Scientists discover sleep switch that builds muscle, burns fat, and boosts brainpower

 Deep sleep does more than help you feel rested. It actively rebuilds your body, strengthening muscles, supporting bone growth, and helping burn fat. For teenagers, it is also essential for reaching full height potential.

At the center of all this is growth hormone, which surges during sleep. But scientists have long puzzled over why poor sleep, especially the early deep stage known as non-REM sleep, leads to lower levels of this critical hormone.

Scientists Discover the Brain Circuit Behind It

Researchers at the University of California, Berkeley, have now uncovered the answer. In a study published in Cell, they mapped the brain circuits that control growth hormone release during sleep and identified a new feedback system that keeps those levels in balance.

This discovery offers a clearer understanding of how sleep and hormones work together. It may also open the door to new treatments for sleep disorders linked to metabolic diseases like diabetes, as well as neurological conditions such as Parkinson's and Alzheimer's.

"People know that growth hormone release is tightly related to sleep, but only through drawing blood and checking growth hormone levels during sleep," said study first author Xinlu Ding, a postdoctoral fellow in UC Berkeley's Department of Neuroscience and the Helen Wills Neuroscience Institute. "We're actually directly recording neural activity in mice to see what's going on. We are providing a basic circuit to work on in the future to develop different treatments."

Lack of sleep does more than leave you tired. Because growth hormone helps control how the body processes sugar and fat, poor sleep can increase the risk of obesity, diabetes, and heart disease.

The Brain Regions Driving Growth Hormone

The system behind this process is buried deep in the hypothalamus, an ancient part of the brain shared by all mammals. Here, specialized neurons release signals that either trigger or suppress growth hormone.

Two key players are growth hormone releasing hormone (GHRH), which stimulates release, and somatostatin, which inhibits it. Together, they coordinate hormone activity across the sleep-wake cycle.

Once growth hormone enters the system, it activates the locus coeruleus, a brainstem region that controls alertness, attention, and cognitive function. Disruptions in this area are linked to a wide range of neurological and psychiatric disorders.

"Understanding the neural circuit for growth hormone release could eventually point toward new hormonal therapies to improve sleep quality or restore normal growth hormone balance," said Daniel Silverman, a UC Berkeley postdoctoral fellow and study co-author. "There are some experimental gene therapies where you target a specific cell type. This circuit could be a novel handle to try to dial back the excitability of the locus coeruleus, which hasn't been talked about before."

How Sleep Stages Control Hormone Release

To study this system, researchers recorded brain activity in mice by inserting electrodes and stimulating neurons with light. Because mice sleep in short bursts throughout the day and night, they provided a detailed view of how growth hormone changes across sleep stages.

The team found that GHRH and somatostatin behave differently depending on whether the brain is in REM or non-REM sleep.

During REM sleep, both hormones increase, leading to a surge in growth hormone. During non-REM sleep, somatostatin drops while GHRH rises more modestly, still boosting hormone levels but in a different pattern.

A Surprising Feedback Loop in the Brain

The researchers also uncovered a feedback loop that links growth hormone to wakefulness. As sleep continues, growth hormone gradually builds up and stimulates the locus coeruleus, nudging the brain toward waking.

But there is a twist. When this brain region becomes too active, it can actually trigger sleepiness instead, creating a delicate balance between sleep and alertness.

"This suggests that sleep and growth hormone form a tightly balanced system: Too little sleep reduces growth hormone release, and too much growth hormone can in turn push the brain toward wakefulness," Silverman said. "Sleep drives growth hormone release, and growth hormone feeds back to regulate wakefulness, and this balance is essential for growth, repair and metabolic health."

Why It Matters for Brain and Body

This balance does more than affect physical growth. Because growth hormone works through brain systems that control alertness, it may also influence how clearly you think and how focused you feel.

Source: ScienceDaily

Scientists find the genetic switch that makes pancreatic cancer resist chemotherapy

 Researchers at Duke-NUS Medical School have discovered a molecular "switch" that determines whether pancreatic cancer cells respond to chemotherapy or resist it. The finding points to a way to potentially shift some of the most treatment resistant tumors into a state where existing drugs can work more effectively.

The study, published in the Journal of Clinical Investigation, explains how this switch operates at a molecular level. The results suggest that pairing targeted therapies with standard chemotherapy may improve outcomes for patients whose tumors no longer respond to treatment.

Why Pancreatic Cancer Is So Difficult to Treat

Pancreatic cancer is one of the deadliest cancers worldwide. In Singapore, it ranks as the ninth most common cancer but the fourth leading cause of cancer related death. Because symptoms often appear late and current treatments have limited impact, most patients depend on chemotherapy, which typically provides only modest benefit.

Over the past decade, scientists have identified two main molecular subtypes of pancreatic cancer, classical and basal. Tumors in the classical subtype tend to be more organized at the cellular level, and patients with this form are more likely to respond to treatment. In contrast, basal subtype tumors are more disorganized and aggressive, and they are often resistant to chemotherapy.

Importantly, pancreatic cancer cells are not fixed in one subtype. They can shift between these states, moving from a more treatable form to a more resistant one. This flexibility is known as cancer cell plasticity.

The Role of GATA6 in Tumor Behavior

The research team focused on a gene called GATA6, which helps maintain pancreatic cancer cells in the more structured and less aggressive classical state. When GATA6 levels are high, tumors tend to grow in a more organized way and are more likely to respond to chemotherapy. When GATA6 levels fall, cells lose that structure, become more aggressive, and are harder to treat.

Professor David Virshup of Duke-NUS's Programme in Cancer & Stem Cell Biology, the study's lead author, said:

"We have known that pancreatic cancer cells can switch between these two states. What we didn't understand was the mechanism driving that switch. By identifying the pathway that suppresses GATA6, we now have a clearer picture of how tumors become resistant -- and potentially how to reverse that process."

KRAS and ERK Pathway Drive the Switch

The researchers traced the switch to a chain of signals inside pancreatic cancer cells. A gene called KRAS, which is mutated in nearly all pancreatic cancers, sends constant growth signals that drive tumor development. KRAS passes these signals through a partner protein known as ERK, which relays the instructions further inside the cell.

When the ERK pathway becomes highly active, it protects another protein that interferes with the production of GATA6. As GATA6 levels drop, cancer cells lose their organized structure, shift toward the more aggressive basal state, and become much less responsive to chemotherapy.

Using genetic screening, molecular analysis in cancer cells, and drug treatments, the team demonstrated that blocking the KRAS and ERK pathway lifts this suppression. When that happens, GATA6 levels rise again. The cancer cells then shift back toward the more organized state and regain sensitivity to chemotherapy.

Combination Therapy Shows Stronger Effects

The study also found that higher levels of GATA6 on their own made pancreatic cancer cells more responsive to treatment. When drugs that inhibit the KRAS and ERK pathway were combined with standard chemotherapy, the anti cancer effects were stronger than with either approach alone. However, this enhanced benefit occurred only when GATA6 was present, highlighting its central role in determining which patients might benefit most from combination therapy.

These findings help clarify why patients with higher GATA6 levels often respond better to certain chemotherapy regimens. They also provide a scientific foundation for ongoing clinical trials that are testing new treatments aimed at KRAS and related pathways.

Professor Lok Sheemei, Duke-NUS' Interim Vice-Dean for Research, said:

"Pancreatic cancer remains one of the toughest cancers to treat. These findings provide a mechanistic explanation for why tumors respond poorly to chemotherapy and offers a rational strategy for combining targeted therapies with existing drugs."

Broader Implications for Other KRAS Driven Cancers

The implications may extend beyond pancreatic cancer. Many other cancers fueled by KRAS mutations show similar shifts in cell behavior and treatment response. Understanding how cancer cells transition between different states could help researchers address therapy resistance in additional cancer types.

Source: ScienceDaily

Hidden sugar patterns on human cells

 Every human cell is covered by a thin layer of sugars called the glycocalyx. This outer coating helps cells interact with their surroundings and may also provide important clues about what is happening inside the cell itself. Researchers at the Max Planck Institute for the Science of Light (MPL) have now created detailed maps of these sugar structures using advanced high resolution microscopy. Their findings, published in Nature Nanotechnology, suggest that changes in the arrangement of these sugars could one day help doctors detect diseases such as cancer.

The glycocalyx surrounds all human cells like a protective outer shell. Rather than remaining fixed in place, these complex sugar molecules constantly shift and reorganize. Scientists in the "Physical Glycosciences" research group, led by Prof. Leonhard Möckl at MPL, study how this sugar coating behaves and what it reveals about cell biology.

To investigate these structures, the team developed a technique called "Glycan Atlasing." Using cutting edge super resolution microscopy, they mapped the glycocalyx at the level of individual sugar molecules across many different types of cells. Their work included cell culture lines, primary human blood cells, and tissue samples.

The resulting maps showed that the glycocalyx changes its molecular arrangement depending on the condition of the cell. For example, immune cells displayed different sugar patterns after being stimulated, similar to what happens during an immune response. According to the researchers, this provides the first direct evidence that the glycocalyx functions almost like a display screen, showing information about a cell's internal state on its outer surface.

Sugar Patterns Could Help Detect Cancer

The team found that these nanoscale sugar patterns could reliably distinguish between different cellular states. Their measurements allowed them to identify separate stages of cancer development, tell the difference between activated and inactive immune cells, and distinguish cancerous regions from healthy regions in human breast tissue.

The findings suggest that the cell surface contains structured biological information that can be read using a standardized approach. "The results provide a promising foundation for the development of future diagnostic methods, as Glycan Atlasing delivers reliable results even in complex samples," explains Möckl, the study leader and corresponding author.

Future Medical Applications

The researchers now plan to expand the method by analyzing additional target structures and automating more of the process. They also hope to study much larger numbers of samples so the technique can eventually be adapted for routine medical use.

"In large-scale studies, we want to investigate which surface patterns are associated with specific disease courses or therapeutic responses and how cell states can be detected early and objectively via the surface," Möckl explains, outlining his team's future plans.

Source: ScienceDaily

New study debunks the biggest fear about yo-yo dieting

 Repeated weight loss followed by weight regain, often called "yo-yo dieting" or weight cycling, has long been viewed as unhealthy and potentially even worse than staying overweight. However, a major new review published in The Lancet Diabetes & Endocrinology argues that this belief is not backed by strong scientific evidence.

In an invited Personal View article, Professor Faidon Magkos of the University of Copenhagen and Professor Norbert Stefan of the German Center for Diabetes Research (DZD), University Hospital Tübingen, and Helmholtz Munich reviewed decades of research involving both humans and animals. After examining the evidence, they found no convincing proof that weight cycling itself causes long-term harm in people with obesity.

"Many people struggling with weight are discouraged from trying to lose weight because they fear 'yo-yo dieting' will lead to muscle loss and somehow damage their metabolism," says Prof. Magkos. "Our review indicates that these fears are largely unsupported. In most cases, the benefits of trying to lose weight clearly outweigh the theoretical risks of weight cycling."

Longstanding fears about yo-yo dieting

For years, weight cycling has been linked to a wide range of health concerns, including greater fat accumulation, faster muscle loss, slower metabolism, and increased risks of diabetes and cardiovascular disease. These concerns have influenced public opinion and even medical advice, leading some people to believe repeated dieting attempts may ultimately cause more harm than benefit.

The new analysis disputes that idea.

What researchers found

The researchers reviewed observational studies, randomized clinical trials, and animal studies focused on repeated weight loss and regain. They looked at how weight cycling affects body weight, body composition, metabolism, and blood sugar control.

"Once you properly account for pre-existing health conditions, aging, and overall exposure to obesity, the supposed harmful effects of weight cycling largely disappear," explains Prof. Stefan.

The review found no consistent evidence that weight cycling leads to excessive loss of lean (muscle) mass or causes lasting metabolic slowdown. In many cases, people who regained weight returned to a body composition similar to where they started, rather than ending up in worse condition. The researchers also found no strong evidence that weight cycling is responsible for the gradual long-term weight gain commonly seen in obesity.

Weight regain versus actual harm

The authors stress an important distinction. Regaining weight can undo many of the positive effects of weight loss, including improvements in blood sugar, blood pressure, and cholesterol levels. But losing those benefits does not necessarily mean a person becomes less healthy than they were before losing weight.

"Regaining weight brings people back toward baseline risk -- not beyond it," says Magkos. "There's a crucial difference between losing benefits and causing harm."

Several large studies also showed that when researchers account for a person's average body weight over time, weight cycling itself is no longer linked to higher risks of diabetes or cardiovascular disease. Instead, excess body fat appears to be the main factor driving metabolic risk.

Implications for obesity drugs and treatment

The findings arrive at a time when newer obesity medications, including GLP-1 and dual incretin agonists, are becoming increasingly common. These drugs can produce significant weight loss, but many patients regain weight after stopping treatment, creating a pattern similar to weight cycling.

According to the researchers, this regain should not automatically be viewed as harmful. Even temporary periods of weight reduction can still provide important health benefits and improve quality of life, even if the weight loss is not permanent.

A reassuring message for patients

Magkos and Stefan say the evidence should encourage people with overweight or obesity not to abandon efforts to lose weight simply because maintaining weight loss can be difficult.

"The idea that 'yo-yo dieting ruins your metabolism' is not supported by robust evidence," they say. "Trying -- and even failing -- to lose weight is not harmful. But giving up altogether may be."

Source: ScienceDaily

Lost 1,200-year-old manuscript contains the first English poem

 Researchers from Trinity College Dublin have uncovered an early 9th century manuscript in Rome containing one of the oldest surviving versions of the earliest known poem written in English.

The manuscript, now housed in the National Central Library of Rome, includes Caedmon's Hymn, a short Old English poem believed to have been composed more than 1,300 years ago. Scholars date the manuscript to between 800 and 830, making it the third oldest surviving copy of the poem ever identified.

What makes the discovery especially important is the way the poem appears in the text. In the two older surviving manuscripts, preserved in Cambridge and St Petersburg, the poem is written mainly in Latin, with the Old English lines added later in the margins or at the end. In the Rome manuscript, however, the Old English version is woven directly into the main Latin text itself.

According to researchers from Trinity's School of English, this suggests that early medieval readers placed significant value on Old English poetry.

The Origins of Caedmon's Hymn

Caedmon's Hymn is a nine line poem praising God for the creation of the world. It was written in Old English, the language spoken in England during the early Middle Ages.

The poem survives today because it was copied into certain manuscripts of Ecclesiastical History of the English People, an 8th century history written in Latin by the English monk Bede.

Tradition holds that the poem was composed by Caedmon, a cowherd from Whitby in present day North Yorkshire, after a divine visitation inspired him to sing.

The newly identified manuscript was discovered by medieval manuscript experts Dr. Elisabetta Magnanti and Dr. Mark Faulkner of Trinity College Dublin. Their findings were published in the open access journal Early Medieval England and its Neighbours by Cambridge University Press.

Dr. Elisabetta Magnanti explained: "I came across conflicting references to Bede's History in Rome, some pointing to its existence and some indicating it was lost. When its existence was confirmed by the library and the manuscript was digitized for us, we were extremely excited to find that the manuscript contained the Old English version of Caedmon's Hymn and that it was embedded in the Latin text.

"The magic of digitization has allowed two researchers in Ireland to recognize the significance of a manuscript now in Rome, containing a poem miraculously composed in Northern England by a shy cowherd a millennium and a half ago. This discovery is a testament to the power of libraries to facilitate new research by digitizing their collections and making them freely available online."

Why the Discovery Matters

Researchers say the find offers rare insight into the earliest history of written English.

Dr. Mark Faulkner said: "About three million words of Old English survive in total, but the vast majority of texts come from the tenth and eleventh centuries. Caedmon's Hymn is almost unique as a survival from the seventh century -- it connects us to the earliest stages of written English. As the oldest known poem in Old English it is today celebrated as the beginning of English literature.

"Unearthing a new early medieval copy of the poem has significant implications for our understanding of Old English and how it was valued. Bede chose not include the original Old English poem in his History, but to translate it into Latin. This manuscript shows that the original Old English poem was reinserted into the Latin within 100 years of Bede finishing his History. It is a sign of how much early readers valued English poetry."

A Manuscript With a Turbulent History

The rediscovered manuscript is one of at least 160 surviving copies of Bede's History. It was produced at the Abbey of Nonantola in northern central Italy sometime between 800 and 830 before eventually making its way to Rome.

Researchers say the manuscript endured a complicated journey over the centuries. During the Napoleonic Wars in the 1810s, it was moved along with other manuscripts to the church of San Bernardo alle Terme in Rome for safekeeping. It was later stolen and passed through several private owners before ultimately being acquired by the National Central Library of Rome.

Because of this tangled ownership history, many Bede scholars had considered the manuscript lost since 1975. Its importance remained unnoticed until the library digitized the document.

Valentina Longo, Curator of Mediaeval and Modern Manuscripts at the National Central Library of Rome, said: "Today, the National Central Library of Rome holds the largest collection of early medieval codices from the benedictine abbey of Nonantola. This collection comprises 45 manuscripts dating from the sixth to the twelfth century, divided between the original Sessoriana collection and the Vittorio Emanuele collection, where the manuscripts recovered following their dispersal due to the 19th-century theft have been housed. The whole Nonantolan collection has been fully digitized and is accessible through the library's website."

Andrea Cappa, Head of Manuscripts and Rare Books Reading Room, National Central Library of Rome, added: "The Central National Library of Rome continually expands its digital collections, providing free access to its resources. The library has already made available digital copies of around 500 manuscripts, and is also completing a major project to digitize the holdings of the National Centre for the Study of the Manuscript, which includes microfilm reproductions of approximately 110,000 manuscripts from 180 Italian libraries. This initiative will give scholars and researchers access to more than 40 million images."

Source: ScienceDaily

Stunning 150-million-year-old stegosaur skull rewrites dinosaur evolution

 Paleontologists from the Fundación Conjunto Paleontológico de Teruel-Dinópolis have published new findings in the scientific journal Vertebrate Zoology describing an extraordinary stegosaur skull discovered in Riodeva (Teruel, Spain). The fossil, which comes from a plated dinosaur that lived about 150 million years ago, is also helping researchers propose a new explanation for how stegosaurs evolved and spread across the world.

Stegosaurs were plant-eating dinosaurs that walked on four legs and are best known for the rows of plates and spikes running from their necks to their tails. The newly studied fossil was uncovered during excavations led by Fundación Dinópolis at the "Están de Colón" site within the Villar del Arzobispo Formation, which dates back to the Late Jurassic period.

Researchers identified the specimen as Dacentrurus armatus, one of Europe's most iconic stegosaurs. The fossil is considered the best-preserved stegosaur skull ever discovered in Europe, a remarkable achievement because dinosaur skulls are extremely delicate and rarely survive intact over millions of years.

Sergio Sánchez Fenollosa, researcher at Fundación Dinópolis and co-author of the study, said: "The detailed study of this exceptional fossil has allowed us to reveal previously unknown aspects of the anatomy of Dacentrurus armatus, the quintessential European stegosaur, which in 2025 marks 150 years since its first description. Dinosaurian skulls are rarely preserved due to the extreme fragility of their bones. This discovery is key to understanding how stegosaurian skulls evolved.

"Furthermore, alongside the anatomical study, we have also proposed a new hypothesis that redefines the evolutionary relationships of stegosaurs worldwide. As a result of this work, we have formalized the definition of a new group called Neostegosauria."

New Dinosaur Evolution Hypothesis

The researchers say Neostegosauria includes medium and large stegosaur species that lived across several continents during different periods of the Jurassic and Early Cretaceous. According to the study, members of this group inhabited areas that are now Africa and Europe during the Middle and Late Jurassic, North America during the Late Jurassic, and Asia during the Late Jurassic and Early Cretaceous.

The team believes this new classification could reshape how scientists understand the evolutionary history and global distribution of plated dinosaurs.

Fossil Site Still Producing Important Discoveries

Alberto Cobos, managing director of Fundación Dinópolis and co-author of the research, emphasized the broader importance of the discovery: "This dual achievement-both the study of an exceptional fossil and the proposal of a new evolutionary hypothesis-positions this research as a global reference in stegosaurian studies.

"This fossil site from Riodeva continues to be a subject of research and still holds numerous relevant fossils, including more postcranial elements from the same adult specimen and, notably, juvenile individuals, a particularly rare combination in this type of dinosaurs. These discoveries continue to exponentially increase the paleontological heritage of the province of Teruel, making it one of the iconic regions for understanding the evolution of life on Earth."

Scientists say the Riodeva fossil site continues to yield valuable material, including additional bones from the same adult dinosaur and rare juvenile remains. Discoveries like these are helping establish Teruel as one of the world's most important locations for studying prehistoric life and dinosaur evolution.

Study Published in Vertebrate Zoology

The research appears in Vertebrate Zoology under the title "New insights into the phylogeny and skull evolution of stegosaurian dinosaurs: An extraordinary cranium from the European Late Jurassic (Dinosauria: Stegosauria)." The paper was authored by paleontologists Sergio Sánchez Fenollosa and Alberto Cobos of Fundación Dinópolis.

The project was supported by Fundación Dinópolis, which is affiliated with the Dept. of Medio Ambiente y Turismo of the Gobierno de Aragón. It also forms part of the activities of Research Group E04-23R FOCONTUR, funded by the Gobierno de Aragón through the Dept. of Empleo, Ciencia y Universidades.

Additional support came from the Unidad de Paleontología de Teruel, funded by the Gobierno de España through the Ministry of Ciencia, Innovación y Universidades. Excavation work at the site also received backing through the project Los yacimientos paleontológicos de la provincia de Teruel como factor de desarrollo territorial (IV), funded jointly by the Gobierno de España and the Gobierno de Aragón through the Teruel Investment Fund via the Dept. of Presidencia, Economía y Justicia.

Source: ScienceDaily

Scientists reverse Alzheimer’s in mice with breakthrough nanotechnology

 An international team of researchers has reported a striking Alzheimer's breakthrough in mice using specially engineered nanoparticles that do much more than deliver medicine. These microscopic particles act as drugs themselves, helping the brain restore its own natural cleaning system and dramatically reducing toxic protein buildup linked to Alzheimer's disease.

The work was led by scientists from the Institute for Bioengineering of Catalonia (IBEC) and West China Hospital Sichuan University (WCHSU), together with collaborators in the United Kingdom. Their findings were published in Signal Transduction and Targeted Therapy.

Instead of focusing directly on damaged neurons, the scientists targeted the blood-brain barrier (BBB), a protective network of cells and blood vessels that controls what enters and leaves the brain. In Alzheimer's disease, this system gradually breaks down, allowing harmful proteins to accumulate and damaging brain function over time.

The researchers designed bioactive nanoparticles called "supramolecular drugs" to help restore this barrier and restart the brain's ability to remove waste.

Repairing the Brain's Cleanup System

The human brain uses enormous amounts of energy. In adults, it consumes around 20% of the body's total energy supply, and in children the figure can reach 60%. To meet those demands, the brain depends on an extremely dense network of blood vessels. Scientists estimate the brain contains roughly one billion capillaries, with nearly every neuron connected to its own blood supply.

Growing evidence suggests these blood vessels play a far larger role in dementia than previously thought. Many researchers now believe vascular damage is not simply a side effect of Alzheimer's disease but may actively drive its progression. Recent studies have also linked blood-brain barrier breakdown to early cognitive decline and increased buildup of toxic proteins.

Under healthy conditions, the blood-brain barrier helps clear waste products from the brain while blocking harmful substances such as toxins and pathogens. One of the most important waste proteins is amyloid-β (Aβ), the sticky material that forms plaques associated with Alzheimer's disease.

In Alzheimer's patients, the brain's waste disposal system begins to fail. As amyloid-β accumulates, neurons become damaged and memory problems worsen.

Alzheimer's Plaques Dropped Within Hours

To test the new therapy, researchers used genetically engineered mice that develop high levels of amyloid-β and progressive cognitive decline similar to Alzheimer's disease in humans.

The animals received only 3 doses of the nanoparticles. The effects appeared quickly.

"Only 1h after the injection we observed a reduction of 50-60% in Aβ amount inside the brain," explains Junyang Chen, first co-author of the study, researcher at the West China Hospital of Sichuan University and PhD student at the University College London (UCL).

The long-term results were even more dramatic. Scientists tracked the animals for months using behavioral and memory tests covering different stages of disease progression.

In one experiment, researchers treated a 12-month-old mouse (equivalent to a 60-year-old human) and evaluated it six months later. By that point, the animal was roughly comparable to a 90-year-old human. Despite its age, the mouse behaved similarly to a healthy animal with no signs of Alzheimer's-related decline.

"The long-term effect comes from restoring the brain's vasculature. We think it works like a cascade: when toxic species such as amyloid-beta (Aβ) accumulate, disease progresses. But once the vasculature is able to function again, it starts clearing Aβ and other harmful molecules, allowing the whole system to recover its balance. What's remarkable is that our nanoparticles act as a drug and seem to activate a feedback mechanism that brings this clearance pathway back to normal levels," said Giuseppe Battaglia, ICREA Research Professor at IBEC, Principal Investigator of the Molecular Bionics Group and leader of the study.

How the Nanoparticles Work

A major focus of the study was a protein called LRP1, which acts like a molecular transport system at the blood-brain barrier. Normally, LRP1 recognizes amyloid-β, binds to it, and moves it out of the brain and into the bloodstream for disposal.

But the process is delicate. If LRP1 binds amyloid-β too strongly, the transport machinery becomes overloaded and breaks down. If the interaction is too weak, waste removal does not occur efficiently enough. Either way, amyloid-β starts piling up in the brain.

The supramolecular nanoparticles were engineered to mimic the natural molecules that interact with LRP1. By doing this, the particles appear to "reset" the transport system, allowing amyloid-β to move out of the brain again.

Source: ScienceDaily