Brain Function Insights

Your brain on AI: One of the first studies measuring what ChatGPT use does to our brain MIT researchers tracked 54 people writing essays using ChatGPT, web search, or just their brains—while monitoring neural activity with EEG. The findings are striking: 🧠 Brain connectivity weakened with more AI support. ChatGPT users showed the least neural engagement. 🔍 Memory collapsed. 83% of ChatGPT users couldn't quote their own essays minutes later, vs. near-perfect recall without AI. ⚡ "Cognitive debt" accumulated. When ChatGPT users later wrote without AI, their brains showed weakened connectivity compared to those who practiced unassisted writing. 🎨 Creativity declined. AI-assisted essays were statistically more uniform and less original. The twist: Strategic timing matters. Using AI after initial self-driven effort preserved better cognitive engagement than consistent AI use from the start. This isn't anti-AI—it's about understanding the trade-offs. While AI-generated essays scored well initially, participants showed signs of cognitive atrophy: diminished critical thinking, reduced memory encoding, and less ownership of their work. The takeaway: We need to enhance, not replace, human thinking as we integrate these powerful tools. Full study here: https://lnkd.in/e-6urMD8 Note: This is a pre-print study awaiting peer review.

We and others have shown that #psychedelics can spark the growth of new synapses in the brain. But there are some deeper questions: where do those new connections actually go? Which specific neural pathways are modified? A new study from the lab is now online at Cell by Cell Press - In this latest work, rather than imaging one synapse at a time, we turned to a more powerful tool for circuit tracing: an engineered rabies virus 🦠, which naturally hops across synaptically connected neurons in the brain. Think of it like the Google Street View self-driving cars, but for neural circuits – roaming widely to show the connected cells in the entire brain.   In the experiment, mice received either #psilocybin or saline control, followed by rabies viral tracing and whole-brain imaging of fluorescently tagged neurons. The psychedelic-induced pattern of rewiring was far from random and revealed several insights:   1) Psilocybin weakens recurrent connections in the cortex, feedback loops that may contribute to the rumination of negative thoughts. 🔄   2) The drug strengthens pathways that carry sensory signals to deeper, action-driving brain regions, tightening the link between perception and behavior. 🎯   3) The circuit reorganization was influenced by neural activity. In a proof-of-concept experiment, we show that manipulating the firing activity can alter psilocybin’s rewiring patterns, demonstrate that it may be possible to sculpt the psychedelic-evoked structural neural plasticity. 💥🧠   We hope the results will change how we think about the therapeutic mechanisms of psychedelics. It is not just more synapses; it is about which circuits are remodeled. Moreover, we have some control over the drug-evoked plasticity when we pair it with neural activity modulation, providing a reason for trying to integrate psychedelics with something like rTMS.   This was a team effort spearheaded by Quan Jiang. With help from collaborators at Allen Institute, UC Irvine, and CUHK. The research was supported by One Mind and National Institute of Mental Health (NIMH).   Link to the paper: https://lnkd.in/eSDMdg5Q

Collaborative innovation combining AI with neuropsychology is proving to be transformative. Six research clusters show specific value and potential: 🌱 Neuroscience and Mental Health: Understanding mental health through neuroimaging and machine learning enables earlier, more precise interventions for conditions like ADHD and depression. By examining correlations in brain function, this research helps identify key markers for cognitive impairments, aiding in early diagnosis and personalized treatment plans. 🔍 Computational Modeling: Computational models simulate decision-making and cognitive markers, which are crucial for neurological conditions like epilepsy. Machine learning applied to seizure detection, for instance, offers a potential breakthrough in predicting and managing epilepsy, helping patients gain better control and care. 🧠 Cognitive Neuroscience: Studies of cognitive decline and neurodegenerative diseases, such as Alzheimer’s, benefit from reinforcement learning models that reveal patterns in brain degeneration. These insights are essential for developing strategies to slow disease progression, offering hope for more effective interventions. 💡 Cognitive Neurology and Neuropsychology: Examining cognitive functions through neuroimaging and machine learning provides deeper insights into disorders like aphasia and neurocognitive deficits. By mapping brain functions and assessing structural changes, these studies advance our understanding of how specific neurological impairments affect behavior and cognition. 💗 Neuropsychological Features: Machine learning models predict mental health outcomes and cognitive declines by analyzing attention and processing speed. This focus on prediction and prevention, especially for conditions like cardiovascular disease impacting cognition, enables proactive care and lifestyle adjustments to mitigate risks. ⚙️ Neurodegenerative Conditions: AI-based predictive models for neurodegenerative diseases like Parkinson’s allow for early, more accurate diagnoses. By analyzing markers in social cognition and emotional processing, this cluster supports personalized interventions, helping to maintain patient quality of life and reduce care burdens. This is only the beginning. This field is absolutely ripe for rapid advance and massive real-world value.

Neurodivergent conditions often overlap — and that matters When someone is struggling, our instinct is often to ask “what is this?” But in neurodiversity, a more helpful question is often “what might this not be?” Neurodivergent conditions frequently overlap, co-occur and mask one another. ADHD, autism, DCD, DLD, dyslexia, dyscalculia, anxiety, tic disorders and the effects of early adversity or brain injury can present with similar outward behaviours — differences in attention, communication, regulation, movement or learning. This is why single-lens thinking is risky. What looks like anxiety may be ADHD overload. What looks like “behaviour” may be unmet communication or sensory needs. What looks like autism may include language disorder, trauma or coordination difficulties alongside it. Good identification is not about labelling fast — it’s about holding multiple hypotheses, understanding functional impact, and recognising that people rarely fit neatly into one box. Diagnosis, where appropriate, should always sit with trained professionals. But for educators, employers and services, the key message is simpler: think intersectionally, support needs early, and avoid assuming one explanation fits all. Neurodiversity is rarely singular — and our systems need to catch up with that reality.

My PhD will focus on something we still only partially understand: the molecular mechanisms linking the oral microbiome, the gut, and neurodegeneration. For years, the scientific and clinical conversation has been centred on the gut–brain axis, often overlooking a critical upstream component. The oral microbiome has largely remained at the margins of this discussion, despite growing evidence that it plays a far more central role than previously assumed. This recent review brings this into sharper focus by showing that oral dysbiosis is not confined to the oral cavity but can actively contribute to systemic and neural processes. Several periodontal pathogens are able to disseminate beyond their local environment, influencing immune regulation and promoting inflammatory cascades that extend to the brain. What is particularly striking is that these mechanisms converge on pathways we already recognise as central to neurodegenerative and neuropsychiatric disorders, including microglial activation, cytokine release, and protein misfolding processes associated with Alzheimer’s and Parkinson’s disease. This shifts the perspective from isolated associations to a more integrated biological framework. The oral microbiome is not simply an additional variable, but part of a continuous system that interacts with the gut, the immune system, and neuroendocrine pathways such as the HPA axis. These interactions form a network in which microbial ecosystems across different body sites contribute to a shared inflammatory and metabolic landscape. What becomes increasingly difficult to justify is the way we continue to approach these domains separately. Oral health, gut health, and brain health are still often treated as distinct areas, both in research and in clinical practice. Yet the biology suggests otherwise. These systems are interconnected, and their interactions may be key to understanding not only disease progression but also potential points of intervention. This is precisely where my work is directed: moving beyond descriptive associations to identify the molecular signals that link these microbial ecosystems to neuroinflammatory processes. The goal is not simply to confirm that a connection exists, but to understand how it operates, and whether it can be meaningfully targeted. If these mechanisms are clarified, oral dysbiosis may no longer be seen as a secondary feature or a coincidental finding, but as a modifiable contributor to neurodegeneration. That shift has significant implications, both for how we conceptualise these conditions and for how we approach prevention and intervention. We are still at an early stage in connecting these layers, but one conclusion is becoming increasingly clear. Brain health cannot be fully understood without considering the broader microbial systems that influence it. #parkinsondisease #oralmicrobiome #gutmicrobiome #neurodegeneration https://lnkd.in/echFjvad

A 65 year old just became the first person to control an iPad using brain signals alone. Mark Jackson was diagnosed with ALS (amyotrophic lateral sclerosis) in 2021. Over time, he developed complete paralysis in both arms and weakness in his neck. No way to swipe a phone. No way to send a text. No way to do things for himself without asking someone else. Until a brain-computer interface by Synchron changed that. Here's how it works: ▶ 1. Device sits inside a brain vein ↳ A small sensor is implanted into one of the veins within Mark's brain through a minimally invasive procedure - not brain surgery. ↳ It reads brain signals from the motor cortex and translates them into digital actions on screen. ↳ Mark now watches Netflix, listens to audiobooks, browses Instagram and Facebook, and texts his kids. All by thinking about the action he wants to take. ▶ 2. Two-way communication creates real-time feedback ↳ Synchron just launched a new version using something called a BCI HID profile - Human Interface Device. ↳ The computer detects the strength and fidelity of Mark's brain signal in real time and presents feedback about where he's looking, what he's thinking about clicking, where he wants to move. For someone who can't move their arms, losing the ability to do things independently is one of the hardest parts of the disease. This technology gives that back. However, the tech is still early. Synchron has completed early feasibility trials and is preparing for pivotal trials before seeking FDA approval - a process that will take several years. But would you trust a brain implant if it gave you back your independence? #entrepreneurship #healthtech #innovation

A recent study reveals that every region of the human brain has a distinct connectivity fingerprint, defined not by its position, but by the network of regions it interacts with. This discovery reframes how we understand brain organization. Rather than assigning singular functions to isolated areas, it emphasizes that cognition and behavior emerge from dynamic patterns of connectivity across the brain. The implications extend far beyond theory. Disruptions in these connectivity patterns could underlie neurological and psychiatric disorders, opening new possibilities for early diagnosis and targeted intervention. For neurotechnology and brain computer interface research, this insight is equally transformative. Accurately replicating or enhancing brain function will depend on understanding the architecture of communication between regions, not just their activation patterns. Ultimately, this finding reinforces a broader truth, that intelligence, whether biological or collective, is not rooted in individual units, but in the relationships that bind them. 📄 Source:Network Neuroscience, 2025 — “Connectivity and Function Are Coupled Across Cognitive Domains Throughout the Brain" #Neuroscience #BrainConnectivity #Neurotechnology #CognitiveScience #AbhijeetSatani

BRAIN CIRCUITS BEHIND PSYCHEDILICS' ANTI-ANXIETY POWER DECODED New research has identified distinct neural circuits for the anti-anxiety and hallucinogenic effects of psychedelics. Using the psychedelic DOI in mice, researchers demonstrated that anxiety reduction persists long after hallucinatory effects subside. By mapping activated brain cells with molecular tagging and reactivating them with light, they pinpointed specific neurons in the prefrontal cortex responsible for anxiety relief. The findings suggest it may be possible to develop psychedelics-based treatments that alleviate anxiety without inducing hallucinations. This study also highlights the complexity of psychedelic effects, involving both direct and downstream neural networks. Key Facts: 1. Anti-anxiety effects of psychedelics persist after hallucinations fade. 2. Neural circuits for anxiety relief involve direct and downstream activation. 3. Optogenetics reactivated anxiety-reducing neurons independently of drugs. Source: https://lnkd.in/g7z6BUWj

How does the gut actually "talk" to the brain? It turns out there are surprisingly sophisticated communication networks at play. The gut microbiota, the trillions of microbes living in your digestive tract, send signals to the brain through a combination of nerve connections and chemical messengers. Two key players in this back-and-forth are the autonomic nervous system and the enteric nervous system, which together keep a constant dialogue going along the microbiota-gut-brain axis. When that dialogue is disrupted, diseases may develop. Researchers have linked breakdowns in gut-brain communication to a range of neuropsychiatric conditions, including depression, social anxiety disorder, schizophrenia, ADHD, autism spectrum disorder (ASD), and even Parkinson's disease. A lot of this comes down to what your gut microbes are producing. Microbial metabolites, the byproducts of bacterial activity, can exert powerful effects throughout the body. For example, short-chain fatty acids (SCFAs) and secondary bile acids help stimulate the release of gut hormones like GLP-1 and PYY. The most famous SCFAs (acetate, propionate, and butyrate) help regulate gut-brain signaling and even shape how the immune system responds. But not all microbial byproducts are beneficial. Secondary bile acids like deoxycholic acid (DCA) and lithocholic acid (LCA), along with polyamines, can weaken the gut's protective lining. When that barrier breaks down, bacterial components like lipopolysaccharide (LPS), peptidoglycan, and flagellin can slip into the bloodstream, setting off immune responses and driving systemic inflammation. Gut bacteria also produce other bioactive compounds worth knowing about. Bacteriocins are small, ribosomally synthesized antimicrobial peptides that bacteria use to compete with one another; some target only closely related species while others have a much broader reach. Tryptophan-derived metabolites like indoles play a role in maintaining gut barrier integrity and keeping inflammation in check. And bacterial-derived histamine has been shown to contribute to visceral pain sensitivity while an enzyme called β-glucuronidase can interfere with the body's ability to detoxify harmful compounds. It's clear that the gut microbiota are far more than digestive artifacts, engaging in crosstalk with every organ system and driving appetite regulation, brain function, immunity, and even social behaviors. If you're not already, it's never too late to start minding your microbes. Reference: O’Riordan et al. "The gut microbiota-immune-brain axis: Therapeutic implications." Cell Reports Medicine, 2025. doi:10.1016/j.xcrm.2025.101982