress response system, involved in tolerance and withdrawal. The executive control system, which regulates impulses and helps make rational decisions. When we eat very tasty foods, the brain releases dopamine into the reward network. Learn to associate that flavor with a pleasant sensation and seek to repeat it. Over time, the circuit is “rewired”: more is needed to feel the same effect, and rational control decreases. Wilcox explains it like this: “Over time, damage to areas of executive control becomes more difficult to resist cravings, just as it is with drugs.” The science behind the debate. In recent years, research into food addiction has exploded. An article from Nature Medicinewhich analyzed almost 300 studies in 36 countries, concluded that ultra-processed foods can “hijack” the brain’s reward systems. The result: cravings, loss of control, and persistent consumption, even when there are negative consequences. Neuroscientist Mark S. Gold and psychologist Ashley Gearhardt, from the University of Michigan, they go further: “We don’t get addicted to apples, but to products designed to hit the brain like a drug.” However, medical consensus has not yet arrived. Neither the WHO nor the American Psychiatric Association recognizes food addiction as an official diagnosis. “Eating is a physiological need —remembers teacher Elisa Rodríguez Ortega—and the boundaries between addiction, bulimia or binge eating remain unclear. In the center of the bullseye. For years, sugar was identified as the great villain of the modern diet. Today, studies point to a more complex scenario: it is not just sugar, but the combination of ingredients, textures and additives in ultra-processed foods. which can make them addictive. These products—industrial blends of fats, salt, sugars, and flavor enhancers—are designed to generate immediate pleasure and encourage repeated intake. According to the Nature reviewthis “hyperpalatable” composition activates the reward system more intensely than natural foods, which would explain why it is so difficult to stop after the first bite. For its part, sugar continues to play a key role. Research, cited in JAMA Internal Medicineshow that an excess of added sugars not only increases the risk of cardiovascular diseases, but also alters the dopaminergic response, reinforcing dependence mechanisms. Qero nor we are all equally prone. Psychologist Michelle S. Hunt, a specialist in food addictions, details that there is a combination of genetic, emotional and environmental factors. “Foods rich in carbohydrates, fats or sugars activate the same areas of the brain as drugs or alcohol. Over time, the brain adjusts its receptors and requires higher doses to feel the same well-being,” he points out. Stress, anxiety and early exposure to ultra-processed foods are other triggers: the brain learns from a young age to associate pleasure with highly tasty products. “People who use food to deal with discomfort are the most vulnerable,” Hunt warns. The border with other types of disorders. Distinguishing food addiction from other eating disorders is not an easy task. According to the Eating Disorder Hope portalin both cases similar signs appear: loss of control, guilt, anxiety and, often, social isolation. a study published in Nature observed that people with bulimia or binge eating episodes present similar changes in the areas of the brain that regulate dopamine. That suggests there could be a common neurobiological basis. Dr. Mark S. Gold sums it up clearly: “Obesity and binge eating are not just behavioral problems; they also share brain mechanisms with other addictions.” For this reason, current treatments combine cognitive-behavioral therapy with cessation programs and emotional support. Reeducation with food. Unlike drugs, total abstinence is not possible: we all need to eat. For this reason, current treatments seek to reeducate the emotional relationship with food. Psychiatrist Kim Dennis runs a clinic where it combines models of addiction and eating disorders: patients learn not to restrict calories extremely – to avoid the rebound effect – but to identify the so-called “trigger” foods, those that unleash uncontrollable cravings. In parallel, drugs are also opening new avenues. Dr. Gold highlights the use of medications such as naltrexone and bupropion, or the newer GLP-1 (such as Ozempic or Mounjaro), which interrupt the link between pleasure and consumption, reducing both food intake and the desire for addictive substances. The final question. Although science has not yet settled the debate, the evidence is increasingly clear: some foods not only nourish or make you fat, they also shape the brain and habits in a profound way. Each bite leaves a mark on the pleasure circuits and the way we learn to eat. It is not about demonizing food or denying pleasure, but about accepting that eating today is an act conditioned by factors that go far beyond appetite. In a world where every flavor is optimized for hooking, true willpower may lie in knowing how to stop before the next bite. Image | Unsplash Xataka | When it comes to meat, science knows there’s something better than protein shakes: lean pork

the strange case of the brain tumor that went unnoticed for 30 years

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Imagine being laughing for no reason at all, no a laugh of joy for having heard a joke, but rather a hollow, distressing laugh that you cannot stop. For a 31-year-old woman, this was his reality since he was a baby and for everyone around her this was a simple ‘tic’ or ‘strange’ behavior on her part. But in the end it turned out to be something much more serious: a brain tumor. A clinical case that is undoubtedly exceptional and that has deserved a publication in the journal Epilepsy & Behavior Case Reports. And it is not only rare because of its symptoms, but also because of the evolution it has had, which a priori has been completely benign. Something that until now had not been documented in anyone, being exceptional. The laughter. Since childhood, the patient experienced episodes of brief, joyless laughter. Before each episode, she felt a tightness in her neck and chest, a kind of “feeling of anguish” that was warning her of what was coming. Seconds later, laughter broke out, during which she remained conscious, but distressed because no one likes to do something they don’t know why they are doing. Furthermore, without controlling the social context where it occurs. It all also adds up to a very distressing condition such as having difficulty breathing, red skin, inability to swallow or even ending up crying while laughing. But within all this there was good news: although in the past the attacks were more frequent, reaching up to 6 or 7 attacks a day that even woke her up at night, over time they became milder and briefer, lasting just one or two seconds. This allowed him to hide them on most occasions. A late diagnosis. For years the cause was a mystery. The woman underwent a brain MRI and several electroencephalograms that were reported as normal. He was even prescribed treatments with levetiracetam and lamotriginewhich had no effect and were abandoned. The key came with a second, more detailed MRI. This time, specialists found the culprit: a tiny 5mm abnormality in the hypothalamus, consistent with a hypothalamic hamartoma (HH). A hamartoma is a congenital malformation, similar to a tumor, which in this case was causing the laughter attacks. The final diagnosis was “gelastic crises secondary to a hypothalamic hamartoma”, that is, a very specific type of epilepsy. A unique case. This case is really special, but not because of what was found in the MRI, but because normally the findings are associated with very serious symptoms such as epileptic seizures or cognitive impairment. But in this case none of these problems developed. On the contrary, he led a completely normal life with university studies and a stable job in the local administration that did not cause him any difficulties. And all this without having prescribed medication. So the question in these cases is mandatory: why? The authors are not at all clear about an answer to this question. The most likely explanation is that the size of the hamartoma was exceptionally small. It has been seen in the literature that hamartomas larger than 1 cm in diameter were associated with more severe crises of the “gelastic plus” type. But the small size together with a very specific location probably explains both the mildness of the attacks and the absence of the rest of the serious symptoms. Images | OurWhisky Foundation In Xataka | That a reporter runs after a pig is the best summary of what we want from AI: videos to break the bank

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 human brain works as a predictive machine. The question is if a Cyborg future awaits us: 1×22 crossover

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We have a new episode of Crossover, the 1×22, and attentive because this time the topic is so interesting and has given so much that we have dedicated the entire program. Thus, this time we have been able to interview the Dr. José Sánchezneuroscientific and disseminator, which investigates How the brain worksemotions and Intelligence. In this interview of just over an hour Sánchez makes us an introduction to his experience with this area and then start with a unique idea: that the brain is a predictive machine. It also speaks to us, of course, artificial intelligence – the generative is of course A predictive machine– And with human emotions, but then the thing gets interesting. And he does it because with him we chat of the impact, present and Neuralink future and brain chips of other rivals. How will that impact our future? Will we end up being something like Cyborgs? We do not know, but before that happens, there is another debate we are talking about: that of social relationships and how these advances can affect mental health. Without a doubt, a spectacular episode that we hope you enjoy as much as we have enjoyed seeing it. Do not hesitate to comment, please, both here and in the YouTube channel itself. On YouTube | Crossover

Our brain also “draws the garbage.” And it is one of the reasons why sleep is so important

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We have known for a long time that sleep is more than rest, it is a vital need such as eating or breathing. Lack of sleep can have devastating consequences on our physical state, but also on our mental state. The big question for many scientists is why, a question that we have not yet answered at all, but in whose resolution we have advanced significantly. Sleep and dementia. A line of research that in recent years has gained importance has been the one that studies the role of the glinphathic system in the relationship between our dream and the appearance of dementia. The key would be in the “cleaning” work that this system exerts in our brain. The glinphathic system. The glinphathic system can be seen in certain contexts such as a cerebral analogue of the Lymphatic system. This forgotten anatomical system exercises different tasks in our body, being one of them to “take out the garbage”, clean the accumulation of waste generated by cells and eliminate harmful substances that may be present in our tissues. The lymphatic system does not extend through our brain, but someone must perform this important task in the central nervous system. A few years ago we began to understand who and how. The problem is that we have not yet managed to find out the most relevant aspects of the call GLINFATIC SYSTEM. Cleaning the plates. This cleaning work could be linked to the appearance of diseases such as Alzheimer’s. In A recent article in The conversationa group of researchers from the Macquarie University formed by Julia Chapman, Camilla Hoyos and Craig Phillips, explained this relationship. This hypothesis is based on the role they play in the appearance of the disorder Beta-amyloid proteins (Aβ). Over time these proteins tend to accumulate in our brain and, if they are not refined, they form plates that hinder the proper neurological functioning, damaging the brain and giving rise to the appearance of the disease. Night work The hypothesis that links sleep and Alzheimer’s way of the glinphathic system is also based on the idea that it is during the dream that the system takes the opportunity to clean impurities and toxins. However, the doubts about what the dream is what this relationship unleashes. As Chapman, Hoyos and Phillips stand out, studies sometimes seem to contradict, for example when measuring if the Aβ levels we find in the brain liquid are greater during sleep or during vigil. From mice to people. One of the problems we find in this line of research is that much of what we know we know it thanks to studies in micewhile the analysis with humans are limited. However, some studies have managed to approach the problem from human biology. An example cited by the team is A study Posted in 2018 in the magazine Proceedings of the National Academy of Sciences (Pnas). In it the team observed how a simple night of sleep deprivation could cause Aβ levels to increase significantly in the hippocampus. The study therefore reinforces the theory that the dream is closely linked to the probability of dementia. The risks of insomnia. The 2018 study was conducted in healthy people who experienced a night of sleep deprivation. So what about people who have insomnia or similar problems? This issue is different and requires a separate study. According to Macquarie’s team, some analysis carried out with people with insomnia and sleep apneas (interruptions caused by breathing problems) have associated these types of problems with a higher risk of dementia or with lower levels of Aβ. This again seems to support the thesis of a relationship between sleep and dementia mediated by this “cleaning system.” Another relevant issue is how sleeping pills influence, if it is at sleeping facilitate the functioning of the glinphathic system or if on the contrary the effect of these does not facilitate their night activity. A study Made in mice and published this year in the magazine Cell points to the second possibility since these compounds They did not activate the appearance of norepinephrinea compound that seems to perform an important rum in this “drain” function of toxins and other harmful compounds for the brain. In Xataka | We have been detecting a relationship between Herpes and Alzheimer’s years. Now we are discovering that treating one helps with the other Image | Craig Adderley / Milad Fakurian

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