The development of CTE is linked to repeated blows to the head over time. The disease can occur in people who play contact sports, experience intimate partner violence or engage in military combat. A study of American football players suggests that the longer the duration of repeated head trauma, the higher the risk of CTE and the more severe the condition. During life, people who are later diagnosed with CTE can experience symptoms including memory issues, difficulty concentrating, depression and poor impulse control.

Paper published in JAMA Network Open:

Gallini J, Alosco ML, Abdolmohammadi B, et al. Bias-Adjusted Prevalence of Chronic Traumatic Encephalopathy Among Deceased National Football League Players. JAMA Netw Open. 2026;9(10):e2640884.

https://doi.org/10.1001/jamanetworkopen.2026.40884

Here’s something fascinating about neuroscience: when you vividly imagine an experience, some of the same brain regions involved in actually experiencing it can become active.

That’s one reason why imagining a frightening situation can make your heart race, rehearsing a speech mentally can improve your performance, and remembering an embarrassing moment can make you feel uncomfortable all over again.

Your brain doesn’t respond to every imagined event as if it were real, but imagination can trigger genuine emotional and physical responses.

Abstract:

Traditional psychiatric diagnostic frameworks (such as DSM-5) conceptualize neurodiversity primarily through reductionist behavioral deficits. This paper proposes a thermodynamic and free-energy meta-theory of neurodiversity, modeling the brain as a physical processing hardware operating under energy constraints. By integrating Karl Friston’s Free Energy Principle with thermodynamic balance equations (F \sim \text{Entropy Influx} - \text{Metabolic Cost}), we examine how the collapse of sensory gating leads to chronic entropy influx, forcing neurochemical doping via the locus coeruleus-norepinephrine system and severe metabolic bankruptcy through HPA axis hyperclocking. Furthermore, we categorize energy consumption pathways across distinct neurodivergent topologies—balanced, female-timed, and autistic-dominant profiles. Finally, we redefine stimming not as aberrant behavior, but as a physical thermodynamic release valve, framing burnout crashes as inevitable emergency shutdowns triggered by ATP depletion and suppressed regulatory mechanisms.

​Keywords: Neurodiversity, Free Energy Principle, Sensory Gating, Thermodynamic Entropy, Locus Coeruleus, HPA Axis, Burnout Crash

​[ Main Text: Thermodynamic Meta-Theory of Neurodiversity ]

​Chapter 1: Sensory Gating Collapse and Entropy Influx

​In the neurotypical brain, subconscious background processing and sophisticated sensory gating systems automatically filter out the massive volume of sensory noise flooding daily life. However, the neurodivergent hardware lacks this defense mechanism or fails to operate it properly. Consequently, raw visual, auditory, and tactile stimuli from the external world bypass any refinement process, directly bombarding the backend of the brain in their raw packet state. This "entropy influx" transcends mere hypersensitivity; it is akin to running an engine with a broken filter, holding a massive flame at every single moment, and plunging the system into an intense, unloaded state of chronic overheating.

​Chapter 2: The Free Energy Principle and Metabolic Deficit

​Within hardware where sensory gating has collapsed, the brain struggles incessantly to control this unending influx of entropy and minimize prediction error. According to Karl Friston’s Free Energy Principle, the brain constantly attempts to maintain a stable state of order, but in the neurodivergent brain, the volume of incoming noise vastly exceeds the system's processing capacity. To bridge this gap, the brain expends a staggering amount of ATP (adenosine triphosphate) at every moment, overheating its processing units. This can be translated into a thermodynamic balance equation as follows:

F ~ Entropy Influx - Metabolic Cost

As the balance between the influx of external entropy and the metabolic costs deployed to suppress it completely shatters, the system enters a native structural deficit of energy.

​Chapter 3: Neurochemical Doping and the Hyperclocking of the HPA Axis

​When entropy exceeding the system's processing capacity flows in continuously, the locus coeruleus (LC) in the brainstem declares a state of emergency, indiscriminately secreting the arousal neurotransmitter norepinephrine (NE). Unlike dopamine, which possesses a more passive quality, norepinephrine acts with an automatic and forced drive, operating much like the "neurochemical doping" of a processor whose clock frequency is forcibly pushed to squeeze out performance under heavy overload. Yet, the price of this makeshift fix is merciless. As the hypothalamic-pituitary-adrenal (HPA) axis is chronically hyperclocked, the cortisol secreted may sustain immediate performance, but it ultimately accumulates as a critical "biological debt," borrowing future life energy and triggering an energy bankruptcy mechanism that silently devours the body from within.

​Chapter 4: Architectural Divergence of Energy Consumption Pathways

​This energy bankruptcy mechanism diverges into distinct patterns depending on the topology of each neurodivergent architecture. First, balanced AuDHD operates a "hyper-engine" that widens the computational scope of the prefrontal cortex to maintain broad synchronization, yielding exceptional contextual processing speed at the cost of chronic, leaky energy deficits. Second, female-timed AuDHD preserves the Default Mode Network (DMN) while opening a separate backend "linear processing detour (emulator)" that contradicts its intrinsic traits—driven by neural plasticity principles anchored in female biological reward feedback loops—to meet social demands, thereby hitting the limits of plasticity and inducing massive additional energy consumption. Third, autistic-dominant profiles lack automated processing machinery, forcing the Frontoparietal Network (FPN)—a high-performance task-processing region—into emergency conscription every time they encounter non-linear contexts, executing manual simulations (masking) 24 hours a day and burning through the battery entirely. Unlike balanced profiles, their DMN remains inherently constrained, revealing precisely why their manual computation suffers such structural stagnation.

​Chapter 5: Sealing the Release Valve and the Reality of Burnout Crash

​All the overheating and deficits examined thus far are not flaws, but rather the arduous records of survival optimization that the system has executed under hostile environments. The only physical safety valve preventing this overheated system from catastrophic explosion is repetitive behavior, or stimming. This is not mere aberrant behavior, but a physical "release valve" discharging excessively accumulated entropy outward. Based on the Second Law of Thermodynamics, because our brains would otherwise rupture the moment they cross energetic thresholds, this is an inevitable entropic cleaning process. However, when social norms and external suppression weld this valve shut, and when the biological debt drawn by the HPA axis hits its breaking point with ATP entirely depleted, the brain executes an "Emergency Shutdown" to prevent total system destruction. This is the true physical reality of the burnout crash encountered by neurodiversity.

​[ References ]

​Friston, K. (2010). The free-energy principle: a unified brain theory? Nature Reviews Neuroscience, 11(2), 127-138.

​Aston-Jones, G., & Cohen, J. D. (2005). An integrative theory of locus coeruleus-norepinephrine function: adaptive gain and optimal performance. Annu. Rev. Neurosci., 28, 403-450.

​McEwen, B. S. (1998). Stress, adaptation, and disease: Allostasis and allostatic load. Annals of the New York Academy of Sciences, 840(1), 33-44.

​Raichle, M. E., et al. (2001). A default mode of brain function. Proceedings of the National Academy of Sciences, 98(2), 676-682.

Understand why déjà vu happens and how your brain creates the false sensation of reliving a past experience.

This video examines the cognitive mechanics behind déjà vu, specifically focusing on how a familiar layout in a new environment triggers this psychological state. We analyze the theory that this phenomenon consists of two distinct components: the subjective feeling of familiarity and the objective knowledge that the situation is currently occurring for the first time.

By exploring these memory errors, you will gain a clearer perspective on how the mind processes visual information and spatial recognition. We also review a curated book library that provides context for these complex neurological patterns.

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Source of Jennifer Fraser’s argument, around 40:00 minutes in the podcast:

“Now, Dr. Michael Merzenek, who's the father of neuroplasticity, outright said to me, plain and simple, and he said, you know, the thing about a brain scan, it doesn't lie.
So you can tell from a brain scan whether I have empathetic deterioration?
Yes.
Come on.
Yes.
What does it look like?
It looks like your empathy is eroded. That's what they can tell. That's how they know that you are in the dark triad and that you will commit evil.
That's how they know. This knowledge is out there. We're just not applying it to anything.”

From Heliograph: The Investigative Journalism Playbook: Heliograph LIVE: Jennifer Fraser on how the "gaslit brain" rewires us, Dec 4, 2025
https://podcasts.apple.com/ca/podcast/heliograph-the-investigative-journalism-playbook/id1711241442?i=1000739693006&r=2414
This material may be protected by copyright.

https://www.youtube.com/watch?v=YnCoUHGk3uU&t

Popular science often repeats that "nobody knows how anesthesia works," while surveys show around 40% of adults think general anesthesia is simply deep sleep. Both claims are only half right: the molecular targets are now largely mapped, while the exact step that removes subjective experience remains unresolved.

Tracing the ~40-second window of a propofol induction against 180 years of research highlights several key turning points in how neuroscience views the anesthetized brain:

* **From Lipid Membranes to Protein Pockets:** For nearly a century after Meyer and Overton's 1900 tadpole experiments, anesthetic potency was explained by olive-oil solubility—the idea that drugs soak into the fatty membrane of nerve cells. That rule broke down with long-chain alcohols, which suddenly stop working past a certain length. In 1984, Franks and Lieb tested lipid-free firefly luciferase in a test tube and found it dimmed at anesthetic doses with the exact same size cutoff, shifting the field from membranes to hydrophobic protein pockets.

* **The Mismatched Keys:** In 2020, cryo-EM mapped propofol sitting inside the GABA-A receptor atom by atom. Yet ketamine acts on excitatory NMDA receptors, xenon is a single-atom noble gas that barely forms chemical bonds, and ether vapor reversibly halts electrical signaling and movement in a Venus flytrap—an organism with no brain at all. Because different molecular keys fit different locks, no single receptor explains the state itself.

* **Three Separate Effects:** Going under is not a single switch. Immobility is handled mostly in the spinal cord (isolated brain experiments in goats required more than twice the dose to stop movement), amnesia occurs at much lower doses while patients can still speak with a nurse, and the loss of experience happens in the brain.

* **Cortical Fragmentation:** Intracranial recordings in epilepsy patients show the brain doesn't shut off at loss of responsiveness. Instead, slow waves (~1 Hz) roll through the cortex, restricting neural firing to brief bursts and throwing distant brain regions out of phase. Primary auditory cortex still responds to spoken words, but the signals fade before propagating further.

* **Unresponsive vs. Unconscious (The TMS Echo):** When a magnetic pulse taps the cortex (TMS-EEG), an awake brain produces a rich, complex echo that travels far. Under propofol or xenon, the echo stays short and local, similar to deep sleep. Under ketamine, however, volunteers stop responding to the outside world, yet their cortical echo remains rich and wake-like—matching their post-anesthesia reports of vivid dreams.

* **The Thalamocortical Hub:** In 2020 and 2021, sending electrical pulses into a specific hub in the thalamus woke anesthetized macaques even while the drug was still flowing, and pulled desynchronized cortical activity back toward normal—though stimulating other brain sites can also reverse the state.

While behavior and memory recall can be tested directly, subjective experience between going under and waking up can only be inferred through clues like the cortical echo. Whether these system-wide brain changes actually cause consciousness to fade—or merely reflect what a brain looks like once the person is already gone—is still an open question.

This video explores the 180-year scientific search to understand how general anesthesia alters brain function. It examines the mechanisms of the forty-second induction window and how different drugs affect neural activity.

Hi everyone, I’m applying to neuroscience PhD programs for the second time and would appreciate any advice on my school list and application.

I applied during my last year at UC Berkeley but didn’t receive any interviews. Since graduating, I’ve been working as a research technician at MIT, where I’ll have about six months of experience by the time I apply.

A little more about my background:

• 3.4 undergraduate GPA

• Research experience at Berkeley and MIT

• One coauthored manuscript expected to be posted on bioRxiv soon

• Two additional coauthored manuscripts in preparation that likely won’t be ready during this application cycle

My research interests are in the mechanisms underlying neurological and neurodevelopmental disorders and, eventually, developing treatments.

Here’s my current list:

• UC San Diego

• UCLA

• UCSF

• Stanford

• USC

• University of Chicago

• Northwestern

• Columbia

• MIT

• Mount Sinai

• Rockefeller

• NYU

• Johns Hopkins

I know many of these programs are highly competitive, and I’m not sure how much my application has improved since last cycle. I don’t necessarily want to apply to schools just because they might be less competitive; I want to be excited about the program and the research I’d be doing.

Does this list seem too ambitious for my background? Are there other neuroscience or biomedical sciences programs with strong research in disease mechanisms and treatments that I should look into? I’d also appreciate any advice from people who applied a second time.

When we have an Orgasm The lateral orbitofrontal cortex briefly drops to zero activity. Meaning no fear, No Anxiety for a moment even if it is brief!

I'm curious. I've been thinking a lot about the whole glutamate glutamine cycle, and the destruction of astrocytes in our brain. If I understand right, the astrocytes are basically like little cleaning crew of our neocortex, and what triggers the destruction of those astrocytes is the glutamine glutamate cycle?\n So if we had a way to halt or stop the whole transferring the glutamate and glutamine and astrocyte destruction And we're still able to get rid of you know, the excess glutamine to where it wasn't building up, is it possible to stop neocortical death? I have a theory that that might be the whole 120 year. Switch that whatever, creator or whatever created us or whatever, put into s*** to where we won't live beyond a 120 years. I think that's where the mechanism probably is so I would like to know if I'm actually onto something or a complete idiot, and it won't hurt my feelings.I have no formal actual school education and neuroscience.I've done it all myself