A recent Huberman Lab guest (their episode will be released soon) who is a world expert on memory teaches that genuine curiosity significantly ramps up levels of neural activity in human brain circuits that release dopamine, which in turn allows deeper, more stable learning.
This makes sense and yet is an often overlooked aspect of “increasing dopamine” for the sake of learning and plasticity. I’m not a big fan of most prescription approaches to dopamine augmentation unless there is a clinical need. Curiosity, however, is something we can all leverage.
You’re not burned out—you’re just taking breaks the wrong way.
Here’s how to fix it, based on science.
Want to perform better? Take better breaks.
Breaks today are where sleep was 15 years ago—underrated and misunderstood. But how you take a break matters.
Most people think more work = more productivity. But research shows that strategic breaks are the real key to staying sharp.
The problem? Most of us take breaks that don’t actually help. Scrolling alone at your desk? Not it.
Here’s how to take a break that actually works:
Move, don’t sit – Walk, stretch, or get outside instead of staying glued to your chair. Movement resets your brain.
Go outside, not inside – Fresh air and sunlight restore energy and boost creativity.
Be social, not solo – Breaks are more effective when taken with someone else.
Fully unplug – Leave your phone. No work talk. No emails. No scrolling. Just a real reset.
Try this: Take a 10-minute walk outside with a colleague. Talk about anything but work. Leave your phone at your desk.
Watch how much better you feel—and perform.
Breaks aren’t a luxury. They’re a performance tool.
Treat them like it.
Got a break routine that works for you? Drop it below
Or send this to someone who needs a real break.
🧠 As a neuroscientist, I find this absolutely incredible.
The first-ever atlas of brain development has just been published and it’s nothing short of breathtaking.
For the first time, researchers have mapped how stem cells transform into neurons during mammalian brain development, tracking hundreds of thousands of cells in humans and mice.
They’ve identified when and how neural progenitors shift from building excitatory to inhibitory neurons and even how glial cells emerge over time.
In essence, they’ve charted the biological choreography of the brain’s birth.
This isn’t just a technical feat.
It’s a window into the deepest question in neuroscience:
➡️ How does a collection of stem cells become a mind?
Projects like the BRAIN Initiative Cell Atlas Network (BICAN) are changing how we understand neurodevelopment, disorders like autism and schizophrenia, and even how we model the brain in vitro.
Every data point in this atlas carries potential for precision medicine, regenerative neuroscience, and the next generation of brain-inspired models.
Truly a landmark moment.
What a time to be doing neuroscience. 🧬
#Neuroscience#BrainDevelopment#StemCells#BRAINInitiative#Neurogenesis#Nature#ScientificDiscovery#Neurobiology
New research shows a protein blamed for Alzheimer’s may actually be crucial for building newborn brains, shaking long-held beliefs
A surprising new study has turned decades of Alzheimer’s dogma on its head. Scientists have discovered that p-tau217, a form of the tau protein long thought to be purely destructive in the brain, is found in astonishingly high levels in healthy newborn babies — even more than in Alzheimer’s patients. This finding suggests p-tau217 isn’t just a marker of disease but may actually be vital for early brain development.
Tau normally acts like scaffolding inside nerve cells, keeping them stable and helping them communicate. But in Alzheimer’s, tau becomes chemically altered into p-tau217, which clumps into tangles that choke brain cells, causing the memory loss and confusion typical of dementia. For years, high levels of p-tau217 have been viewed as a surefire sign of trouble. But this new research, led by the University of Gothenburg, shows that’s not the whole story.
Analyzing blood samples from over 400 people — from premature babies to seniors with Alzheimer’s — researchers found premature infants had the highest p-tau217 levels of all. These levels then plunged during the first months of life, stayed very low through adulthood, and only rose modestly again in Alzheimer’s patients. The fact that newborns can handle sky-high p-tau217 without damage suggests it plays a key role in wiring up the brain’s early networks, especially in regions tied to movement and touch.
This discovery could completely reshape how we diagnose and treat Alzheimer’s. It means high p-tau217 isn’t always a red flag — in babies, it’s part of healthy growth. More importantly, if we can figure out why infant brains tolerate or even need these levels without forming harmful tangles, we might uncover new ways to protect aging brains. Instead of only attacking tau as the villain, researchers may start asking how to keep its youthful, brain-building properties alive for longer.
Research References :
PMID: 40574977
PMCID: PMC12198956
The potential dual role of tau phosphorylation: plasma phosphorylated-tau217 in newborns and Alzheimer’s disease, Brain Communications, Volume 7, Issue 3, 2025, fcaf221,
𝐍𝐨, 𝐲𝐨𝐮𝐫 𝐛𝐫𝐚𝐢𝐧 𝐝𝐨𝐞𝐬 𝐧𝐨𝐭 𝐩𝐞𝐫𝐟𝐨𝐫𝐦 𝐛𝐞𝐭𝐭𝐞𝐫 𝐚𝐟𝐭𝐞𝐫 𝐋𝐋𝐌 𝐨𝐫 𝐝𝐮𝐫𝐢𝐧𝐠 𝐋𝐋𝐌 𝐮𝐬𝐞.
See our paper for more results: "Your Brain on ChatGPT: Accumulation of Cognitive Debt when Using an AI Assistant for Essay Writing Task" (link in the comments).
For 4 months, 54 students were divided into three groups: ChatGPT, Google -ai, and Brain-only. Across 3 sessions, each wrote essays on SAT prompts. In an optional 4th session, participants switched: LLM users used no tools (LLM-to-Brain), and Brain-only group used ChatGPT (Brain-to-LLM).
👇
𝐈. 𝐍𝐋𝐏 𝐚𝐧𝐝 𝐄𝐬𝐬𝐚𝐲 𝐂𝐨𝐧𝐭𝐞𝐧𝐭
- LLM Group: Essays were highly homogeneous within each topic, showing little variation. Participants often relied on the same expressions or ideas.
- Brain-only Group: Diverse and varied approaches across participants and topics.
- Search Engine Group: Essays were shaped by search engine-optimized content; their ontology overlapped with the LLM group but not with the Brain-only group.
𝐈𝐈. 𝐄𝐬𝐬𝐚𝐲 𝐒𝐜𝐨𝐫𝐢𝐧𝐠 (𝐓𝐞𝐚𝐜𝐡𝐞𝐫𝐬 𝐯𝐬. 𝐀𝐈 𝐉𝐮𝐝𝐠𝐞)
- Teachers detected patterns typical of AI-generated content and scoring LLM essays lower for originality and structure.
- AI Judge gave consistently higher scores to LLM essays, missing human-recognized stylistic traits.
𝐈𝐈𝐈: 𝐄𝐄𝐆 𝐀𝐧𝐚𝐥𝐲𝐬𝐢𝐬
Connectivity: Brain-only group showed the highest neural connectivity, especially in alpha, theta, and delta bands. LLM users had the weakest connectivity, up to 55% lower in low-frequency networks. Search Engine group showed high visual cortex engagement, aligned with web-based information gathering.
𝑺𝒆𝒔𝒔𝒊𝒐𝒏 4 𝑹𝒆𝒔𝒖𝒍𝒕𝒔:
- LLM-to-Brain (🤖🤖🤖🧠) participants underperformed cognitively with reduced alpha/beta activity and poor content recall.
- Brain-to-LLM (🧠🧠🧠🤖) participants showed strong re-engagement, better memory recall, and efficient tool use.
LLM-to-Brain participants had potential limitations in achieving robust neural synchronization essential for complex cognitive tasks.
Results for Brain-to-LLM participants suggest that strategic timing of AI tool introduction following initial self-driven effort may enhance engagement and neural integration.
𝐈𝐕. 𝐁𝐞𝐡𝐚𝐯𝐢𝐨𝐫𝐚𝐥 𝐚𝐧𝐝 𝐂𝐨𝐠𝐧𝐢𝐭𝐢𝐯𝐞 𝐄𝐧𝐠𝐚𝐠𝐞𝐦𝐞𝐧𝐭
- Quoting Ability: LLM users failed to quote accurately, while Brain-only participants showed robust recall and quoting skills.
- Ownership: Brain-only group claimed full ownership of their work; LLM users expressed either no ownership or partial ownership.
- Critical Thinking: Brain-only participants cared more about 𝘸𝘩𝘢𝘵 and 𝘸𝘩𝘺 they wrote; LLM users focused on 𝘩𝘰𝘸.
- Cognitive Debt: Repeated LLM use led to shallow content repetition and reduced critical engagement. This suggests a buildup of "cognitive debt", deferring mental effort at the cost of long-term cognitive depth.
Support and share! ❤️
#MIT#AI#Brain#Neuroscience#CognitiveDebt
People are suffering—yet many still deny that hours with ChatGPT reshape how we focus, create and critique. A new MIT study, “Your Brain on ChatGPT: Accumulation of Cognitive Debt when Using an AI Assistant for Essay-Writing,” offers clear neurological evidence that the denial is misplaced.
Read the study (lengthy but far more enjoyable than a conventional manuscript, with a dedicated TL;DR and a summarizing table for the LLM): https://lnkd.in/g6PBVwVe
🧠 What the researchers did
- Fifty-four students wrote SAT-style essays across four sessions while high-density EEG tracked information flow among 32 brain regions.
- Three tools were compared: no aid (“Brain-only”), Google search, and GPT-4o.
- In Session 4 the groups were flipped: students who had written unaided now rewrote with GPT (Brain→LLM), while habitual GPT users had to write solo (LLM→Brain).
⚡ Key findings
- Creativity offloaded, networks dimmed. Pure GPT use produced the weakest fronto-parietal and temporal connectivity of all conditions, signalling lighter executive control and shallower semantic processing.
- Order matters. When students first wrestled with ideas on their own and then revised with GPT, brain-wide connectivity surged and exceeded every earlier GPT session. Conversely, writers who began with GPT and later worked without it showed the lowest coordination and leaned on GPT-favoured vocabulary, making their essays linguistically bland despite high grades.
- Memory and ownership collapse. In their very first GPT session, none of the AI-assisted writers could quote a sentence they had just penned, whereas almost every solo writer could; the deficit persisted even after practice.
- Cognitive debt accumulates. Repeated GPT use narrowed topic exploration and diversity; when AI crutches were removed, writers struggled to recover the breadth and depth of earlier human-only work.
🌱 So what?
The study frames this tradeoff as cognitive debt: convenience today taxes our ability to learn, remember, and think later. Critically, the order of tool use matters. Starting with one’s ideas and then layering AI support can keep neural circuits firing on all cylinders, while starting with AI may stunt the networks that make creativity and critical reasoning uniquely human.
🤔 Where does that leave creativity?
If AI drafts faster than we can think, our value shifts from typing first passes to deciding which ideas matter, why they matter, and when to switch the autopilot off. Hybrid routines—alternate tools-free phases with AI phases—may give us the best of both worlds: speed without surrendering cognitive agency.
Further reading: Lively discussion (debate) between neuroethicist Nita Farahany and CEO of The Atlantic, Nicholas Thompson, “The Most Interesting Thing in AI” podcast. The big (and maybe the final) question for us is: What is humanity when AI takes over all the creative processes?
Podcast link: https://lnkd.in/emeQkcK6
𝐌𝐚𝐬𝐥𝐨𝐰’𝐬 𝐇𝐢𝐞𝐫𝐚𝐫𝐜𝐡𝐲 𝐨𝐟 𝐑𝐞𝐠𝐮𝐥𝐚𝐭𝐢𝐨𝐧
🧠 𝐖𝐡𝐲 𝐒𝐨𝐦𝐞 𝐊𝐢𝐝𝐬 𝐒𝐭𝐫𝐮𝐠𝐠𝐥𝐞 𝐭𝐨 𝐅𝐨𝐜𝐮𝐬: 𝐈𝐭’𝐬 𝐍𝐨𝐭 𝐉𝐮𝐬𝐭 𝐁𝐞𝐡𝐚𝐯𝐢𝐨𝐫
As an occupational therapist, I often hear things like:
“They just need to concentrate.”
“They’re being defiant.”
“They’re not trying hard enough.”
But what if it’s not defiance?
What if it’s dysregulation?
👉 Many children aren’t “choosing” to be unfocused or reactive.
They’re stuck in survival mode and their nervous system is doing its best to cope.
That’s why I created this visual:
Maslow’s Hierarchy of Regulation
✨ Because co-regulation comes before concentration.
Before a child can sit, attend, or learn, they need:
🔻 Physiological Regulation : Are they tired, hungry, or overstimulated?
🔻 Safety & Predictability : Do they feel safe and know what to expect?
🔻 Connection & Co-Regulation : Is someone helping them regulate and feel secure?
🔻 Self-Esteem & Capability : Do they feel like they can succeed?
✅ Only then can a child access their higher brain functions focus, planning, memory, and learning.
In therapy, we don’t just look at the surface.
We ask:
“What is this behavior telling us about what the child needs?”
Because a dysregulated child isn’t being difficult They’re asking for support in the only way they know how.
💡 When we meet their needs, we unlock their potential.
#OccupationalTherapy#ChildDevelopment#Maslow#EmotionalRegulation#CoRegulation#PediatricTherapy#SchoolOT#BehaviorIsCommunication#NeurodiversityAffirming#TherapyInRealLife#OTMatters#SensorySupport#ExecutiveFunction
Our new study shows that SARS-CoV-2 spike protein accumulates & persists in the body for years after infection, especially in the skull-meninges-brain axis, potentially driving long COVID. mRNA vaccines help but cannot stop it🔬🧠🦠🧵👇
🔬 Using our cutting-edge DISCO tissue clearing technology, we mapped spike protein presence in mouse models and human post-mortem tissues. Key findings:
1️⃣ Spike protein accumulates in the skull marrow niches and skull-meninges connections (SMCs), a newly discovered route into the brain.
2️⃣ Spike protein persists in brain tissue even when PCR tests show no viral presence, indicating a longer half-life than viral particles.
3️⃣ The spike protein is associated with vascular, inflammatory changes and neuronal injury, leading to proteomic changes linked to neurodegeneration.
4️⃣ Long COVID patients exhibited elevated neurodegeneration markers in cerebrospinal fluid, such as Tau protein and NfL.
5️⃣ mRNA vaccines (e.g., BioNTech/Pfizer) significantly reduced spike protein accumulation but did not eliminate it completely.
These findings open pathways for new diagnostic and therapeutic strategies to tackle long COVID and its neurological sequelae. For instance:
• Neural injury markers in cerebrospinal fluid could help evaluate long COVID.
• Spike protein removal or inhibition could become a therapeutic focus.
Read the full study in Cell Host & Microbe:
🔗 https://lnkd.in/dPYc5uVW
Let’s work together to uncover more about the lasting impact of COVID-19 and drive solutions for those suffering from its long-term effects.
#COVID19#LongCOVID#Neuroscience#DISCO#Clearing#Immunology#AIinScience#Proteomics
Before a psychiatric diagnosis can be made, it has to survive a medical workup. This is one of the most important, and most consistently missed, steps in mental health care.
The brain runs on glucose, oxygen, hormones, nutrients, and an immune system it shares with every other organ. When any of those inputs are disrupted, the brain produces symptoms indistinguishable from psychiatric illness.
Examples of what gets missed every day:
⚕️ Hypothyroidism can present as depression. Studies show up to 26.2% of depressed patients have abnormal thyroid function. Treating the thyroid condition should be the first step.
⚕️ Hyperthyroidism can look like anxiety or mania: racing thoughts, insomnia, irritability, and palpitations mimicking panic disorder or hypomania.
⚕️ Iron deficiency can mimic ADHD or depression. Iron is important in dopamine synthesis, and testing without ferritin levels routinely misses this etiology.
⚕️ B12 deficiency can manifest as depression, cognitive decline, and in severe cases psychosis. Neurological impairment can occur at levels considered normal by standard reference ranges.
⚕️ Sleep apnea can present as depression and ADHD: cognitive fog and low energy are driven by chronic hypoxia and fragmented sleep.
⚕️ POTS and dysautonomia can look like anxiety, depression, and cognitive dysfunction, driven by cerebral hypoperfusion when upright, not primary psychiatric illness.
⚕️ PANDAS/PANS manifests as sudden-onset OCD, tics, anxiety, and behavioral change in children. The hallmark is dramatic onset, often overnight, following streptococcal or other infection.
⚕️ Autoimmune encephalitis can present as psychosis. 75% of anti-NMDA receptor encephalitis patients first present to a psychiatrist. It is treatable, but can be fatal when missed.
⚕️ Cushing's disease can look like bipolar disorder: cortisol excess produces mood instability, insomnia, and cognitive impairment.
Here's what a basic workup for any psychiatric condition should include:
→ CBC, CMP, TSH, free T4, B12, folate, vitamin D, iron studies with ferritin, fasting glucose, HbA1c, lipid panel, CRP, urinalysis, toxicology screen.
Suspected POTS:
→ Orthostatic vitals (supine, sitting, standing at 1, 3, and 10 minutes); tilt table test if indicated.
Suspected PANDAS/PANS:
→ Throat culture, rapid strep, ASO titer, anti-DNase B antibody, CBC with differential, ANA, ESR, CRP, mycoplasma IgM/IgG.
First-episode psychosis:
→ Add ANA, anti-NMDA antibodies, HIV, RPR, neuroimaging.
Treating a medical condition as a psychiatric one can cost years of a patient's life. The most evidence-based first step in mental health care is ruling out the medical conditions that produce psychiatric symptoms. We should be doing it every time.
Follow me Britton Ashley Arey, MD MBA for evidence-based perspectives on psychiatry, mental health, and the science of the mind.
#Psychiatry#MentalHealth#IntegratedCare#MindBodyMedicine#MentalHealthAwarenessMonth