Brain Cells Measure Axons to Build the Perfect Myelin Sheath

 Ask your competent? doctor EXACTLY HOW MUCH MYELIN was destroyed in your stroke! And then the EXACT REPAIR PROTOCOLS!

Doesn't know either, right?  Then, PURE INCOMPETENCE!

Does your doctor know anything useful about your stroke and recovery? Not even an objective damage diagnosis, like a 3d map of your dead and damaged areas!

Brain Cells Measure Axons to Build the Perfect Myelin Sheath

Summary:

Researchers at SUNY Upstate Medical University have resolved a long-standing neurobiology puzzle: how the central nervous system gauges axon diameter to control myelin sheath length. The study reveals that oligodendrocytes utilize the mechanosensitive protein Piezo1 to sense the physical caliber of nerve fibers during early development, scaling myelin segment length accordingly to ensure rapid, efficient neural signaling.

Key Facts:

• The “Molecular Ruler”: Oligodendrocytes use the mechanosensitive ion channel protein Piezo1 to detect the caliber and diameter of nerve fibers, dictating how far to extend each individual myelin segment.
• Timing Matters Most: Piezo1 is critically active during early stages of myelination, when myelinating glial cells are actively wrapping and elongating their lipid membranes along axons.
• Target for Remyelination: Decoding the physical and molecular cues governing sheath length provides a biological blueprint for promoting proper myelin regeneration in demyelinating conditions like multiple sclerosis (MS).

Source: SUNY Upstate Medical University

In the central nervous system, rapid and synchronized communication depends on myelin—the multilayered lipid sheath synthesized by specialized glial cells known as oligodendrocytes. Wrapping tightly around axons like insulation on electrical wiring, myelin enables action potentials to leap rapidly between the nodes of Ranvier via saltatory conduction.

For decades, neuroanatomists have observed a fundamental structural rule across vertebrate nervous systems: thicker axons invariably support longer myelin segments, whereas thinner fibers host shorter ones. This architectural precision is essential for tuning the arrival times of neural impulses across complex brain circuits.

However, a fundamental mechanistic question remained unanswered: How do oligodendrocytes physically detect the caliber of an axon, and how does that sensory signal instruct them on how long to build each sheath?

In a study published in PLOS Biology, a research team at SUNY Upstate Medical University identified the molecular sensor orchestrating this process: a mechanosensitive ion channel protein known as Piezo1.

Piezo1 Functions as an Axonal Sensor

Led by senior author Marie Bechler, Ph.D., assistant professor of cell and developmental biology, neuroscience, and physiology, the investigators examined how developing oligodendrocytes interpret physical mechanical cues presented by surrounding axons.

Using advanced cellular modeling assisted by Upstate’s Electron Microscopy Core, first author Amanda R. Young, Ph.D., alongside Bechler demonstrated that oligodendrocytes rely on Piezo1 to gauge axon diameter. As an oligodendrocyte membrane wraps around a wider axon, the increased mechanical curvature and membrane tension activate Piezo1, signaling the cell to extend the myelin sheath to an appropriate, proportional length.

The researchers determined that Piezo1 acts during the critical initial phases of myelination. During this early developmental window, oligodendrocytes actively sample axonal caliber and drive the longitudinal extension of the wrapping membrane before stabilizing into mature sheaths.

Implications for Multiple Sclerosis and Myelin Repair

When myelin degrades, as seen in autoimmune demyelinating conditions like multiple sclerosis (MS), action potential propagation stumbles or fails altogether. Deprived of the metabolic and trophic support normally provided by oligodendrocytes, denuded axons progressively degenerate, causing sensory loss, severe fatigue, visual impairment, motor dysfunction, and cognitive deficits.

Current MS therapeutics primarily focus on suppressing immune attacks, but restoring lost myelin, remyelination, remains a major hurdle. In chronic lesions, newly formed remyelinated sheaths are characteristically abnormally thin and short, which can limit the full recovery of neural conduction velocity.

“Numerous neurological conditions across our lifespan disrupt oligodendrocyte cells and the myelin sheaths they form,” said Dr. Bechler. “Our research aims to understand the impact of these changes compared to the healthy nervous system as well as to find ways to promote myelin sheath growth in diseases where myelin is lost or damaged.”

By illuminating how the mechanosensor Piezo1 coordinates sheath elongation, the study provides a foundation for targeted strategies designed not only to encourage oligodendrocytes to remyelinate bare axons, but to construct sheaths of the proper dimensions to restore optimal nervous system function.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this neuroscience Research:

• Media Contact: Matthew Sheiffer
• Source: State University of New York
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: PLOS Biology (Sept 21, 2026). “Myelin sheath lengths in the central nervous system scale to axon diameter via oligodendroglial Piezo1.” Authors: Amanda R. Young, Ashley Galfano, Jacob Reyngoudt, Ryan W. Lewis, Martha Cash, Beckam Polis, Myah Zalusky, Avipsha Datta, and Marie E. Bechler.
• DOI: 10.1371/journal.pbio.3003992

Stroke drug shows potential MS benefits - myelin repair

 Ask your  competent? doctor EXAXTLY HOW MUCH MYELIN WAS DAMAGED IN YOUR STROKE! And the EXACT REPAIR PROTOCOLS!

No knowledge is a fireable offense all the way to the board of directors!

Stroke drug shows potential MS benefits

A stroke drug may help preserve and repair myelin damaged by multiple sclerosis, according to a review of animal studies.

Nimodipine was also linked to reduced inflammation, nerve damage and disease severity in several of the studies reviewed.

Myelin is the protective coating around nerve fibres that is damaged in multiple sclerosis, or MS, disrupting communication between the brain and the rest of the body.

Researchers in Iran reviewed five animal studies investigating whether nimodipine, a prescription medicine used to prevent blood vessel spasms after bleeding in the brain, could have potential as an MS treatment.

In MS, the immune system mistakenly attacks the myelin sheath, causing inflammation and nerve damage that can lead to a wide range of neurological symptoms.

Most current MS treatments work by modifying the immune system. While they can reduce relapses and slow disease progression, they generally do not directly repair myelin that has already been lost.

Nimodipine works by relaxing narrowed blood vessels to improve blood flow to injured brain tissue.

Previous research has suggested that the drug may also reduce inflammation and nerve damage while supporting myelin repair.

Four of the five studies involved rodents with experimental autoimmune encephalomyelitis, or EAE, a condition commonly used to model MS.

The fifth used cuprizone, a toxin that causes demyelination, meaning the loss of the protective myelin coating around nerves.

The studies differed substantially in the animals and disease models used, nimodipine doses, treatment methods and outcome measures, so researchers could not combine the results into a single statistical analysis.

Instead, they carried out a narrative review of the results.

Overall, nimodipine was linked to reduced disease severity in the EAE models.

One study found that the drug reduced the severity of relapsing-remitting EAE and lessened disease severity during the early active phase.

Other studies reported reduced relapse rates, fewer sensory and motor problems and effects suggesting protection of nerve cells.

Nimodipine was also linked to less myelin loss and fewer demyelinated nerve fibres.

In one study, treatment increased the number of nerve fibres showing signs of remyelination, the process through which damaged myelin is rebuilt.

The findings were accompanied by increased activity in genes linked to myelin and higher numbers of cells involved in myelin regeneration.

Animals treated with nimodipine also showed fewer signs of inflammation in the brain and spinal cord and lower blood levels of some inflammation-related proteins.

The drug was also linked to improved blood flow and oxygen levels in the spinal cord, while one study found reduced clinical scores and improved motor performance.

In the cuprizone model, nimodipine was linked to fewer reactive immune cells in the brain and faster, more complete myelin repair.

The researchers called for further studies to reproduce the findings and early-stage human trials to determine whether nimodipine can safely provide similar benefits for people with MS.

The researchers wrote: “These findings underscore the potential of drug repositioning to uncover novel clinical mechanisms for nimodipine and expand its therapeutic applications to other diseases, such as MS.

“Preclinical evidence suggests that nimodipine may attenuate disease severity and demyelination and may promote repair-related processes in rodent models relevant to MS.”

‘Dancing molecules’ successfully repair severe spinal cord injuries

 So, do we have anyone in stroke with two functioning neurons that can look at this and suggest using it for stroke? NO, WE DON'T! Nothing will be done; there is NO leadership or strategy anywhere in stroke! Just plan on never having a stroke!

‘Dancing molecules’ successfully repair severe spinal cord injuries

After single injection, paralyzed animals regained ability to walk within four weeks

Northwestern University researchers have developed a new injectable therapy that harnesses “dancing molecules” to reverse paralysis and repair tissue after severe spinal cord injuries. 

In a new study, researchers administered a single injection to tissues surrounding the spinal cords of paralyzed mice. Just four weeks later, the animals regained the ability to walk.

Five key developments

By sending bioactive signals to trigger cells to repair and regenerate, the breakthrough therapy dramatically improved severely injured spinal cords in five key ways:

1. The severed extensions of neurons, called axons, regenerated
2. Scar tissue, which can create a physical barrier to regeneration and repair, significantly diminished
3. Myelin, the insulating layer of axons that is important in transmitting electrical signals efficiently, reformed around cells(We need this)
4. Functional blood vessels formed to deliver nutrients to cells at the injury site(We need this)
5. More motor neurons survived

After the therapy performs its function, the materials biodegrade into nutrients for the cells within 12 weeks and then completely disappear from the body without noticeable side effects. This is the first study in which researchers controlled the collective motion of molecules through changes in chemical structure to increase a therapeutic’s efficacy.

“Our research aims to find a therapy that can prevent individuals from becoming paralyzed after major trauma or disease,” said Northwestern’s Samuel I. Stupp, who led the study. “For decades, this has remained a major challenge for scientists because our body’s central nervous system, which includes the brain and spinal cord, does not have any significant capacity to repair itself after injury or after the onset of a degenerative disease. We are going straight to the FDA to start the process of getting this new therapy approved for use in human patients, who currently have very few treatment options.”

Stupp is Board of Trustees Professor of Materials Science and Engineering, Chemistry, Medicine and Biomedical Engineering at Northwestern, where he is founding director of the Simpson Querrey Institute for BioNanotechnology (SQI) and its affiliated research center, the Center for Regenerative Nanomedicine. He has appointments in the McCormick School of Engineering, Weinberg College of Arts and Sciences and Feinberg School of Medicine.

Life expectancy has not improved since the 1980s

According to the National Spinal Cord Injury Statistical Center, nearly 300,000 people are currently living with a spinal cord injury in the United States. Life for these patients can be extraordinarily difficult. Less than 3% of people with complete injury ever recover basic physical functions. And approximately 30% are re-hospitalized at least once during any given year after the initial injury, costing millions of dollars in average lifetime health care costs per patient. Life expectancy for people with spinal cord injuries is significantly lower than people without spinal cord injuries and has not improved since the 1980s.

“Currently, there are no therapeutics that trigger spinal cord regeneration,” said Stupp, an expert in regenerative medicine. “I wanted to make a difference on the outcomes of spinal cord injury and to tackle this problem, given the tremendous impact it could have on the lives of patients. Also, new science to address spinal cord injury could have impact on strategies for neurodegenerative diseases and stroke.”

‘Dancing molecules’ hit moving targets

The secret behind Stupp’s new breakthrough therapeutic is tuning the motion of molecules, so they can find and properly engage constantly moving cellular receptors. Injected as a liquid, the therapy immediately gels into a complex network of nanofibers that mimic the extracellular matrix of the spinal cord. By matching the matrix’s structure, mimicking the motion of biological molecules and incorporating signals for receptors, the synthetic materials are able to communicate with cells.

“Receptors in neurons and other cells constantly move around,” Stupp said. “The key innovation in our research, which has never been done before, is to control the collective motion of more than 100,000 molecules within our nanofibers. By making the molecules move, ‘dance’ or even leap temporarily out of these structures, known as supramolecular polymers, they are able to connect more effectively with receptors.”

Stupp and his team found that fine-tuning the molecules’ motion within the nanofiber network to make them more agile resulted in greater therapeutic efficacy in paralyzed mice. They also confirmed that formulations of their therapy with enhanced molecular motion performed better during in vitro tests with human cells, indicating increased bioactivity and cellular signaling.

“Given that cells themselves and their receptors are in constant motion, you can imagine that molecules moving more rapidly would encounter these receptors more often,” Stupp said. “If the molecules are sluggish and not as ‘social,’ they may never come into contact with the cells.” 

Signals mimic natural proteins

Once connected to the receptors, the moving molecules trigger two cascading signals, both of which are critical to spinal cord repair. One signal prompts the long tails of neurons in the spinal cord, called axons, to regenerate. Similar to electrical cables, axons send signals between the brain and the rest of the body. Severing or damaging axons can result in the loss of feeling in the body or even paralysis. Repairing axons, on the other hand, increases communication between the body and brain.

The second signal helps neurons survive after injury because it causes other cell types to proliferate, promoting the regrowth of lost blood vessels that feed neurons and critical cells for tissue repair. The therapy also induces myelin to rebuild around axons and reduces glial scarring, which acts as a physical barrier that prevents the spinal cord from healing. 

“The signals used in the study mimic the natural proteins that are needed to induce the desired biological responses. However, proteins have extremely short half-lives and are expensive to produce,” said Zaida Álvarez, the study’s first author and former research assistant professor in Stupp’s laboratory. “Our synthetic signals are short, modified peptides that — when bonded together by the thousands — will survive for weeks to deliver bioactivity. The end result is a therapy that is less expensive to produce and lasts much longer.” 

Universal application

While the new therapy could be used to prevent paralysis after major trauma (automobile accidents, falls, sports accidents and gunshot wounds) as well as from diseases, Stupp believes the underlying discovery — that “supramolecular motion” is a key factor in bioactivity — can be applied to other therapies and targets.

“The central nervous system tissues we have successfully regenerated in the injured spinal cord are similar to those in the brain affected by stroke and neurodegenerative diseases, such as ALS, Parkinson’s disease and Alzheimer’s disease,” Stupp said. “Beyond that, our fundamental discovery about controlling the motion of molecular assemblies to enhance cell signaling could be applied universally across biomedical targets.” 

Other Northwestern study authors include Evangelos Kiskinis, assistant professor of neurology and neuroscience in Feinberg; research technician Feng Chen; postdoctoral researchers Ivan Sasselli, Alberto Ortega and Zois Syrgiannis; and graduate students Alexandra Kolberg-Edelbrock, Ruomeng Qiu and Stacey Chin. Peter Mirau of the Air Force Research Laboratories and Steven Weigand of Argonne National Laboratory also are co-authors. 

Scientists Uncover How Glucose Influences Myelin Formation and Function

 Your competent? doctor has informed you of the EXACT DAMAGE to your myelin post stroke and the EXACT PROTOCOLS TO FIX THAT, right? Oh NO, nothing of the sort? So your doctor is ignoring your damage and doing nothing? Sounds like vast incompetence to me!

demyelinating (24 posts to May 2012)

demyelination (12 posts to November 2021)

myelin (79 posts to April 2011)

myelin regeneration (3 posts to August 2024)

myelin repair (5 posts to January 2025)

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

Scientists Uncover How Glucose Influences Myelin Formation and Function

Glucose Levels Signal the Growth of Myelin

 

Ask your competent? doctor EXACTLY how much myelin damage you have post stroke and THE EXACT PROTOCOLS TO FIX THAT DAMAGE!

demyelinating (24 posts to May 2012)

demyelination (12 posts to November 2021)

myelin (79 posts to April 2011)

myelin regeneration (3 posts to August 2024)

myelin repair (5 posts to January 2025)

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

Glucose Levels Signal the Growth of Myelin

Summary: Scientists have long wondered why myelin, the brain’s essential insulation, develops at different speeds in different regions. A new study reveals that glucose isn’t just fuel; it’s a traffic signal.

High sugar levels tell stem-like cells to multiply, while low sugar levels signal them to stop dividing and start maturing into myelin-forming cells. This metabolic “gear shift” ensures the brain’s wiring is built at exactly the right time and place.

Key Facts

• The Glucose Signal: In the developing brain, regions with high glucose levels act as nurseries for Oligodendrocyte Progenitor Cells (OPCs), causing them to divide rapidly. When glucose levels drop, these cells receive the signal to mature into myelin-producing oligodendrocytes.
• The ACLY Enzyme: The researchers identified an enzyme called ATP-citrate lyase (ACLY) as the key translator. It turns glucose into a molecule (acetyl-CoA) that enters the cell nucleus to “turn on” the genes needed for multiplication.
• Metabolic Switch: Once the cells mature, they stop relying on glucose for development. Instead, they switch to alternative fuels like ketone bodies to actually build the myelin membrane.
• Ketogenic Rescue: In mice lacking the ACLY enzyme, myelin production was stunted. However, when these mice were placed on a ketogenic diet, the alternative fuel source bypassed the glucose bottleneck and improved the myelin deficits.
• Critical Windows: The developmental stage studied (32–40 weeks in human gestation) is a high-risk period for premature babies. Understanding this metabolic signal could lead to new ways to protect the white matter of preemies.

Source: CUNY

Researchers at the Advanced Science Research Center at the CUNY Graduate Center (CUNY ASRC) have uncovered a surprising link between low brain sugar levels and the development of myelin — the protective coating that allows nerve cells to communicate rapidly and efficiently.

The study, set for publication in Nature Neuroscience, reveals that the glucose-sensing ability of stem-like cells during early development helps them determine whether they should multiply and remain undifferentiated or mature into myelin-forming cells, thereby shaping brain development.

Myelin is the membrane of specialized cells called oligodendrocytes, which arise from progenitor cells, called oligodendrocyte progenitor cells (OPCs). Myelination begins before birth and continues into adulthood, supporting critical milestones such as sitting, crawling, walking, and talking.

Scientists have long puzzled over why myelin forms at different times in different brain regions. The CUNY ASRC team discovered that local changes in glucose (the brain’s main energy source) act as a signal that directs behavior during development.

Using advanced technology at the CUNY ASRC MALDI Imaging Core Facility (co-directed by professors Rinat Abzalimov and Ye He), the researchers mapped glucose levels across developing mouse brains. They found that glucose levels vary by region and over time. Areas with higher glucose levels had more actively dividing OPCs while areas with lower glucose levels contained cells beginning to mature into myelin-producing oligodendrocytes.

“Our findings show that glucose is not just fuel for the brain, it’s also a signal for the cells to divide,” said lead author Sami Sauma, a postdoctoral researcher with the CUNY ASRC Neuroscience Initiative who received his Ph.D. from Graduate Center.

“We found that when glucose levels are high in a particular brain region, progenitors use it to drive proliferation. As glucose levels shift, the same cells switch gears and begin maturing. It’s a beautifully coordinated metabolic system that helps shape brain development.”

At the center of this process is an enzyme called ATP-citrate lyase (ACLY). ACLY converts glucose-derived molecules into acetyl-CoA in the cell nucleus, enabling chemical changes to DNA-associated proteins that activate genes required for cell proliferation.

When the researchers genetically deleted ACLY in OPCs, those cells could no longer multiply effectively. As a result, mice showed a temporary reduction in myelin due to a smaller pool of progenitor cells. Remarkably, however, the cells were still able to mature into myelin-producing oligodendrocytes by switching to alternative metabolic sources.The team discovered that while progenitor cells depend on glucose-derived acetyl-CoA to multiply, mature oligodendrocytes rely on acetyl-CoA generated outside the nucleus from other fuels, such as ketone bodies, to produce myelin.

In fact, when transgenic mice lacking the ACLY enzyme in OPCs were placed on a ketogenic diet, which increases ketone levels in the blood, their myelin deficits improved.

“This study reveals that the same cell lineage interprets different metabolic signals at distinct stages of development,” said Patrizia Casaccia, founding director of the CUNY ASRC Neuroscience Initiative and Einstein Professor of Biology at the CUNY Graduate Center.

“By understanding how glucose and alternative energy sources regulate proliferation and myelin formation, we are uncovering new metabolic strategies that could be harnessed to protect myelin in the developing brain and even promote repair in disease states.”

The developmental window studied in mouse models corresponds to approximately 32 to 40 weeks of human gestation, which is a critical period when premature birth can result in white matter injury. The findings suggest that metabolic support during this vulnerable stage could help protect progenitor cells responsible for building myelin.

The implications may also extend to neurological disorders characterized by myelin loss in children and adults, including multiple sclerosis. By targeting the metabolic pathways that regulate progenitor cell proliferation and oligodendrocyte maturation, researchers may be able to design new therapies to enhance myelin repair.

As scientists continue to uncover how metabolism shapes brain development, this research highlights a powerful and potentially modifiable influence on how the brain builds its essential wiring.

Funding: The study was supported by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health.

Key Questions Answered:

Q: Does “low brain sugar” mean I should avoid sugar during pregnancy?

A: No. “Low sugar” in this context refers to localized, natural metabolic shifts within specific brain regions as they develop. This study is about how cells sense sugar, not a recommendation to change dietary intake. The brain always requires a steady supply of glucose to function.

Q: Could a ketogenic diet help treat myelin-related diseases like MS?

A: The study found that ketones can provide an alternative “fuel” for myelin formation when the primary glucose pathway is broken. While this is promising for neonatal brain injury and potentially Multiple Sclerosis, more research is needed before the ketogenic diet can be prescribed as a standardized clinical treatment for myelin repair.

Q: Why do different parts of the brain develop myelin at different times?

A: This study provides a major clue: glucose levels vary across the brain in a timed sequence. By mapping these “glucose gradients,” researchers showed that the brain essentially uses sugar levels to orchestrate the construction of its electrical wiring in a specific, prioritized order.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.About this neuroscience research news

Author: Shawn Rhea
Source: CUNY
Contact: Shawn Rhea – CUNY
Image: The image is credited to Sami Sauma

Original Research: Closed access.
“Glucose-dependent spatial and temporal modulation of oligodendrocyte progenitor cell proliferation via ACLY-regulated histone acetylation” by Sami Sauma, Stephanie Stransky, Ipek Selcen, Simone Sidoli, Rinat Abzalimov, Ye He & Patrizia Casaccia. Nature Neuroscience
DOI:10.1038/s41593-026-02263-7

Gene mutation that aids high-altitude survival could repair myelin sheath damage

Ask your competent? doctor EXACTLY how much myelin damage you have post stroke and THE EXACT PROTOCOLS TO FIX THAT DAMAGE!

demyelinating (24 posts to May 2012)

demyelination (12 posts to November 2021)

myelin (79 posts to April 2011)

myelin regeneration (3 posts to August 2024)

myelin repair (5 posts to January 2025)

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

Gene mutation that aids high-altitude survival could repair myelin sheath damage

A genetic mutation that helps animals like yaks and Tibetan antelopes survive at high altitudes may hold the key to repairing nerve damage in conditions such as cerebral paralysis and multiple sclerosis (MS). The finding, publishing March 13 in the Cell Press journal Neuron, reveals a naturally existing pathway that promotes regeneration after nerve damage and could open new doors for treating diseases like MS by leveraging molecules that are already present in the human body. 

"Evolution is a great gift from nature, providing a rich diversity of genes that help organisms adapt to different environments," says corresponding author Liang Zhang of Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine. "There is still so much to learn from naturally occurring genetic adaptations." 

The myelin sheath is a protective layer that surrounds nerve fibers in the brain and spinal cord, allowing nerve signals to transmit efficiently. Insufficient oxygen during brain development can damage this layer, leading to conditions like cerebral paralysis in newborns. 

More to Consider

Watch Experts Discuss Complement Inhibition in PNHMedlive

In adults, injuries to the myelin sheath are tied to MS, an autoimmune disease in which the immune system mistakenly attacks and destroys the myelin sheath. Reduced blood flow to the brain, often associated with aging, can also damage myelin, contributing to conditions such as cerebral small vessel disease and vascular dementia. 

In previous studies, researchers have found that animals living on the Tibetan Plateau-which has an average elevation of 14,700 feet-carry a mutation on a gene called Retsat. Scientists suspected that this mutation helps animals like yaks and Tibetan antelopes maintain healthy brain function despite chronically low oxygen levels. 

Zhang and his team set off to investigate if this mutation could prevent myelin sheath damage. They exposed newborn mice to low-oxygen conditions equivalent to elevations above 13,000 feet for about a week. Mice carrying the Retsat mutation performed significantly better in learning, memory, and social behavior tests than those with the standard version of the gene. Brain analyses also revealed that the high-altitude gene mice had higher levels of myelin surrounding their nerve fibers. 

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The researchers then examined whether the Retsat mutation could repair myelin sheath damage similar to that seen in MS. They found that in mice carrying the mutation, the myelin sheath regenerated much faster and more completely after injury. The injury sites also had more mature oligodendrocytes, a type of cell responsible for producing myelin. 

Further investigation showed that mice with the mutation produced higher levels of ATDR, a metabolite derived from vitamin A, in their brains. The Retsat mutation appeared to increase the enzymatic activity that converts vitamin A into its metabolites, which in turn promotes the production and maturation of myelin-producing oligodendrocytes. When the team gave ATDR to mice with an MS-like disease, their disease severity decreased, and they showed improved motor function. 

Current treatments for MS mainly focus on suppressing immune activity, notes Zhang. "ATDR is something everyone already has in their body. Our findings suggest that there may be an alternative approach that uses naturally occurring molecules to treat diseases related to myelin damage," he says. 

This work was supported by the National Science and Technology Major Project, the National Natural Science Foundation of China, the China Postdoctoral Science Foundation, Shanghai Post-doctoral Excellence Program, the Natural Science Foundation of Shanghai, the 2024 Tibet Autonomous Region Science and Technology Plan Key R&D and Transformation Project, the Open Research Fund of Navy Medical University Basic Medical College, Yunnan Revitalization Talent Support Program Science & Technology Champion Project and the Yunnan Revitalization Talent Support Program. 

Source:

Cell Press

Journal reference:

Li, D., et al. (2026). A gain-of-function Retsat variant from high-altitude adaptation promotes myelination via a neuronal dihydroretinoic acid-RXR-γ pathway. Neuron. DOI: 10.1016/j.neuron.2026.01.013. https://www.cell.com/neuron/fulltext/S0896-6273(26)00013-9

High-Altitude Gene Helps Heal Myelin Damage

 Ask your incompetent? doctor EXACTLY HOW THEY ARE RECOVERING YOUR MYELIN DAMAGE post stroke! Oh, NOTHING DOING! And your incompetent? board of directors has no method to validate competence in their hospital?

demyelinating (24 posts to May 2012)

demyelination (12 posts to November 2021)

High-Altitude Gene Helps Heal Myelin Damage

Summary: Evolutionary adaptations that allow animals like yaks and Tibetan antelopes to thrive at 14,700 feet may provide a breakthrough for human neurodegenerative diseases. A study reveals that a mutation in the Retsat gene—common in high-altitude species—protects the brain from low oxygen and promotes the regeneration of the myelin sheath.

By identifying a specific metabolite called ATDR (derived from Vitamin A), researchers successfully repaired nerve damage in mouse models(So, your competent? doctor will immediately initiate further research in human testing of this! Oh NO! Nothing will occur because incompetence!) of Multiple Sclerosis (MS) and cerebral paralysis, offering a natural pathway to heal the brain from within.

Key Facts

• The Retsat Mutation: Animals on the Tibetan Plateau carry a specific mutation on the Retsat gene that maintains healthy brain function despite chronic oxygen deprivation.
• Myelin Protection: In newborn mice exposed to thin-air conditions (13,000+ feet), those with the Retsat mutation showed significantly better learning, memory, and higher myelin density.
• The ATDR Breakthrough: The mutation increases enzymatic activity that converts Vitamin A into ATDR. This molecule triggers the maturation of oligodendrocytes—the “factory” cells that build and repair myelin.
• MS Treatment Potential: When mice with an MS-like disease were given ATDR, their motor function improved and their disease severity decreased.
• A Natural Alternative: Unlike current MS treatments that focus on suppressing the immune system, ATDR leverages a molecule already present in the human body to actively repair damage.

Source: Cell Press

A genetic mutation that helps animals like yaks and Tibetan antelopes survive at high altitudes may hold the key to repairing nerve damage in conditions such as cerebral paralysis and multiple sclerosis (MS). 

The finding, publishing March 13 in the Cell Press journal Neuron, reveals a naturally existing pathway that promotes regeneration after nerve damage and could open new doors for treating diseases like MS by leveraging molecules that are already present in the human body. 

Research reveals that the Retsat mutation found in high-altitude animals promotes the production of ATDR, a molecule that stimulates oligodendrocytes to repair the myelin sheath. Credit: Neuroscience News

“Evolution is a great gift from nature, providing a rich diversity of genes that help organisms adapt to different environments,” says corresponding author Liang Zhang of Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine. “There is still so much to learn from naturally occurring genetic adaptations.” 

The myelin sheath is a protective layer that surrounds nerve fibers in the brain and spinal cord, allowing nerve signals to transmit efficiently. Insufficient oxygen during brain development can damage this layer, leading to conditions like cerebral paralysis in newborns. 

In adults, injuries to the myelin sheath are tied to MS, an autoimmune disease in which the immune system mistakenly attacks and destroys the myelin sheath. Reduced blood flow to the brain, often associated with aging, can also damage myelin, contributing to conditions such as cerebral small vessel disease and vascular dementia. 

In previous studies, researchers have found that animals living on the Tibetan Plateau—which has an average elevation of 14,700 feet—carry a mutation on a gene called Retsat. Scientists suspected that this mutation helps animals like yaks and Tibetan antelopes maintain healthy brain function despite chronically low oxygen levels.  

Zhang and his team set off to investigate if this mutation could prevent myelin sheath damage. They exposed newborn mice to low-oxygen conditions equivalent to elevations above 13,000 feet for about a week. 

Mice carrying the Retsat mutation performed significantly better in learning, memory, and social behavior tests than those with the standard version of the gene. Brain analyses also revealed that the high-altitude gene mice had higher levels of myelin surrounding their nerve fibers.  

The researchers then examined whether the Retsat mutation could repair myelin sheath damage similar to that seen in MS. They found that in mice carrying the mutation, the myelin sheath regenerated much faster and more completely after injury. The injury sites also had more mature oligodendrocytes, a type of cell responsible for producing myelin. 

Further investigation showed that mice with the mutation produced higher levels of ATDR, a metabolite derived from vitamin A, in their brains. The Retsat mutation appeared to increase the enzymatic activity that converts vitamin A into its metabolites, which in turn promotes the production and maturation of myelin-producing oligodendrocytes. When the team gave ATDR to mice with an MS-like disease, their disease severity decreased, and they showed improved motor function. 

Current treatments for MS mainly focus on suppressing immune activity, notes Zhang. “ATDR is something everyone already has in their body. Our findings suggest that there may be an alternative approach that uses naturally occurring molecules to treat diseases related to myelin damage,” he says.  

Funding:

This work was supported by the National Science and Technology Major Project, the National Natural Science Foundation of China, the China Postdoctoral Science Foundation, Shanghai Post-doctoral Excellence Program, the Natural Science Foundation of Shanghai, the 2024 Tibet Autonomous Region Science and Technology Plan Key R&D and Transformation Project, the Open Research Fund of Navy Medical University Basic Medical College, Yunnan Revitalization Talent Support Program Science & 

Key Questions Answered:

Q: How does a “yak gene” help with a human disease like MS?

A: It’s all about surviving harsh conditions. High-altitude animals evolved to protect their brain’s “wiring” (the myelin sheath) even when oxygen is low. Humans with MS suffer from damage to that same wiring. By studying how yaks keep their myelin healthy, scientists found a “repair switch” in the Retsat gene that we can potentially flip in humans using natural molecules.

Q: Is this just another way to suppress the immune system?

A: No, and that’s the exciting part. Most MS drugs just stop the immune system from attacking the brain. This discovery is about regeneration. It focuses on the cells that actually rebuild the protective coating around your nerves, meaning it could actually heal the damage that has already been done.

Q: Can I just take more Vitamin A to get these benefits?

A: Not necessarily. The secret isn’t just having Vitamin A; it’s the brain’s ability to convert it into the specific metabolite ATDR. The Retsat mutation makes that conversion super-efficient. The goal for future medicine is to provide ATDR directly to the brain to kickstart the repair process without needing the genetic mutation.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this genetics and neurology research news

Author: Julia Grimmett
Source: Cell Press
Contact: Julia Grimmett – Cell Press
Image: The image is credited to Neuroscience News

Original Research: Open access.
“A Gain-of-Function Retsat Variant from High-Altitude Adaptation Promotes Myelination via a Neuronal Dihydroretinoic Acid-RXR-γ Pathway” by Daopeng Li, Wenxiu Dai, Li Li, Zhihao Zhou, Zhenghao Li, Chenzhao He, Xiangying Li, Xiaoyun Lu, Qiuying Huang, Yanqin Zhu, Debao Wu, Jiaquan Lu, Yiting Yuan, Yanghanchen Zhao, Wenbiao Zhang, Zhiping Zeng, Qiuying Huang, Xuemin Wang, Peng Shi, and Liang Zhang. Neuron
DOI:10.1016/j.neuron.2026.01.013

Psychedelics Remodel Myelin to Heal PTSD

 Your competent? doctor is already prescribing psychedelics, right?

DMT (8 posts to November 2020)

ecstasy (19 posts to November 2012)

LSD (5 posts to September 2018)

CerAxon (5 posts to January 2012)

citicoline (15 posts to October 2011)

magic mushrooms (10 posts to October 2014) 

psilocybin (14 posts to May 2014)

Psychedelics (25 posts to August 2018)

And knows of the need for myelin repair post stroke!

myelin (79 posts to April 2011)

myelin regeneration (3 posts to August 2024)

myelin repair (5 posts to January 2025)

And knows all about preventing and fixing your PTSD!

Since there is a 23% chance of stroke survivors getting PTSD what is your doctor's treatment plan?

OH NO, your doctor is incompetent in all points! What will you do to correct that problem?

Psychedelics Remodel Myelin to Heal PTSD

Summary: For years, scientists have focused on how psychedelics “rewire” neurons. But a groundbreaking study has found a “missing link” in long-term PTSD recovery: myelin remodeling. Researchers discovered that psilocybin and MDMA do more than just alter brain activity; they trigger the physical repair of myelin—the insulating layer that protects nerve fibers and synchronizes brain signals.

By “re-insulating” the circuits that have been frayed by trauma, these drugs help harmonize the rhythm of brain networks, turning a temporary “psychedelic window” into a permanent structural recovery.

Key Facts

• The “Missing Link”: While psychedelics provide rapid relief, long-term stability requires circuit-level repair. This study identifies adaptive myelination as the key to sustaining those benefits.
• Brain Synchronization: Myelin acts as the brain’s insulation. Remodeling this layer allows disrupted brain circuits (common in PTSD) to synchronize and harmonize their electrical rhythms again.
• Mechanistic Proof: Researchers used a rat model to show that blocking myelin repair prevented the long-term anti-anxiety effects of psilocybin and MDMA, proving that structural repair is necessary for recovery.
• Oligodendrocytes Matter: The study shifts the focus from neurons to oligodendrocytes—the cells that produce myelin—as the “gatekeepers” of long-lasting psychedelic healing.
• Anti-Inflammatory Effects: In addition to repairing insulation, both drugs were found to reduce astrocyte reactivity, lowering brain inflammation associated with chronic stress.

Source: Elsevier

Post-traumatic stress disorder (PTSD) is not only characterized by strongly encoded traumatic memories, but also by disrupted coordination across brain networks.

New research shows that treatment with psychedelic drugs triggers a large-scale reconfiguration of brain network dynamics driven by the remodeling of myelin—the neuronal insulation layer.

The findings from the novel study in Biological Psychiatry show enhancing myelination might be a viable strategy to augment or sustain the therapeutic effects of psychedelic-assisted treatments for PTSD and related disorders.

Psilocybin and 3,4-methylenedioxymethamphetamine (MDMA) produce rapid clinical effects in patients with PTSD. However, durable benefits require circuit-level stabilization.

As the underlying cellular mechanisms remain incompletely understood, the current study identifies myelin as the missing link bridging the short-lived psychedelic experience and longer-term maintenance of healthier neural network dynamics.

The study shows that activity-dependent oligodendrogenesis and myelin remodeling can tune the disrupted timing and persistent response to threat observed in PTSD by synchronizing and harmonizing the rhythm of brain circuits.

John Krystal, MD, Editor of Biological Psychiatry, explains, “The focus of psychedelic and MDMA research has been the effects of these drugs on neurons and neuroplasticity. This work has largely ignored a potentially important role for other cell types in the neurobiology of their therapeutic effects.

“Oligodendrocytes play a number of roles in the brain, which produce the myelin that insulates neurons. Subgroups of oligodendrocytes take up glutamate and contribute to glutamate homeostasis, protecting the brain from neurotoxicity. Another group of oligodendrocytes is involved in immune and inflammatory functions in the brain.”

Researchers used a rat model of contextual fear conditioning and administered repeated low doses of psilocybin or MDMA. They then quantified anxiety-like and exploration behaviors and assessed spatial learning and memory.

The results showed that anxiety-like behaviors were reduced—a shift accompanied by changes in oligodendrocyte biology and multi-omic (genetic) signatures towards myelin remodeling in the dentate gyrus (part of the hippocampus, the brain’s memory center).

“To test whether myelin integrity was simply associated with behavioral change—or actually required for it—we combined the drug interventions with models that either damaged brain insulation (demyelination) or chemically enhanced it (promyelination) to see how these changes affected recovery,” explains lead investigator Mehmet Bostancıklıoğlu, PhD, Department of Physiology, Gaziantep University Faculty of Medicine, Gaziantep, Turkey.

Using high-powered microscopy and genetic analysis, the researchers confirmed both psilocybin and MDMA trigger physical myelin repair. Furthermore, a serotonin receptor 5-HT_2A blockade prevented both the behavioral and myelin-associated effects.

When the team used a different drug (anisomycin) to block the formation of fear memories, anxiety decreased, but the myelin remained unrepaired. This suggests that while memories can be suppressed, biological recovery requires the structural support of myelin.

“Taken together, this moves oligodendrocytes and adaptive myelination from ‘background correlates’ to a mechanistically testable gate on the durability of psychedelic-associated circuit change,” notes Dr. Bostancıklıoğlu.

“The implication of oligodendrocytes in the therapeutic effects of psychedelics and MDMA is important because of their many functions in the brain, including myelin formation, glutamate homeostasis, and neuroinflammation. The dependency of the therapeutic effects of these drugs in animals may suggest that myelin compromise may undermine their efficacy,” adds Dr. Krystal.

“Overall, these data suggest that psychedelics and MDMA, like selective serotonin reuptake inhibitors (SSRIs) and ketamine, may promote the recovery from stress-related damage to myelin, contributing to clinical recovery.”

The study also found that psilocybin and MDMA reduce astrocyte reactivity that can cause inflammation.

The investigators point out that enhancing myelination would not be expected to replace psychotherapy; rather, it could support consolidation and maintenance of healthier network communication after the acute psychedelic session, when the brain is transitioning from destabilization back towards reintegration.

Dr. Bostancıklıoğlu concludes, “We often talk about psychedelics as ‘opening a window’ for brain plasticity. Recent work emphasizes that these drugs can acutely loosen entrenched network patterns and then leave a sub-acute period in which experience can reshape circuits.

“What we show here is that myelin-producing cells may be an underappreciated part of that story—helping translate a transient window into longer-lasting circuit change, at least in a fear-based rat model.”

Key Questions Answered:

Q: Do psychedelics just “mask” traumatic memories?

A: No—this study shows they actually help fix the wiring. Trauma “frays” the insulation (myelin) of your brain’s communication lines, leading to static and mistimed signals. Psychedelics like psilocybin and MDMA trigger the brain to physically re-wrap those wires, allowing for clearer, calmer communication.

Q: Why is “neural insulation” so important for PTSD?

A: In PTSD, the brain’s fear circuits are often “over-active” and poorly timed. Myelin ensures that signals travel at the right speed. By repairing this insulation, the brain can better synchronize its networks, helping to “turn down the volume” on persistent threat responses.

Q: Does this mean I can just take psilocybin and be cured?

A: Not quite. The researchers emphasize that these drugs “open a window” of plasticity. The physical repair of myelin provides the structural support needed for that window to stay open, but it works best alongside therapy to reintegrate those healthier network patterns.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this PTSD and psychedelics research news

Author: Eileen Leahy
Source: Elsevier
Contact: Eileen Leahy – Elsevier
Image: The image is credited to Neuroscience News

Original Research: Open access.
“MDMA and Psilocybin Regulate Oligodendrocyte-Lineage Cell Numbers and Anxiety-Like Behaviors in a Rat Model of Fear” by Mehmet Bostancıklıoğlu, Davut Sinan Kaplan, Ramazan Bal, Elif Yiğit, Hasan Ulusal, and Ebru Temiz. Biological Psychiatry
DOI:10.1016/j.biopsych.2026.01.016