Bryan Johnson took ketamine and monitored his brain activity for 15 days, recording the experience and sharing about it on X.

Johnson is a 47-year-old longevity-obsessed entrepreneur, known for sharing biohacking content across his social media channels. His most recent health experiment involved treatment with the popularized horse tranquilizer.

As he shared in a tweet, he wanted to test what happens to the brain before, during, and after ketamine treatment.

Ketamine has gained popularity as a fast-acting treatment for depression, PTSD, and chronic pain. Unlike traditional antidepressants, it works quickly by targeting the brain’s glutamate system to restore neural connections.

To monitor his brain activity, Johnson used his self-invented Kernel Flow—a form of non-invasive brain interface technology worn on the head.

While the trial is limited to members of families with genetic mutations that all but guarantee they will develop Alzheimer’s at a young age, typically in their 30s, 40s or 50s, the researchers expect that the study’s results will inform prevention and treatment efforts for all forms of Alzheimer’s disease.

Called the Primary Prevention Trial, the new study investigates whether remternetug — an investigational antibody being developed by Eli Lilly and Company — can remove plaques of a key Alzheimer’s protein called amyloid beta from the brain or block them from accumulating in the first place. Both genetic and nongenetic forms of Alzheimer’s disease start with amyloid slowly collecting in the brain two decades before memory and thinking problems arise. By clearing out low levels of amyloid beta plaques or preventing them from accumulating during the early, asymptomatic phase of the disease, or both, the researchers hope to interrupt the disease process at the earliest stage and spare people from ever developing symptoms.

“We have seen tremendous progress in the treatment of Alzheimer disease in the past few years,” said Eric McDade, DO, a professor of neurology and the trial’s principal investigator. “Two amyloid-targeting drugs were shown to slow symptoms of the disease and have now been approved by the Food and Drug Administration (FDA) as treatments for people with mild cognitive impairment or mild dementia due to Alzheimer’s disease. This provides strong support for our hypothesis that intervening when amyloid beta plaques are at the very earliest stage, long before symptoms arise, could prevent symptoms from emerging in the first place.”

The trial is part of the Knight Family Dominantly Inherited Alzheimer Network-Trials Unit (Knight Family DIAN-TU), a clinical trials platform designed to find medicines to prevent or treat Alzheimer’s disease. It is closely associated with DIAN, a National Institutes of Health (NIH)-funded international research network led by WashU Medicine that involves research institutes in North America, Australia, Europe, Asia and South America. DIAN follows families with mutations in any of three genes that cause Alzheimer’s at a young age. A child born into such a family has a 50% chance of inheriting such a mutation, and those who do so typically develop signs of dementia near the same age his or her parent did. All the participants in the Primary Prevention Trial come from such families.

“My grandfather passed away from Alzheimer’s, and so did his mother and all but one of his brothers,” said Hannah Richardson, 24, a participant in the Primary Prevention Trial. “My mom and my uncle have been participating in DIAN trials since I was about 10 years old. My mom was always very open about her diagnosis and how it spurred her advocacy for Alzheimer’s research, and I’ve always known I wanted to follow in her footsteps. I am happy to be involved in the Primary Prevention Trial and be involved in research because I know how important it is.”

A recent large-scale study published in Science Advances has revealed a connection between genetic variations associated with dyslexia and structural differences in the brain. These differences were found in areas involved in motor coordination, vision, and language. This provides new insights into the neurological underpinnings of this common learning difficulty.

Dyslexia is a common learning difficulty that primarily affects the skills involved in accurate and fluent word reading and spelling. It’s characterized by challenges with phonological awareness (the ability to recognize and manipulate the sounds in spoken language), verbal memory, and verbal processing speed. People with dyslexia may struggle to decode words, recognize familiar words automatically, and spell words correctly. Importantly, dyslexia is not related to a person’s overall intelligence. It’s considered a neurodevelopmental condition, meaning it arises from differences in how the brain develops and processes information, particularly related to language.

Genetic disposition to dyslexia is associated with brain structure in the general population.

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Researchers have identified a key pathway that links how neurons send signals to each other, or synaptic activity, to the expression of genes necessary for long-term changes in the brain, providing crucial insights into the molecular processes underlying memory formation.

“These findings illuminate a critical mechanism that connects local synaptic activity to the broader gene expression changes necessary for learning and memory,” said Mark Dell’Acqua, professor of pharmacology at the University of Colorado Anschutz Medical Campus and senior author of the study. “This paper is mainly a basic science finding of a fundamental process of what nerve cells do. Understanding this relay system not only enhances our knowledge of brain function but could also better inform therapeutic treatments for cognitive disorders.”

The nucleus where the genes that modify neuron function are controlled is a long distance away from where neurons receive input from their synapses, which are located in distant dendrites that extend like branches from the trunk of a tree. This research focuses on the cAMP-response element binding protein (CREB), a transcription factor known to regulate genes vital for dynamic changes at synapses which is essential for neuronal communication. Despite CREB’s well-documented role in supporting learning and memory, the exact mechanisms leading to CREB activation during neuronal activity remain unclear.

Using advanced microscopy techniques, graduate student Katlin Zent in Dr. Dell’Acqua’s research group revealed a crucial relay mechanism involving the activation of receptors and ion channels generating calcium signals that rapidly communicates from synapses in remote dendrite branches to the nucleus in the neuron cell body.

“Going forward, this research will enable us to better examine the way these pathways are utilized in different disease states,” said Dell’Acqua. “We could see exactly what parts of this new mechanism are interfered with and where, giving us a better idea of how this pathway affecting learning and memory is impacted. This research highlights potential targets for interventions aimed at conditions like Alzheimer’s disease and other memory-related disorders.”

+ Decoding the secrets of DNA, CRISPR gene editing allows scientists to target specific genes linked to aging. By modifying these genes, researchers aim to prevent conditions that come with aging. Envision a future where genetic risks for age-related diseases are minimized through precise DNA editing.

It is possible to regenerate cells using stem cells, which can turn into a variety of types. In recent trials, stem cells showed promise in regenerating aged tissues like cartilage. Scientists hope to develop therapies that might slow down physical decline and maintain vitality longer by using this potential.

Nanobots could someday be the future of healthcare by targeting damaged cells directly as they move through your bloodstream. Researchers are currently exploring how nanobots might repair cellular damage and improve overall health, potentially reversing some age-related effects at the cellular level.

As the protective ends of chromosomes, telomeres shorten over time. When they become too short, cells stop functioning. In laboratory studies, researchers have extended the lifespan of animals by using telomere extension techniques. Though still experimental, this research could pave the way for human applications in slowing aging.

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They found that when people with aphantasia try to conjure an image in their mind’s eye, the primary visual cortex – the part of the brain that processes picture-like visual information – is activated, but any images that are produced remain unconscious to the individual.

Published today in Current Biology, opens in a new window, the study, carried out by scientists at UNSW and South China Normal University, used a range of techniques to measure brain activity. Their findings challenge the existing theory that activity in the primary visual cortex directly produces conscious visual imagery.

“People with aphantasia actually do seem to have images of a sort, they remain too weak or distorted to become conscious or be measured by our standard measurement techniques,” says Prof. Joel Pearson, a co-author of the study based at UNSW’s School of Psychology, opens in a new window. “This may be because the visual cortex is wired differently, as evidenced by the data in this new study. This research not only deepens our understanding of the brain but also pushes the boundaries of how we think about imagination and consciousness.”

DLB is a common cause of dementia. It starts by the abnormal accumulation of the protein alpha-synuclein in the brain. This produces degeneration of the brain and causes problems with thinking, movement, and behavior. Eventually, the disease leads to dementia and death. Doctors use a imaging technique called FDG-PET to assess how the brain is affected in DLB. However, until now, there was no information on how these brain changes develop over time.

The study, led by Dr. Daniel Ferreira at the Department of Neurobiology, Care Sciences and Society, followed 35 patients with DLB, 37 patients with early-stage DLB (called prodromal DLB), and 100 healthy people from Mayo Clinic (USA), for an average of 3.8 years. The researchers found that brain degeneration starts early in prodromal DLB and worsens as the disease progresses.

“We discovered that people with prodromal DLB had faster degeneration in certain brain areas compared to healthy individuals,” said Dr. Ferreira.” This information is crucial for monitoring disease progression from early stages and planning clinical trials for new treatments.”

longitudinal FDG-PET metabolic change along the lewy body.

“Synchron’s vision is to scale neurotechnology to empower humans to connect to the world, and the NVIDIA Holoscan platform provides the ideal foundation,” said Tom Oxley, M.D., Ph.D., CEO & Founder, Synchron. “Through this work, we’re setting a new benchmark for what BCIs can achieve.”

NEW YORK—(BUSINESS WIRE)— Synchron, a category-defining brain-computer interface (BCI) company, announced today a step forward in implantable BCI technology to drive the future of neurotechnology. Synchron’s BCI technology, in combination with the NVIDIA Holoscan platform, is poised to redefine the possibilities of real-time neural interaction and intelligent edge processing.

Synchron will leverage NVIDIA Holoscan to advance a next-generation implantable BCI in two key domains. First, Synchron will enhance real-time edge AI capabilities for on-device neural processing, improving signal processing and multi-AI inference technology. This will reduce system latency, bolster privacy, and provide users with a more responsive and intuitive BCI experience. NVIDIA Holoscan provides Synchron with: (i) a unified framework supporting diverse AI models and data modalities; (ii) an optimized application framework, from seamless sensor I/O integration, GPU-direct data ingestion, to accelerated computing and real-time AI.

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The work, published today in Nature, marks a significant step forward in our ability to study how the human body takes shape during early development.

The notochord, a rod-shaped tissue, is a crucial part of the scaffold of the developing body. It is a defining feature of all animals with backbones and plays a critical role in organising the tissue in the developing embryo.

Despite its importance, the complexity of the structure has meant it has been missing in previous lab-grown models of human trunk development.

In this research, the scientists first analysed chicken embryos to understand exactly how the notochord forms naturally. By comparing this with existing published information from mouse and monkey embryos, they established the timing and sequence of the molecular signals needed to create notochord tissue.