Today's selection explores the biological mechanics of neurodevelopment, ranging from the protective effects of ADHD medication and sleep-cycle interventions to new insights into how brain cells manage memory and nerve insulation (Blog Name: Living on the Spectrum).
The Transmitter’s Rising Stars of Neuroscience 2025
Diverse Research Directions
The 2025 cohort of early-career researchers includes scientists focusing on the physical and developmental roots of neurodivergence. Christian Cazares uses brain organoids to identify biomarkers of cortical dysfunction, while Theanne Griffith examines how sensory proprioception—the body's sense of its own position—influences the central nervous system. Other honorees, such as Halie Olson and Shailee Jain, investigate language development in toddlers and AI-based models of language processing.
Community Advocacy
Beyond laboratory work, these researchers lead initiatives to increase accessibility and representation in science. Several honorees founded organizations like "Black In Neuro" and "Arabs in Neuroscience," focusing on mentorship and improving diversity within the neuroscience community.
Microglia Implicated in Infantile Amnesia
Research Findings
A study using mouse models suggests that microglia, the brain's immune cells, act as a mediator between maternal immune activation and the retention of early memories. Typically, rodents experience "infantile amnesia," where the earliest memories are lost. However, immune responses during pregnancy appear to cause these memories to persist, a phenomenon associated with autism-like behaviors in the study.
Biological Mechanisms
Researchers found that deactivating microglia or blocking specific receptors (CX3CR1) could either allow early memories to persist in typical mice or reverse the effects of maternal immune activation. This suggests microglia might influence memory by altering the extracellular matrix or interfering with the formation of new engrams, rather than just through synaptic pruning.
Significance & Limitations
While the study provides a link between immune responses and memory development, some experts question the use of minocycline due to its lack of specificity. The findings point toward a complex system where multiple mechanisms likely drive how the brain retains or discards early life experiences.
Mechanosensors Regulate Individual Steps in Myelination
Core Findings
Oligodendrocytes, the cells responsible for nerve insulation, use physical pressure to determine how much myelin to wrap around nerve fibers. This process relies on a mechanosensor called TMEM63A. When this receptor is absent, these cells fail to calibrate myelin thickness to the size of the nerve fiber, leading to improper insulation.
Clinical Relevance
This mechanical process is directly linked to infantile hypomyelinating leukodystrophy 19, a rare disorder where the brain produces insufficient myelin. Understanding how TMEM63A and other sensors like PIEZO function may clarify how the brain coordinates complex stages of neural insulation during development.
Bendy Bodies, ADHD Brains
Physical and Neurological Overlap
Research shows a significant correlation between ADHD and joint hypermobility, where joints have an unusually large range of motion. Nearly 80% of adult females with ADHD are hypermobile. Neurodivergent individuals are four times more likely to have hypermobility, which often stems from genetic differences in connective tissue.
Co-occurring Symptoms
Hypermobility often appears alongside Dysautonomia, specifically POTS (postural orthostatic tachycardia syndrome), which causes heart rate spikes upon standing. Brain imaging reveals that hypermobile individuals often have structural differences in the amygdala and insula, areas responsible for processing fear, emotion, and sensory perception—patterns frequently seen in ADHD and autism.
Management and Support
Effective management strategies focus on improving core strength and proprioception through physical therapy and Pilates. In some cases, clinicians use medications to address associated pain, muscle spasms, or anxiety related to these physical differences.
No, Stimulants Don’t Cause Brain Damage
Protective Effects
Scientific research indicates that prescription stimulant medications used for ADHD do not cause brain damage when taken as instructed. Imaging studies suggest these medications may actually have a protective effect, reducing brain abnormalities associated with ADHD and bringing activation patterns closer to those of neurotypical individuals.
Source of Misconceptions
Concerns about neurotoxicity generally stem from studies involving extremely high doses injected into rodents or the use of illicit substances like cocaine. These differ significantly from prescription medications in terms of chemical structure, delivery speed, and dosage. Evidence suggests that following a prescribed treatment plan can prevent the long-term difficulties associated with untreated ADHD.
Circadian Rhythm Disorder and ADHD
Biological Timing Differences
Approximately 73-78% of individuals with ADHD experience delayed sleep-wake cycles. Studies show that melatonin production starts roughly 90 minutes later in adults and 45 minutes later in children with ADHD compared to neurotypical peers. Morning cortisol rhythms, which regulate alertness, are also delayed.
Chronotherapy Approaches
Interventions timed to biological rhythms have shown success in reducing symptoms. Low-dose melatonin (0.5 mg) reduced adult ADHD symptoms by 14% and advanced sleep timing. For children, higher doses (3-6 mg) improved mood and behavior. Using a 10,000 lux light lamp in the morning, combined with consistent wake times and evening light restriction, can effectively shift sleep phases earlier.
Clinical Recommendations
Experts suggest routine screening for sleep disturbances in ADHD patients. These low-risk, accessible interventions serve as a useful addition to traditional treatments to help manage the overall symptoms of the condition.
Podcast Transcript
Aaron: Hello everyone, and welcome to the show. I am Aaron.
Jamie: And I am Jamie.
Aaron: You know, Jamie, I was looking through some of the latest updates in neuroscience this week, and I felt a strange mix of emotions. On one hand, some of the biology is incredibly dense—almost intimidating—but on the other hand, there’s this sense of momentum. It feels like we are finally starting to look under the hood of how the brain actually builds itself.
Jamie: I know exactly what you mean. It can feel like a lot of data, but when you zoom out, the picture becomes more about people. I actually saw the Transmitter recently released their 2025 "Rising Stars of Neuroscience" list. It’s a group of 25 early-career researchers, and what struck me wasn’t just their lab work, but how many of them are focusing specifically on things our listeners care about—like language development in toddlers and how the brain processes sensory information.
Aaron: I noticed that too. I think it was Christian Cazares who is using those lab-grown mini-brains—organoids—to study how the brain’s "wiring" might look different in neurodevelopmental conditions. It’s fascinating because it’s not just about finding a "cause," but understanding the diversity of how brains grow. And researchers like Theanne Griffith are looking at proprioception—that "sixth sense" of knowing where your body is in space.
Jamie: That’s a huge one for the SPD and ADHD communities. And it’s not just the science; these "Rising Stars" are also leading groups like "Black In Neuro" and "Arabs in Neuroscience." It feels like the field is trying to become as diverse as the people it studies.
Aaron: It’s heartening to see that shift in the culture of science. But speaking of the "wiring" of the brain, I came across something about microglia and memory that left me a bit confused. We usually think of microglia as the "trash collectors" or the immune cells of the brain, right? But this new study with mice suggests they have a weird role in how we remember things from when we were babies.
Jamie: It’s a really intriguing study. They looked at "infantile amnesia," which is the reason most of us don’t remember being two years old. Usually, the brain "cleans out" those early memories. But in this study, they found that if there was an immune response during pregnancy—what they call maternal immune activation—those early memories actually stuck around in the offspring.
Aaron: Wait, so the memories stay when they’re supposed to fade? That sounds like it could be a good thing, but I’m guessing it’s more complicated.
Jamie: Right, it’s not necessarily "better" memory; it’s a change in how the brain matures. They found that microglia seem to be the ones deciding which memories stay and which go. When they used an antibiotic or blocked a specific receptor to "quiet" the microglia, they could actually reverse that memory retention. Now, some scientists are cautious because the drugs used aren’t perfectly specific, but it suggests that the immune system and memory are much more intertwined than we realized.
Aaron: That really highlights how sensitive the developing brain is to its environment. It reminds me of another study you sent over about "myelin." I always thought of myelin as just the insulation on a wire, like the plastic coating on a charger cable. But it turns out it’s a lot more... mechanical?
Jamie: Exactly. We usually think of brain growth as a chemical process, but this research on oligodendrocytes—the cells that make myelin—shows they actually "feel" their way around. They use a sensor called TMEM63A to measure the physical diameter of a nerve fiber. It’s like they are checking the size of the pipe to decide exactly how much insulation to wrap around it.
Aaron: So if that sensor isn’t working, the insulation is all wrong?
Jamie: Right. If that mechanical "sensing" fails, you get improper myelination, which is linked to some very rare neurodevelopmental disorders. It’s a reminder that the brain is a physical structure that responds to pressure and touch at a microscopic level.
Aaron: You know, that word "proprioception" keeps coming up—that sense of where the body is. It’s a perfect bridge to something I’ve heard many parents and adults in the ADHD community talk about: being "double-jointed" or really flexible. I saw a study recently that says this isn’t just a coincidence.
Jamie: It’s a very real connection. Research shows that neurodivergent individuals, especially those with ADHD, are about four times more likely to have joint hypermobility. In fact, in one study, nearly 80% of adult females with ADHD were found to be hypermobile. It’s often related to things like Ehlers-Danlos syndrome or Hypermobility Spectrum Disorder.
Aaron: 80%? That’s massive. I think for a lot of people, they just thought they were clumsy or "stretchy," but this suggests it’s tied to the way the brain is wired, too.
Jamie: It is. Brain imaging has actually shown that people with hypermobility often have structural differences in the amygdala, which processes emotions, and the insula, which handles sensory perception. It’s almost like the body’s "internal GPS" is calibrated differently. This can lead to extra fatigue, anxiety, and even issues with the autonomic nervous system, like POTS, where your heart rate spikes when you stand up.
Aaron: It makes so much sense why someone might feel "anxious" when their body is actually just struggling to regulate its physical position and heart rate. It’s not "all in your head," it’s in your joints and your nervous system.
Jamie: Precisely. And that’s why management often involves things like Pilates or physical therapy to build core strength and help the brain "find" the body’s position better.
Aaron: Speaking of ADHD, I want to pivot to something that often causes a lot of stress for parents: medication. There’s always this lingering fear, isn't there? That these stimulants might be "damaging" the brain in the long run.
Jamie: It’s a very common and very understandable concern. But the actual research on this is quite reassuring. When scientists look at the brains of people taking prescribed stimulants for ADHD, they don’t see damage. In many cases, they actually see the opposite. The medication can have a "protective" effect, helping the brain’s structure and activation patterns look more like those of neurotypical individuals over time.
Aaron: So where does the "neurotoxicity" fear come from then? Is it just old wives' tales?
Jamie: Well, it mostly comes from studies where rodents were given massive, injected doses—way higher than what a human would take—or from looking at the illicit use of street drugs like cocaine. Prescription meds move through the body much more slowly and at much lower doses. The evidence suggests that the risks of untreated ADHD—the persistent struggles with school, work, and safety—are often much more significant than the risks of the medication itself.
Aaron: That’s a helpful distinction. But even if someone is on medication, sleep always seems to be the final boss for people with ADHD. I was reading that nearly 75% of people with ADHD have a "delayed" sleep cycle. They aren't just "night owls" by choice; it’s biological.
Jamie: It really is. Their internal clock, or circadian rhythm, is often shifted back. For example, the "melatonin onset"—the time the brain starts producing sleep hormones—can be 45 to 90 minutes later than in neurotypical people. Even their morning cortisol, which helps us wake up, peaks later.
Aaron: I’ve seen some talk about "chronotherapy." Is that just a fancy way of saying "get more sleep"?
Jamie: Not exactly. It’s about timing. Using low-dose melatonin, around 0.5 milligrams, several hours before bed has been shown to help shift that clock forward. And one of the most interesting tools is bright light therapy—using a 10,000 lux lamp first thing in the morning. It tells the brain "the day has started," which can actually improve ADHD symptoms during the day by 14% in some cases.
Aaron: It’s fascinating that something as simple as a bright light or a tiny dose of melatonin could have a double-digit impact on focus. It’s not a replacement for traditional treatment, but it sounds like a very accessible "add-on."
Jamie: Exactly. It’s low-risk and addresses the biological reality of how these brains are timed.
Aaron: Well, we’ve covered a lot of ground today—from lab-grown brains and immune cells to stretchy joints and morning sunlight. It’s a lot to take in, but it’s a good reminder that neurodevelopment isn't just one thing. It’s a whole ecosystem.
Jamie: It really is. And while the science is always evolving, the focus seems to be shifting toward understanding each person’s unique biological "rhythm" and "wiring" rather than just looking at a diagnosis.
Aaron: I think that’s a great place to leave it for today. Thank you all for listening and joining us in this quiet corner to chat. If you want to dive deeper into any of the studies or researchers we mentioned, you can find the summaries and original links on our episode page.
Jamie: We hope this helps you feel a little more informed and a little less overwhelmed. We’ll see you next time.
Aaron: Goodbye everyone.
Jamie: Goodbye.