Do we need to change the way we think about consciousness?
Using patient-derived induced pluripotent stem cells, the researchers generated advanced models known as 3D assembloids of two key brain areas: the cortex, which is essential for movement and higher-order thinking, and the hippocampus, which supports learning and memory. The results revealed strikingly different effects depending on the brain region.
In cortical models, the SCN8A variants made neurons hyperactive, mimicking seizure activity. In hippocampal models, however, the variants disrupted the brain rhythms associated with learning and memory. This disruption stemmed from a selective loss of specific hippocampal inhibitory neurons — the brain’s traffic cops that regulate neural activity.
These findings may help explain why patients with epilepsy often struggle with symptoms beyond seizures.
To confirm their findings, the researchers compared brain recordings from people with epilepsy to stem cell-derived hippocampal assembloids. They looked at seizure-prone regions of the patients’ hippocampi as well as regions unaffected by seizures. Abnormal brain rhythms appeared in both the patients’ seizure “hot spots” and in assembloids carrying SCN8A variants. In contrast, seizure-free brain regions and assembloids without the variants showed normal activity.
For families of children with severe epilepsy, controlling seizures is often just the beginning of their challenges. Even in cases where powerful medications can reduce seizures, many children continue to face difficulties with learning, behavior and sleep that can be just as disruptive to daily life.
New stem cell-based research published in Cell Reports, provides an early step toward understanding why current treatments often fall short, pointing to the distinct effects that single disease-causing gene variants can have across different regions of the brain.
Brain damage caused by blocked blood vessels may be treatable using injections of stem cells, according to a new study by researchers from the University of Zurich and the University of Southern California.
The results could one day help patients who have experienced some forms of stroke recover lost functions.
Using mice with stroke-induced brain damage, the researchers found that injections of human stem cells could successfully develop into immature brain cells. The results were dramatic: most of the implanted cells remained in place, developing features of fully functioning neurons and communicating with surrounding cells.
A person will have Alzheimer’s years before ever knowing it. The disorienting erasure of memories, language, thoughts—in essence, all that makes up one’s unique sense of self—is the final act of this enigmatic disease that spends decades disrupting vital processes and dismantling the brain’s delicate structure.
Once symptoms surface and doctors make a diagnosis, though, it can often be too late. Damage is widespread, impossible to reverse. No cure exists.
Attempts to develop drugs that clear away toxic accumulations of amyloid-beta and tau proteins—hallmarks of the disease that cause neurons to die—have ended in hundreds of failed clinical trials. Today, some scientists are skeptical over whether removing amyloid plaques is even enough. Others have a hunch that the best line of attack won’t target just one aspect of the disease, but many of them, all at once.
Interesting paper where microintravascular electrodes were inserted into cortical veins of pigs to record somatosensory and visual neuronal activity as well as selectively stimulate motor areas. Compared to electrocorticography, this is a less invasive approach with similar capabilities. #neurotech [ https://doi.org/10.1002/aisy.202500487](https://doi.org/10.1002/aisy.202500487)
Intravascular electroencephalography (ivEEG) with microintravascular electrodes enhances neural monitoring, functional mapping, and brain–computer interfaces (BCIs), offering a minimally invasive approach to assess cortical activities; however, this approach remains unrealized. Current ivEEG methods using electrode-attached stents are limited to recording from large vessels, such as the superior sagittal sinus (SSS), restricting access to cortical regions essential for precise BCI control, such as those for hand and mouth movements. Here, ivEEG signals from small and soft cortical veins (CV-ivEEGs) in eight pigs using microintravascular electrodes are recorded, achieving higher resting-state signal power and greater spatial resolution of somatosensory evoked potentials (SEPs) compared to SSS-based ivEEG. Additionally, ivEEG recorded from deep veins clearly captures visual evoked potentials. Furthermore, comparisons between CV-ivEEG and electrocorticography (ECoG) using epidural and subdural electrodes in two pigs demonstrate that CV-ivEEG captures cortical SEPs comparable to ECoG. Targeted electrical stimulation via cortical vein electrodes induces specific contralateral muscle contractions in five anesthetized pigs, confirming selective motor-region stimulation with minimal invasiveness. The findings suggest that ivEEG with microintravascular electrodes is capable of accessing diverse cortical areas and capturing localized neural activity with high signal fidelity for minimally invasive cortical mapping and BCI.
The study investigates how people (“receivers” / “detectors”) evaluate deceptive information depending on social distance (friend vs. stranger) and context (whether the outcome involves gains or losses).
Receivers were more likely to fall for deception in gain contexts than in loss contexts. That is, when there is a possible reward, people are less vigilant / more prone to be deceived.
Key brain regions involved: Dorsolateral Prefrontal Cortex (DLPFC, risk evaluation), Orbitofrontal Cortex (OFC, reward processing), Frontal Pole Area (FPA, intention understanding). Differences in activity/connectivity in these regions were associated with how people evaluated deceptive vs truthful information, and depending on social distance.
Preventing deception requires understanding how lie detectors process social information across social distance. Although the outcomes of such information are crucial, how detectors evaluate gains or losses from close versus distant others remains unclear. Using a sender-receiver paradigm and fNIRS hyperscanning, we recruited 66 healthy adult dyads (32 male and 34 female dyads) to investigate how perceived social distance modulates the neural basis in receivers (the detector) during deceptive gain–loss evaluation. The results showed that detectors were more prone to deception in gain contexts, with these differences mediated by connectivity in risk evaluation (Dorsolateral Prefrontal Cortex, DLPFC), reward-processing (Orbitofrontal Cortex, OFC), and intention-understanding regions (Frontal Pole Area, FPA). Hyperscanning analyses revealed that friend dyads exhibited higher interpersonal neural synchrony (INS) in these regions than stranger dyads. In gain contexts, friend dyads showed enhanced INS in the OFC, whereas in loss contexts, enhanced INS was observed in the DLPFC. Trial-level analysis revealed that the INS during the current trial effectively predicted the successful deception of that trial. We constructed a series of regression models and found that INS provides superior predictive power over single-brain measures. The INS-based Support Vector Regression model achieved an accuracy of 86.66% in predicting deception. This indicates that increased trust at closer social distances reduces vigilance and fosters relationship-oriented social information processing. As the first to identify INS as a neural marker for deception from the detector’s perspective, this work advances Interpersonal Deception Theory and offers a neuroscientific basis for credit risk management.
Significance Statement Using a sender–receiver paradigm and fNIRS hyperscanning, we investigated deception from the detector’s perspective across social distances and gain–loss contexts. Our findings reveal that interpersonal neural synchrony (INS) between the dorsolateral and orbitofrontal prefrontal cortices reliably predicts whether deception succeeds. We further analyzed the predictive power of INS at the trial level and found that deception susceptibility was first apparent in the early stages of verbal communication. These results suggest that deception is not solely shaped by individual vigilance but emerges from dynamic neural coupling during interaction. This study identifies INS as a neural signature of deception susceptibility and bridges behavioral models with neural computation, offering implications for deception detection in real-world social contexts.