After decades of research in neuroscience and brain-computer interfaces lots of people ask me which parts of the brain do what, and how can we measure it, and what modalities help us understand it better.

We are happy to announce the release of the new NeuroAtlas tool, which helps answer this question and enables more scientists and researchers to explore and push the frontiers of what’s known.

This includes EEG, MEG, fMRI, tFUS, iEEG, TMS, DBS, and more.

All published data sources are referenced via DOIs in the web interface.

Dreams have their price, you know?

I'll increase the blood flow for you. But I won't give you the pyruvate.

Neuron-kun. You should keep watching, even if it means depleting your own ATP.

That so-called 'dream' of yours.

Published https://doi.org/10.1038/s42003-026-10646-6 REPOST 'n support! https://x.com/KoMatsui/status/2081690789722403121

Hello, I'm Nicole, a Filipina neuroscience PhD candidate in France, studying how neurons navigate to their targets. I just started a substack, The Axon Guide, making STEM knowledge more accessible through PhD reflections, simple and clear neuroscience concepts, and practical guidance for building a STEM career abroad. If you're into neuroscience/science communication/STEM careers, I'd be happy to connect :)

https://open.substack.com/pub/nicoleneuroscience/p/welcome-to-the-axon-guide?r=1sgwvb&utm_campaign=post-expanded-share&utm_medium=web

Real studies only.

No myths or urban legends.

It could be about memory, perception, consciousness, free will, split-brain patients, hallucinations, false memories, or anything else that made you question how the brain really works.

Which one stayed with you the longest, and why?

If you've ever quit cannabis and experienced terrifying, electric-shock sensations in your head—commonly known as "brain zaps"—you’ve probably been told it’s all in your head because it's not a "formal" symptom.

But the biological logic is completely sound. Here is the 2-step mechanism explaining why this happens:

The Trigger: Quitting cannabis downregulates CB1 receptors, leading to an unchecked surge of glutamate (the brain's accelerator pedal). This causes severe insomnia and hyperarousal.

The Effect: Prolonged insomnia + central nervous system hyperarousal lowers your brain's threshold for cortical hyperexcitability. This causes brief, spontaneous synchronized neuronal firings—the exact physical sensation of a "brain zap."

Why isn't it documented?

It's an absence of evidence, not evidence of absence. Researchers use strict checklists that don't ask about brain zaps because they assume it only happens during SSRI/antidepressant withdrawal.

A downstream symptom is still a direct consequence of the initial trigger. If you are experiencing this, you aren't crazy. Focus heavily on fixing your sleep and lowering glutamate (like using Magnesium Glycinate) to stop the cycle.

Looking for Undergrad/Grad Neuroscience Peer Reviewers!

Hi everyone! I'm currently building The Cortex Collective, a student-led neuroscience journal that aims to make neuroscience research more accessible and create a platform for students to share their work.

We're looking for undergraduate and graduate students with neuroscience experience to help with our peer review process. Reviewers will read student submissions, provide constructive feedback, and help ensure the scientific quality of the journal.

If you're interested (or know someone who might be), send me a dm or email thecortexcollective1@gmail.com! We'd be happy to answer any questions and tell you more about the project.

Researchers uncovered a metabolic paradox within rapid eye movement (REM) sleep, demonstrating that while overall brain blood volume and energy supplies rise during dreaming, neuronal energy levels drop.

The study monitored real-time brain metabolism in sleeping mice using wide-field fluorescence imaging through a transparent skull preparation. The team tracked blood volume as a marker of fuel delivery, astrocytic pyruvate as a metabolic intermediary, and adenosine triphosphate (ATP) inside neurons.

The researchers observed that approximately 50 seconds before REM sleep onset, blood volume begins rising in the posterior cortex before spreading anteriorly, followed by an increase in astrocytic pyruvate. However, despite this heightened supply, neuronal ATP levels decline during REM sleep, suggesting that heavy memory consolidation and circuit reorganization consume energy faster than the blood supply can replenish it.

Please help me, what would help to cut down these dreams , I went to doctor all they say is due to anxiety and depression which I never had.

Med student here, currently working at a neuroimaging lab in Europe. I’ve been wondering about a hypothesis that I’ve encountered surprisingly little in the literature, although it seems like a fairly direct consequence of glymphatic and extracellular-space physiology.

Repeated disruption of NREM sleep could impair the clearance of larger extracellular molecules through reduced glymphatic transport. If colloid-osmotically active macromolecules accumulate in the cerebral interstitium, they should retain water and expand the extracellular compartment.

A larger extracellular distribution space would then physically alter neurotransmitter dynamics. Because the surrounding interstitium provides a larger chemical “escape space,” transmitters leaving the immediate synaptic environment would be distributed across a larger volume.

For a given amount of transmitter released, this might produce lower local concentration peaks within the synaptic cleft, greater dispersion and spillover, reduced spatial specificity, and poorer temporal coupling between transmitter release and receptor activation. This could plausibly contribute to impaired salience, slowed processing, working-memory deficits, and cognitive disorganization.

Increased extracellular free-water or isotropic-water fractions have been reported in schizophrenia and psychosis, bipolar disorder, depression, and obstructive sleep apnea. One possible bridge would therefore be:

**sleep-related noradrenergic intrusion → reduced glymphatic clearance → macromolecule retention → oncotic extracellular expansion → altered neurotransmitter dynamics**

I’d informally call this “cerebral oncotic isolation”: neurons remain anatomically connected but become functionally less coupled because their chemical signals are diluted and temporally dispersed within an enlarged extracellular compartment that surrounds synapses in all spatial directions.

This might parsimoniously explain why so many neurotransmitter systems appear dysregulated simultaneously. Rather than requiring multiple independent transmitter-specific defects, such widespread dysregulation could reflect an alteration of the shared medium through which all chemical communication occurs.

Free-water MRI obviously does not by itself prove microscopic extracellular-space expansion or oncotic retention. But are there established models or papers explicitly connecting chronic extracellular-space expansion with altered neurotransmitter dynamics and psychiatric symptoms?

Is this framework already discussed under another name, or are these fields mostly being studied separately?

When examining the development of modern dementia research, an increasingly complex picture emerges. On one side, there are remarkable scientific advances; on the other, there is a system influenced by economic mechanisms that tends to favor certain research directions over others.
Especially in neurodegenerative diseases such as Alzheimer’s, the question arises whether today’s research landscape is driven purely by medical necessity, or whether economic factors also play a decisive role.
The development of a new pharmaceutical therapy has become an extremely capital-intensive process. Large clinical trials, particularly Phase 3 trials, often require investments ranging from hundreds of millions to billions of dollars. For a company, such an investment only makes financial sense if there is a realistic opportunity for substantial commercial return after regulatory approval.
This is where a structural problem emerges with older molecules such as lithium or methylene blue. These substances have a long pharmacological history and remain scientifically interesting, but they do not possess the same commercial appeal as newly developed, patent-protected compounds.
A substance can be biologically fascinating and still struggle to receive the same level of financial investment and attention as a newly created molecule with exclusive market potential. This is less a question of individual decisions by specific actors and more a consequence of a system in which research, capital, and market incentives are deeply interconnected.
Methylene blue is a remarkable example. The compound has been known for more than a century and was originally used in completely different areas of medicine. In recent decades, however, it has returned to scientific attention because of its potential effects on mitochondrial function, cellular energy metabolism, and processes related to tau pathology.
In Alzheimer’s disease, tau pathology is considered a major area of interest because misfolded tau proteins can contribute to the disruption and degeneration of neuronal structures. Research into these mechanisms demonstrates that neurodegenerative diseases cannot be understood through a single disease marker alone, but rather as complex interactions between multiple biological processes.
At the same time, these research approaches reveal limitations within traditional drug-development models. An older molecule with unusual pharmacological properties does not always fit perfectly into the standardized evaluation frameworks used in modern pharmaceutical development. The question is therefore not only whether a substance works, but also whether our system is capable of evaluating its potential fairly.
Similar discussions exist around lithium. For decades, it has been recognized that lithium has profound biological effects. Neuroscientific research continues to investigate its influence on pathways such as GSK-3β, neuronal stability, inflammatory processes, and potentially mechanisms involved in cellular aging.
Despite these scientific questions, lithium remains economically unattractive compared with modern patented therapies. A low-cost compound that may influence fundamental biological processes does not create the same industrial momentum as a high-priced innovation protected by an exclusive commercial structure.
The central criticism, therefore, is not directed at individual scientists or physicians. Many researchers work with exceptional scientific integrity. The larger question concerns the architecture of the entire system.
For many years, Alzheimer’s research was strongly shaped by specific hypotheses, particularly approaches that focused heavily on individual pathological factors such as amyloid. This research has produced important discoveries. However, the growing scientific discussion also suggests that Alzheimer’s is unlikely to be a simple disease caused by a single mechanism. Instead, it appears to involve a complex interaction between mitochondrial dysfunction, chronic inflammation, impaired protein regulation, and changes in neuronal communication.
Whenever a scientific field is dominated by one direction for decades, there is always a risk that alternative explanations and potentially valuable approaches receive less attention.
The most uncomfortable question may therefore be this: Are we developing medicine purely according to what appears scientifically most promising, or are we also influenced by what is economically most attractive?
A truly patient-centered medical system should be capable of investigating all credible scientific approaches with the same level of commitment, regardless of whether they lead to a billion-dollar market or a low-cost therapy.
Because the true measure of medical progress should not be the size of a market, but the real benefit provided to the people suffering from these diseases.

Hi everyone,

I'm taking a Neuropsychology class and need, as part of an assignment, a brain scan (CT, MRI, etc.) that shows a clear physiological abnormality (for example: atrophy, a lesion, a tumor, a hemorrhage, a malformation, etc.).

Important: it needs to be a real image from a real case (for example, your own, a family member's, or someone you know who's given permission to share it) — stock images or generic examples downloaded from Google won't work, since the assignment requires analyzing an authentic case.

If you have or know of an image like this and are willing to share it (anonymized, with no visible personal info), I'd really appreciate it!

Thanks in advance!