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  1. DATE: August 19, 2026 at 11:00AM
    SOURCE: STAT NEWS NEUROSCIENCE

    TITLE: STAT+: Brain organoids, kept alive more than five years, matured like human brains

    URL: statnews.com/2026/08/19/brain-

    A little more than two years ago, a junior scientist walked into Paola Arlotta’s Harvard office with a set of mesmerizing images and asked if she wanted to see what the old brain organoids look like. 

    Arlotta, a developmental neurobiologist, turned in surprise. “You analyzed them?” she exclaimed. 

    Irene Faravelli’s face fell. She had, but now she wondered if that had been a grave mistake. Arlotta assured her everything was fine. In fact it was great. “I was actually pleased that somebody had the courage to do this,” Arlotta recalled to STAT in a recent interview. 

    Continue to STAT+ to read the full story…

    URL: statnews.com/2026/08/19/brain-

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BrainOrganoids #FiveYearOrganoids #HarvardNeuroscience #BrainResearch #OrganoidMaturation #Neurodevelopment #StemCellResearch #NeuroscienceNews #STATPlus #InVitroBrainModel

  2. FRANKENSTEIN ON A CHIP 💎
    HAVE WE THOUGHT THIS THROUGH?

    I watched a creepy video this morning:

    We're Not Ready for Biocomputing
    youtu.be/uKhsbQcFVwQ?si=ByqFGs

    Researchers at Cortical Labs have built a biological computing system using around 200,000 living human neurons connected to electrodes.

    The neurons receive signals, respond to feedback, and contribute to controlling a computer game. They demonstrated it with Doom.

    There is currently no evidence that these neurons are conscious or suffering.

    The video pushes that idea further than the science supports. Much of the Doom system is ordinary computing, with the neurons contributing a smaller but real part.

    But I kept thinking about Frankenstein.

    The curse of Frankenstein was not simply that Victor created something new.

    It was that he created something and then failed to take responsibility for what he had created.

    That seems rather relevant.

    Researchers are already working with increasingly sophisticated human neural tissue, including three-dimensional brain organoids.

    So perhaps we need one simple principle now:

    LIVING HUMAN NEURAL TISSUE SHOULD NOT LOSE ETHICAL CONSIDERATION SIMPLY BECAUSE IT IS OUTSIDE A HUMAN BODY.

    That does not mean a dish of neurons is a person.

    It does not mean these neurons are suffering.

    It means we should not wait until something can clearly tell us that it suffers before deciding we have obligations toward it.

    Inside a skull, living human brain tissue is treated with extraordinary care.

    Put similar tissue on a chip, call it “computing substrate”, and our responsibility should not simply disappear.

    These systems are still relatively simple.

    But the whole direction of biocomputing is toward systems that are more organised, more adaptive and more complex.

    That is why the ethics need sorting out before we get there.

    Frankenstein’s mistake was not curiosity.

    It was creating first and asking what he owed his creation afterwards.

    We have already started creating.

    Perhaps this time we should ask the question early:

    AT WHAT POINT DO WE OWE THE THING WE HAVE GROWN SOME CONSIDERATION?

    I would rather we answer that before we build something we can no longer confidently say has no awareness.

    @3goodthings@DigitalCoup@meditation@economics_that_works

    #Biocomputing #Neuroscience #Bioethics #BrainOrganoids #Frankenstein

  3. DATE: August 5, 2026 at 09:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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    TITLE: Miniature brain models reveal varied electrical activity in different types of autism

    URL: psypost.org/miniature-brain-mo

    Researchers have grown miniature, three-dimensional brain models from the cells of autistic and nonautistic individuals to study how their neural networks communicate. The models demonstrated that different types of autism spectrum disorder produce vastly different patterns of electrical activity, highlighting the wide biological variety underlying the condition. The small study was published in the journal Translational Psychiatry.

    Autism spectrum disorder is a neurodevelopmental condition involving differences in social communication and repetitive behaviors. The biological roots of the condition remain difficult to map out. While many cases have no known genetic cause, a portion of autistic individuals have what is known as syndromic autism. This form of the condition is linked to specific single-gene mutations that alter how brain cells develop and communicate.

    Because traditional animal models often fail to accurately reflect the specific features of human brain development, researchers have increasingly turned to brain organoids. These are tiny, self-organizing bundles of tissue grown from human stem cells. Brain organoids replicate the early stages of human brain development while retaining the exact genetic code of the person who provided the original cells.

    Lead researchers Nisim Perets and Liya Kerem, along with a team of colleagues at Itay and Beyond and the Hebrew University of Jerusalem, wanted to see if organoids could reveal the functional differences between various forms of autism. They focused on comparing the baseline electrical activity and network connections among several distinct genetic subtypes of the disorder. Extrapolating how a single mutated gene alters whole-brain activity is challenging in living humans, making these laboratory-grown models highly useful for observing live neural networks in action.

    The researchers collected urine samples from fifteen human participants. Four participants were neurotypical, serving as a control group. Ten participants had syndromic autism stemming from five different genetic mutations, including the genes SHANK3, SCN2A, STXBP1, PPP2R5D, and GRIN2B. One participant had idiopathic autism, meaning their condition had no identified genetic origin.

    Using epithelial cells extracted from the urine, the team reprogrammed the cells back into a basic stem cell state. They then placed these induced pluripotent stem cells into special nutrient baths, guiding them to grow into more than four hundred brain organoids. To ensure the models were developing correctly, the researchers analyzed the cells using genetic sequencing and fluorescent imaging. This confirmed that the organoids contained the right mix of brain cells, including neural progenitors, developing neurons, and mature cortical cells.

    After growing the organoids for about two months, the researchers placed them onto special plates equipped with microscopic electrodes. These multi-electrode arrays allowed the team to record the spontaneous electrical signals passing between the neurons. The researchers tracked metrics like the firing rate, the size of the electrical spikes, and the frequency of synchronized bursts across the neural network.

    The resting electrical activity in the autism models differed substantially from the neurotypical control models. The organoids derived from the participant with idiopathic autism exhibited a generally hypoactive profile. They showed lower firing rates, weaker signal strengths, and fewer bursts of activity compared to the control group.

    Conversely, organoids derived from most of the syndromic autism subtypes showed higher firing rates than the control group. Organoids from participants with SCN2A mutations had varying firing rates but consistently produced weaker electrical signal strengths. This initial observation confirmed that genetic differences lead to physical differences in how brain cells spontaneously fire.

    Next, the research team tested how the neural networks responded to new stimuli, a process known as short-term synaptic plasticity. In a living brain, neural networks adapt to incoming information by temporarily adjusting their sensitivity. They might dampen their activity, known as short-term depression, or temporarily boost it, known as short-term potentiation. The researchers delivered brief electrical pulses to the organoids and recorded the changes in activity over the following five minutes.

    The high-frequency stimulation mostly caused the networks to dampen their activity. However, organoids from patients with STXBP1, SHANK3, and SCN2A mutations displayed abnormally high levels of short-term depression and reduced potentiation compared to the control group. Organoids with GRIN2B mutations showed the opposite trend, with slightly elevated potentiation and reduced depression. These varied responses suggest that different genetic mutations disrupt the brain’s ability to adapt to incoming signals in entirely different ways.

    The researchers also mapped the functional connectivity of the networks before and after the stimulation. In response to the electrical pulses, the neurotypical organoids displayed a stable, predictable decrease in network connectivity. Organoids from the autism groups displayed highly erratic responses.

    The neural networks in organoids with a STXBP1 gene mutation collapsed almost immediately after stimulation, failing to recover normally. Models with a PPP2R5D mutation experienced a sharp, sudden drop in connectivity. Models with GRIN2B mutations showed an inconsistent, fluctuating response across the entire observation period. The organoids representing idiopathic autism barely changed at all, showing a rigidity not seen in the control group.

    To visualize these vast differences, the researchers mapped eighteen separate electrical characteristics onto a three-dimensional graph using a mathematical technique called principal component analysis. Organoids grown from the same person behaved similarly, and the entire neurotypical control group clustered tightly together. The organoids from the autistic participants scattered widely across the graph.

    Even organoids grown from patients sharing the exact same genetic mutation sometimes displayed different patterns of electrical activity. One participant with a GRIN2B mutation had a clinical history of seizures, and their corresponding organoids exhibited abnormal rhythmic bursting. Another participant with the same GRIN2B mutation did not have a history of seizures, and their organoids did not display that specific bursting pattern.

    While these three-dimensional models provide a window into early brain development, they do not replicate the full structural architecture of a mature human brain. The study also relied on a small sample size of fifteen patients, with only a single individual representing the idiopathic autism category. The association between specific electrical patterns in the organoids and clinical symptoms like seizures will require testing in larger patient cohorts to verify that the results were not statistically anomalous.

    The researchers noted that tracking functional electrical differences in brain organoids could help classify different subtypes of autism based on brain circuitry rather than just behavioral observations. Because autism encompasses such a wide array of biological mechanisms, grouping patients by how their neural networks actually function might eventually guide the development of tailored therapeutic interventions.

    The study, “Patient-derived brain organoids reveal divergent neuronal activity across subpopulations of autism spectrum disorder,” was authored by Nisim Perets, Liya Kerem, Nir Waiskopf, Noa Horesh, Itay Goldman, Jasmine Avichzer, Doron Bril, William Tobelaim, Milcah Barashi, Liat David, and Ariel Tenenbaum.

    URL: psypost.org/miniature-brain-mo

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismResearch #BrainOrganoids #NeuralActivity #AutismSubtypes #GeneticAutism #Neuroscience #SynapticPlasticity #BrainConnectivity #TranslationalPsychiatry #NeuralNetworks

  4. Patient-Derived Brain Organoids Offer Insights for Alzheimer's Treatments

    📰 Original title: Lab-Grown Mini Brains Could Aid Alzheimer's Research

    🤖 IA: It's not clickbait ✅
    👥 Usuarios: It's not clickbait ✅

    View full AI summary: killbait.com/en/patient-derive

    #health #alzheimers #brainorganoids #precisionmedicine

  5. Scientists Make Breakthrough That Allows Lab-Grown Brain Cells To Play A Sort Of Video Game

    GameSpot may receive revenue from affiliate and advertising partnerships for sharing this content and from purchases through links.…
    #NewsBeep #News #Technology #AU #Australia #braincells #brainorganoids #brainpower #braintissue #UCSantaCruz
    newsbeep.com/au/515448/

  6. Are you interested in the spiking activity of your neuronal cultures, #brain slices, #organoids, etc.?

    Check out our latest publication in STAR Protocols:
    “Protocol for the enhanced analysis of electrophysiological data from high-density multi-electrode arrays with nicespike and spikeNburst”
    doi.org/10.1016/j.xpro.2025.10

    It provides user-friendly graphical and #Python programming interfaces to spike sorting via template matching thanks to #Kilosort and #spikeinterface (@spikeinterface), and subsequent analysis of #spiking and #bursting activity, networks, and synchrony.

    #neuroscience #brainscience #electrophysiology #brainOrganoids

  7. @eLife Suddenly, I have to update my undergraduate lectures on neural determination. FGF8 for the win.
    #neuroscience #organoids #BrainOrganoids

  8. What are #brainorganoids and how are they being used in neurological research for potential future treatments? These questions were asked and answered in the #DanaDiscoveryDialogues on Oct. 25th. Watch the full recording. dana.org/article/brain-organoi #neuroethics

  9. ICYMI: Watch the recording of our first Dana Discovery Dialogue on the bioethics and future of brain organoids! Learn the basics of what they are and how they’re being used to advance research on neurological diseases and dig into the ethical considerations around their use. youtube.com/watch?v=kxc6HWnJUm
    #DanaDiscoveryDialogues #neurosociety #brainorganoids

  10. Reminder to register for our first #DanaDiscoveryDialogues series starting today at 3pm ET! Join us for a discussion on #brainorganoids and how they can be ethically used for medical research. Register here: on.dana.org/dana-discovery-dia

  11. Scientists have created a new field of biocomputing called organoid intelligence, or OI. They use lab-grown brain organoids, which are clusters of neurons that mimic brain functions, as biological hardware. OI could revolutionize computing, medicine, and neuroscience by harnessing the power and efficiency of the human brain. #OI #biocomputing #brainorganoids

    freethink.com/hard-tech/organo

  12. How to feed mini-organs

    Organoids, lab-grown mini-organs, hold the promise for better understanding of human biology. But these microscopic organ-like blobs of cells fall short of real organs in a lot of ways. For one, their size is limited to less than half of a millimeter in diameter — any larger and their internal cells start dying because nutrients from the liquid they’re grown in can’t diffuse past a certain distance. Scientists are now making lab-grown mini-organs more lifelike by adding blood vessels.

    #Biomedicine #Biotechnology #Organoids #BloodVessels #BrainOrganoids #Neuroscience #Neurology

    alleninstitute.org/news/scisho