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Astrocytes are star-shaped glial cells in the central nervous system that support neuronal function, maintain the blood-brain barrier, and contribute to brain repair and homeostasis. The evolution of these cells throughout the progression of Alzheimer’s disease (AD) is still poorly understood, particularly when compared to that of neurons and other cell types.

Researchers at Massachusetts General Hospital, the Massachusetts Alzheimer’s Disease Research Center, Harvard Medical School and Abbvie Inc. set out to fill this gap in the literature.

Their paper, published in Nature Neuroscience, provides one of the most detailed accounts to date of how different astrocyte subclusters respond to AD across different brain regions and disease stages, providing valuable insights into the cellular dynamics of the disease.

Large language models (LLMs) can synthesize vast amounts of information. Luo et al. show that LLMs—especially BrainGPT, an LLM the authors tuned on the neuroscience literature—outperform experts in predicting neuroscience results and could assist scientists in making future discoveries.

Boosting the endocannabinoid 2-AG in the brain can counteract opioid addiction while preserving their pain relief, a Weill Cornell Medicine study finds. This approach, tested in mice using the chemical JZL184, may lead to safer treatments for pain management.

The natural enhancement of chemicals produced by the body, known as endocannabinoids, may mitigate the addictive properties of opioids like morphine and oxycodone while preserving their pain-relieving effects, according to researchers from Weill Cornell Medicine in collaboration with The Center for Youth Mental Health at NewYork-Presbyterian. Endocannabinoids interact with cannabinoid receptors found throughout the body, which play a role in regulating functions such as learning and memory, emotions, sleep, immune response, and appetite.

Opioids prescribed to control pain can become addictive because they not only dull pain, but also produce a sense of euphoria. The preclinical study, published recently in the journal Science Advances, may lead to a new type of therapeutic that could be taken with an opioid regimen to only reduce the reward aspect of opioids.

The Tbx1 gene influences brain volume and social behavior in autism and schizophrenia, with its deficiency linked to amygdala shrinkage and impaired social incentive evaluation.

A study published in Molecular Psychiatry has linked changes in brain volume to differences in social behavior associated with psychiatric conditions like autism spectrum disorder and schizophrenia.

The research, led by Noboru Hiroi, Ph.D., a professor in the Department of Pharmacology at the Joe R. and Teresa Lozano Long School of Medicine at The University of Texas Health Science Center at San Antonio (UT Health San Antonio), revealed that a deficiency in a specific gene was connected to social behavior differences in mice. These behavioral differences are similar to those often observed in psychiatric disorders.

Researchers have developed a method using viruses to track neuronal development in frogs, shedding light on the evolution of vertebrate nervous systems and offering comparative insights with mammals.

Although viruses are typically associated with illnesses, not all viruses are harmful or cause disease. Some are instrumental in therapeutic treatments and vaccinations. In scientific research, viruses are often used to infect certain cells, genetically modify them, or visualize neurons in the organism’s central nervous system (CNS)—the command center made up of the brain, spinal cord, and nerves.

The highlighting process has now been successfully applied to amphibians, which are crucial for understanding the brain and spinal cord of tetrapods—four-limbed animals, including humans. This has been shown in a new study by an international EDGE consortium jointly led by the Sweeney Lab at the Institute of Science and Technology Austria (ISTA) and the Tosches Lab at Columbia University.

Scientists have discovered that cosmic filaments, the largest known structures in the universe, are rotating. These massive, twisting filaments of dark matter and galaxies stretch across hundreds of millions of light-years and play a crucial role in channeling matter to galaxy clusters. The finding challenges existing theories, as it was previously believed that rotation could not occur on such large scales. The research was confirmed through both computer simulations and real-world data, and it opens up new questions about how these giant structures acquire their spin.

After reading the article, a Reddit user named Kane gained more than 100 upvotes with this comment: “What if galaxy clusters are like neuron and glial clusters in a brain. And dark matter is basically the equivalent of a synapse. It connects galaxies and matter together and is responsible for sending quantum information back and forth like a signal chain.”

Though Elon Musk’s Neuralink put wireless brain implants in the spotlight — in early 2024, Musk announced his company’s first implant was successful — the research and development of these devices has spanned decades. The BrainGate clinical trials have been underway for 20 years, and the consortium’s wireless implant marks the first time a person has used an implant with high bandwidth capabilities.

Wireless technologies are opening doors in neuroscience, enabling new capabilities in communication, treatment, and research. Because wireless implants can monitor the brain for long periods of time, they offer a unique opportunity to examine neural dynamics, increasing our understanding of the human mind. Their cord-free design also benefits people hoping to use these devices outside a research setting and improve their quality of life.

The first brain implant is credited to neurologist Phil Kennedy, who had the device surgically affixed to his brain. Today, wired implants are less invasive and widely used. They can help prevent seizures, manage OCD symptoms, and treat movement disorders.

Dr. Marta di Forti: “Our study indicates that daily users of high potency cannabis are at increased risk of developing psychosis independently from their polygenic risk score for schizophrenia.”


Is there a connection between cannabis use and developing psychosis? This is what a recent study published in Psychological Medicine hopes to address as an international team of researchers investigated how frequent cannabis use combined with a genetic predisposition for schizophrenia could lead to developing psychosis later in life. This study holds the potential to help researchers, medical professionals, and the public better understand how to identify the signs of psychosis in cannabis users and take necessary steps to address them as soon as possible.

For the study, the researchers conducted an observational study by obtaining data records of almost 150,000 individuals registered in United Kingdom and European Union medical databanks, one of which was the European Network of National Schizophrenia Networks Studying Gene-Environment Interactions (EU-GEI), to examine records regarding patients who self-reported use and psychosis diagnoses. In the end, the researchers discovered a connection between individuals who self-reported lifetime frequent cannabis use and psychosis diagnoses, specifically regarding high potency cannabis which contains 10 percent or greater Delta-9 tetrahydrocannabinol (THC).

“These are important findings at a time of increasing use and potency of cannabis worldwide,” said Dr. Marta di Forti, who is a Professor of Drug use, Genetics, and Psychosis at King’s College London and a co-author on the study. “Our study indicates that daily users of high potency cannabis are at increased risk of developing psychosis independently from their polygenic risk score for schizophrenia. Nevertheless, the polygenic risk score for schizophrenia might, in the near future, become useful to identify those at risk for psychosis among less frequent users to enable early preventative measures to be put in place.”

And it’s not from Neuralink.

Recently, Semafor received an extraordinary iMessage. It was from Rodney Gorham, a paralyzed ALS patient, and he had sent it directly from his brain. Gorham has a brain implant called Stentrode. Unlike previous generations of brain-computer interfaces, the Stentrode, from the neurotechnology company Synchron, can be implanted without invasive brain surgery. But… what *are* brain-computer interfaces? How do they work? And where is this novel technology going?

A specific brain mechanism modulates how animals respond empathetically to others’ emotions. This is the latest finding from the research unit Genetics of Cognition, led by Francesco Papaleo, Principal Investigator at the Istituto Italiano di Tecnologia (IIT – Italian Institute of Technology) and affiliated with IRCCS Ospedale Policlinico San Martino in Genova. The study, recently published in Nature Neuroscience, provides new insights into psychiatric conditions where this socio-cognitive skill is impaired, such as post-traumatic stress disorder (PTSD), autism, and schizophrenia.

Psychological studies have shown that the way humans respond to others’ emotions is strongly influenced by their own past emotional experiences. When a similar emotional situation—such as a past stressful event—is observed in another person, we can react in two different ways. On one hand, it may generate empathy, enhancing the ability to understand others’ problems and increasing sensitivity to others altered emotions. On the other hand, it may induce self-distress resulting into an avoidance towards others.

The research group at IIT has demonstrated that a similar phenomenon also occurs in animals: recalling a negative experience strongly influences how an individual responds to another who is experiencing that same altered emotional state. More specifically, animals exhibit different reactions only if the negative event they experienced in the past is identical to the one they observe in others. This indicates that even animals can specifically recognize an emotional state and react accordingly even without directly seeing the triggering stimuli.