Researchers successfully restore the brain's 'sweet layer' and recover memory

Aging can bring plenty of surprises, but few people suspect that part of the trouble might involve sugar. Researchers have learned that the brain’s protective coating of sugars loses some of its heft with age, and that this sugar loss might undermine the brain’s defenses.

Nobel laureate Carolyn Bertozzi, from Stanford University, became curious about this sugary armor and looked into whether replenishing it could tighten the brain’s protective barrier.

That barrier, called the blood-brain barrier, is designed to let in necessary nutrients while blocking harmful substances. This sugar coat, known as the glycocalyx, sits on cells that form the blood-brain barrier. A recent study in mice found that the glycocalyx becomes thinner over time, leaving gaps that invite unwanted molecules to slip in.

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Tree of life necklace

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Brain-friendly cities

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Blessings

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Tiny Genetic Code Disruption Alters Brain Wiring and Behavior

A small genetic sequence called mini-exon B plays a surprisingly crucial role in how neurons form synaptic connections, according to new research. Scientists found that deleting this four–amino acid segment from a synapse-building protein, PTPδ, disrupted neural activity and led to anxiety-like behaviors in mice.
The mini-exon enables PTPδ to bind with another protein, IL1RAP, forming a complex critical for excitatory synapse development. This discovery helps explain how subtle changes in genetic splicing may contribute to neurodevelopmental disorders like autism, ADHD, and OCD.

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The brain’s ability to think, feel, and move depends on a delicate balance of electrical and chemical signals. These signals travel across synapses, where one neuron passes a message to the next. Proteins like PTPδ help these synapses form properly by acting like molecular Velcro—linking neurons together with precise alignment.

In their study, the researchers genetically engineered mice to delete mini-exon B from the PTPδ gene. The results were dramatic: Mice missing mini-exon B entirely had a survival rate of less than 30% after birth, highlighting its essential role in early brain development and viability.

On the other hand, mice with one copy of the gene altered survived into adulthood but displayed clear behavioral changes, including anxiety-like behavior and reduced movement.

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Is Risk-Taking Behavior Contagious?

Why do we sometimes decide to take risks and other times choose to play it safe? In a new study, Caltech researchers explored the neural mechanisms of one possible explanation: a contagion effect.

O’Doherty and his colleagues found that the participants were much more likely to make the gamble for more money in the “Self” trial when they had previously observed a risk-taking peer in the “Observe” trial. The researchers noticed that after the subjects observed the actions of a peer, their preferences for risk-taking or risk-averse behaviors began to reflect those of the observed peer—a so-called contagion effect. “By observing others behaving in a risk-seeking or risk-averse fashion, we become in turn more or less prone to risky behavior,” says Shinsuke Suzuki.

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By combining computational modeling of the data from the “Self” behavioral trials with the fMRI data, the researchers determined that a region of the brain called the caudate nucleus responds to the degree of risk in the gamble; for example, a riskier gamble resulted in a higher level of observed activity in the caudate nucleus, while a less risky gamble resulted in a lower level of activity. Additionally, the more likely the participants were to make a gamble, the more sensitively activity in the caudate nucleus responded to risk. “This showed that, in addition to the behavioral shift, the neural processing of risk in the caudate is also altered. Also, both the behavioral and neural responses to taking risks can be changed through passively observing the behavior of others,” Suzuki says.

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▪️واقعا جالب است که تصمیماتی که در زندگی میگیریم تابعی است از میزان ریسک پذیری افرادی که با آنها زندگی می کنیم و تعامل نزدیک داریم. با ایجاد تغییر و افزایش تعامل خود با افراد خطر پذیر جرات گرفتن تصمیمات ریسکی تر را پیدا می کنیم و برعکس. افرادی که با آنها زندگی می کنید چه میزان دل و جرات دارند؟ شما هم مثل مثل اونها شدید نه؟

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We often dismiss such disturbing murders as the result mental illness, or rather comfortably conclude that an otherwise normal person “snapped,” or became momentarily deranged. Self-delusion may be easier than accepting the alternative. “I think anyone is capable of it,” University of Alaska forensic psychologist Bruno Kappes told me when I asked how we can comprehend someone suddenly snapping in a violent murderous rage.

The fact is, rage can explode without warning. Overpowering judgment, compassion, fear, and pain, the fiery emotion serves one purpose — violence, both in words and actions. It may help explain why homicide is responsible for nearly 16,000 deaths in this country every year, according to the U.S. Centers for Disease Control and Prevention. And it may definitely help explain why people are far more likely to be murdered by a friend or acquaintance than by a stranger.

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It’s important to acknowledge that powerful emotions like rage and fear can lend us power in a crisis. They can give a petite woman the strength to move a car and free a trapped child or drive a soldier against normal instinct to run into a hail of bullets to save a comrade in jeopardy. Such rapid-response brain circuitry undoubtedly played a role when U.S. Air Force Staff Sargent Spencer Stone and two friends subdued a fellow train passenger — a terrorist armed with an AK-47 and a knife — in France last summer. “I really wasn’t thinking,” Stone told me. “It wasn’t a conscious decision — I just went. It was automated.” Stone and fellow Americans Anthony Sadler and Alek Skarlatos, were all recognized for heroism in that case. But sometimes this automatic lifesaving response can misfire and lead to a story of unexpected tragedy rather than heroism.

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▪️داستان به‌ قتل رسیدن Geoff Farrar توسط David DiPaolo داستان عجیب و تامل برانگیزی است. دیوید به مدت ۲۰ سال زیر نظر جیاف آموزش کوهنوردی دیده است ولی یک روز...

حتما بخونید.

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Mosaic Brain Evolution Drives Learning in Tropical Butterfly

Researchers have discovered that Heliconius butterflies, known for feeding on both nectar and pollen, show mosaic brain evolution with specialized neural expansions linked to enhanced learning and memory abilities. This expansion occurs in specific brain structures called mushroom bodies, which are key for long-term visual memory and spatial learning.

By analyzing these butterflies’ brain circuits, scientists found that certain cells, known as Kenyon cells, grew at different rates, helping the butterflies navigate complex feeding routes. As part of this behaviour, they demonstrate a remarkable ability to learn and remember spatial information about their food sources—skills previously connected to the expansion of a brain structure called the mushroom bodies, responsible for learning. These findings highlight how brain structure adaptations support cognitive innovations, offering new insights into neural evolution.

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