This Is What Happened When People Ran At A Surprisingly Easy Pace by mindbodygreen

 Did your incompetent? doctor have ANYTHING  that would get you running again? I'd need my spasticity cured! I bet your doctor didn't even ask you if you wanted to run again, THAT IS HOW FUCKING INCOMPETENT S/HE IS!

Maybe something from this book?

Tommye-K. Mayer book; 'Teaching Me to Run'.

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!

This Is What Happened When People Ran At A Surprisingly Easy Pace

Nanoparticles regenerate neurons and improve cognition in Alzheimer’s mice

Will your competent? doctor and hospital get followup research initiated that will create protocols that prevent Alzheimers or be used in recovering from a stroke?

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!

Your doctor is responsible for preventing this! Is s/he willing to prevent this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

 Nanoparticles regenerate neurons and improve cognition in Alzheimer’s mice

The adult human brain has limited capacity to repair or regenerate neurons lost to Alzheimer's disease, the most common type of dementia. Existing treatments can slow disease progression but do not reverse cognitive decline. In a study publishing in the Cell Press journal Cell Biomaterials on August 26, researchers show that engineered nanoparticles can not only regenerate neurons in human brain organoids but also restore neural circuits and improve cognition in mice. 

The new neurons can become mature and survive. We also confirmed much higher neuron density in the brains of treated mice." 

Peisheng Xu, corresponding author, professor of pharmaceutics, University of South Carolina

Xu's team studied a polymer nanogel system called Nano-ERASER that uses antibodies to degrade targeted proteins. They used the system to permeate the blood-brain barrier and enter astrocytes, which are star-shaped support cells abundant in the central nervous system. Within the astrocytes, Nano-ERASER deployed antibodies to break down a protein called PTBP1, triggering the astrocytes to convert to neurons. 

Compared to gene-editing tools like CRISPR, Nano-ERASER does not modify DNA and its cell reprogramming is reversible. 

"We hope this can be more effective and also safer," Xu says. "We don't need to worry about the potential side effects caused on the genetic level." 

First, the researchers applied Nano-ERASER to human astrocyte cultures, as well as human organoids designed to mimic brains with Alzheimer's disease. In both models, PTBP1 levels were reduced, prompting the conversion of astrocytes to neurons. Further testing revealed these new neurons were functional. 

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Next, the team treated mice with Alzheimer's disease. Over several weeks, their nesting skills recovered, and they completed a water maze more efficiently than before, suggesting improved learning and memory. In addition, the mouse brains showed increased neuron density and reduced neuroinflammation and amyloid-beta protein buildup, a hallmark of Alzheimer's disease. 

"After just two injections, these mice became smarter," Xu says. "Even after one injection, we already saw these mice's behavior differ from that of the nontreated ones." 

The findings mark a critical step in regenerative neuroscience, Xu says, in part because previous research has debated whether PTBP1 suppression alone could induce in vivo neuroregeneration. 

Though this study does not prove that Nano-ERASER treats Alzheimer's disease in humans, Xu says it offers a roadmap for a potential cure. He and his colleagues plan to evaluate the platform for longer-term efficacy, test it in nonhuman primates, and one day begin human clinical trials. 

"If we can advance it to the clinic, then we can have hope for patients with Alzheimer's disease," Xu says. 

Source:

Cell Press

Journal reference:

Wang, M., et al. (2026). Reverse the progression of Alzheimer’s disease through Nano-ERASER-based adult neuroregeneration. Cell Biomaterials. DOI: 10.1016/j.celbio.2026.100575. https://www.cell.com/cell-biomaterials/fulltext/S3050-5623(26)00231-X

Disrupted brain-immune signaling may help drive neurodegeneration

 Will your competent? doctor and hospital get followup research initiated that will create protocols that prevent neurodegeneration?

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!

Disrupted brain-immune signaling may help drive neurodegeneration

From gut-primed T cells to microglial signaling and persistent gene-regulatory states, researchers map an intricate immune network that connects the brain with the rest of the body.

Immune cells communicate across a continuous, bidirectional circuit between the CNS and periphery. Immune cells from across the body engage CNS tissues and, in turn, are shaped by signals returning from the brain. (Left) Under peripheral equilibrium, immune effectors mobilized from visceral organs, secondary lymphoid organs, hematopoietic tissues, and the peripheral nervous system (PNS) - including CD4⁺ and CD8⁺ T cells, B cells, monocytes (top 3 cell types), NK cells, dendritic cells, mast cells, neutrophils, and innate lymphoid cells (bottom cluster of cells) - engage the CNS in a homeostatic dialogue that supports neural cell health, plasticity, and repair, sustaining a protective environment. (Right) Age-associated dysfunction across the same peripheral compartments reshapes this circuit: altered immune effectors enter the CNS and contribute to shifting the local environment toward a degenerative state in which microglia adopt disease-associated programs, astrocytes become reactive, and neurons accumulate pathology. This model underscores how the same circuitry can yield protective or pathogenic outcomes and that neurodegeneration is downstream of dysfunctional brain-immune crosstalk. Study: Neurodegeneration as a dysregulation of neuroimmune crosstalk

Want to read later? Download your PDF copy by clicking here.

A recent perspective published in the journal Cell synthesizes scientific evidence suggesting that neurodegeneration involves intricate crosstalk between neurons and immune cells, linking the brain to peripheral immunity through bidirectional exchange. Strategies that restore immune homeostasis or recalibrate neuroimmune signaling may potentially slow neurodegeneration and promote recovery.

Historically, immune dysregulation has often been considered a consequence of neurodegenerative disorders. Recent studies, however, are beginning to change this scientific mindset, suggesting that disordered communication between the brain and immune cells may also contribute to disease onset and progression. The authors describe immune dysfunction as a “concause” of neurodegeneration, meaning it may interact with neuronal and glial vulnerabilities without necessarily being the initial trigger. It is essential to advance understanding of the pathophysiology of neurodegenerative diseases to inform therapeutic development and the development of immune-based strategies.

In this perspective, researchers examined brain-immune interactions and their potential role in neurodegeneration. They organized emerging evidence into three frameworks: “outside-in” effects driven by peripheral immunity, “inside-out” signaling coordinated by brain-resident microglia, and “locked-in” gene regulatory programs that can stabilize maladaptive neuroimmune states.

The brain-immune communication network

The brain continuously communicates with peripheral immune networks. Components of the CNS, including the choroid plexus, meninges, and lymphatic and vascular structures, interact with immune cells to relay signals related to neural needs.

Helper and cytotoxic T cells can enter CNS border regions and, under defined conditions, the brain parenchyma. Brain-immune communication supports neural integrity but can promote pathology when dysregulated. Microglia and BAMs provide surveillance, while lymphocytes confer antigen specificity and immunological memory.

Cytokines, complement, and MHC-I are traditionally linked to immunity, but CNS cells also produce or sense these molecules during neural activity. Innate lymphoid cells in the dura can respond to injury, while the choroid plexus helps regulate inflammatory signaling. In mice, increased neuronal activity may draw antibody-secreting B-lineage cells into the hippocampus during synaptic remodeling.

The gut also influences brain immunity. T cells educated in gut-associated immune tissues can subsequently traffic to the borders of the CNS and, under certain conditions, into the brain, while plasma cells secreting IgA antibodies protect blood vessels in the meninges. In addition, changes in the gut microbiome could influence immune activity and microglial function. Through the GBA, the gut and brain are in constant dialogue with each other. The vagus nerve conveys immunity-related information from the intestines to the brain. Reward-related neural pathways can, in turn, influence peripheral immune activity.

Brain-immune interactions in neurodegenerative disease

T cell activity has been implicated in PD, AD, ALS, and dementia with Lewy bodies (DLB). In ALS4, an inherited form of ALS, cytotoxic T cells are detected early in the blood and brain and expand as the disease progresses, consistent with antigen-driven responses.

Prehospital tranexamic acid in trauma and traumatic brain injury: a systematic review with meta-analysis of randomized comparative evidence

 Your competent? doctor put together a protocol on this years ago, right? NO? 

• tranexamic acid (17 posts to March 2013)

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!

Prehospital tranexamic acid in trauma and traumatic brain injury: a systematic review with meta-analysis of randomized comparative evidence

• Khalid Nabeel Almulhim &
• Mohammed Almulhim 

• 12 Accesses

• Explore all metrics 

We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply.

Abstract

Background

Tranexamic acid (TXA) is commonly used in trauma care to decrease bleeding, but its effectiveness and safety in prehospital settings, notably in traumatic brain injury (TBI), remain controversial. This review aimed to systematically evaluate the evidence on prehospital tranexamic acid (TXA) use in trauma and traumatic brain injury (TBI), with quantitative meta-analysis restricted to randomized comparative evidence and non-randomized evidence summarized narratively.

Methods

We conducted a systematic review with quantitative meta-analysis restricted to independent randomized comparative studies evaluating prehospital TXA versus placebo, usual care, or no TXA. Observational studies, secondary analyses, and survey studies were summarized separately and were not pooled with randomized trials in the primary efficacy or safety meta-analysis. outcomes included mortality (28/30-day, in-hospital), thromboembolic events, seizures, and neurological consequences. Risk of bias was evaluated using Cochrane risk of bias tools for randomized controlled trials (RoB2) and non-randomized studies by Risk Of Bias In Non-randomized Studies of Interventions (ROBINS-I).

Results

Twenty-one reports met the broad review criteria. The RCT-only analysis of 28- or 30-day mortality included three independent parent randomized trials: PATCH-Trauma/Gruen et al. 2023, STAAMP/Guyette et al. 2021, and ROC-TXA/Rowell et al. 2020. Prehospital TXA was associated with lower 28- or 30-day mortality (RR 0.81, 95% CI 0.68–0.95). The TBI mortality result was derived solely from ROC-TXA/Rowell et al. 2020 and was therefore a single-study estimate rather than a pooled estimate (RR 0.87, 95% CI 0.64–1.20). In-hospital mortality was reported only by STAAMP/Guyette et al. 2021 and was also a single-study estimate (RR 0.87, 95% CI 0.57–1.33). No statistically significant increase in thromboembolic events or seizures was demonstrated. However, the DVT and PE point estimates were above the null, and their wide confidence intervals did not exclude a clinically relevant increase in thromboembolic risk.

Conclusion

Prehospital TXA may reduce 28- or 30-day mortality in selected broader trauma populations, particularly among patients at risk of hemorrhage. No statistically significant increase in thromboembolic events or seizures was demonstrated; however, clinically relevant thromboembolic harm cannot be excluded because the DVT and PE point estimates were above the null, and the confidence intervals were wide.

A Novel Curcumin-Based Formulation Offers Protection Against Neurodegeneration in Rat Models of AlCl3 Induced Alzheimer’s Disease

 How long will it take for your competent? doctor/hospital to get human testing going for stroke related neurodegeneration? NEVER? So your stroke medical 'professionals' are useless?

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!

 A Novel Curcumin-Based Formulation Offers Protection Against Neurodegeneration in Rat Models of AlCl3Induced Alzheimer’s Disease

Mohamed Arif1*, V. Gayathri2, Radhika Ravindran3,P. Kalaivani2, R. Siva2, Shonam Tamrakar2 1Gidaa Life Sciences Private Limited, 287, 9th Cross, Bapuji Layout Near Chandra Layout, Vijayanagara, Bangalore, Karnataka 560040, India. 2Centre for Toxicology and Developmental Research, Sri Ramachandra Institute of Higher Education and Research (Deemed to be University), No. 1, Ramachandra Nagar, Porur, Chennai 600116, Tamil Nadu, India. 3Tissue Engineering and Biomaterials Lab, Department of Biotechnology, IIT Madras, India. *Corresponding Author: Mohamed Arif, Gidaa Life Sciences Private Limited, 287, 9th Cross, Bapuji Layout Near Chandra Layout, Vijayanagara, Bangalore, Karnataka 560040, India. DOI: https://doi.org/10.58624/SVOANE.2026.07.030 Received: July 31, 2026 Published: August 18, 2026 Citation: Arif M, Gayathri V, Ravindran R, Kalaivani P, Siva R, Tamrakar S. A Novel Curcumin-Based Formulation Offers Protection Against Neurodegeneration in Rat Models of AlCl3-Induced Alzheimer’s Disease. SVOA Neurology 2026, 7:4, 220-238. doi.org/10.58624/SVOANE.2026.07.030 

 Abstract 

The exact mechanisms underlying Alzheimer’s disease (AD) pathogenesis are not fully understood, and effective disease-modifying treatments remain lacking despite decades of AD research. Therefore, alternative therapeutic approaches that may target multiple mechanisms of action underlying AD and have a better safety profile than synthetic drugs, such as phytotherapy, are being explored. We aimed to assess the neuroprotective properties of a novel curcumin formulation fortified with andrographolides and piperine (MAG XXI) in rat models of aluminium chloride–induced AD. Overall, 30 male Wistar rats were included and divided into five groups (a healthy control group, a non-treated AD group, and three AD groups treated with donepezil or 200/400 mg/kg body weight of MAG XXI). The Morris water maze, passive avoidance, and elevated plus maze tests were performed on the rats. Tissue samples from the cortex and hippocampus of the rats were then subjected to biochemical evaluation of neuronal, oxidative stress, and inflammatory markers. Compared to non-treated rats, donepezil-treated rats and high-dose (400 mg/kg body weight) MAG XXI–treated rats showed a mild but significant improvement in the Morris water maze and elevated plus maze test findings and a marked and significant improvement in the passive avoidance task results. Furthermore, oxidative stress markers, inflammatory markers, and neuronal markers improved overall in the donepezil-treated group and in both MAG XXI–treated groups. Notably, the improvement in the oxidative stress markers was more marked with MAG XXI (both doses) than with donepezil. Histopathological examination revealed lower incidence rates of neurofibrillary tangles, gliosis, and neuronal degeneration in the high-dose MAG XXI and donepezil groups. Notably, cresyl staining revealed minimal-to-mild cell dispersion in the donepezil group, whereas normal neuronal cells with well-lineated cell bodies and Nissl substance were observed in the high dose MAG XXI group. No adverse events were noted in the MAG XXI groups. MAG XXI could be a promising alternative for AD treatment because it appears to exhibit neuroprotective properties, as demonstrated by its ability to alleviate oxidative stress and neuroinflammation. However, further clinical trials involving humans are necessary to corroborate the present study’s results

Mini 'arteries-on-a-chip' could help predict a person's risk of stroke

 Have your competent? doctor lay out a path to stroke recovery with all this chip based research.

• BBB on a chip (1 post to February 2017)
• Brain on a chip (9 posts to October 2012)
• Lab on a Chip (3 posts to May 2012)

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!

Mini 'arteries-on-a-chip' could help predict a person's risk of stroke

Researchers have pioneered a way to create miniaturized copies of a person's carotid artery that could help doctors predict and manage the patient's stroke risk, a new study suggests.

In the research, published in July in the journal Cell Biomaterials, scientists used these "arteries-on-a-chip" to monitor how real blood flows through a patient's carotid arteries, which carry blood to the brain, face and neck. This could enable doctors to identify not just how and what type of clots form in that specific patient, but also determine which medications would be most effective in dealing with the blockage.

While the technique is currently a proof-of-concept, someday, it could help medical practitioners to better tailor treatments for each patient.

"When the inner lining of an artery is damaged, material underneath the cells, including collagen, becomes exposed to the blood," Zhao said. A bloodborne protein called von Willebrand factor (VWF) grabs hold of platelets from the flowing blood. Those platelets then stick together and recruit more platelets, building a clot, he said.

But forming a clot is only half the story; it's what this mass does next that determines the risk to the patient.

In some cases, the growing ball of clotted blood will stay firmly rooted to the artery wall, slightly impeding blood flow but not posing any immediate danger. However, if tiny fragments break off this static clot, they can travel toward the brain, where they risk blocking smaller vessels and thus causing a stroke.

"Clinically, we are very good at imaging how narrow an artery is," Zhao said, "but narrowing alone does not tell us exactly how a clot will behave."

This is where artery-on-a-chip models come in, he said. Rather than relying purely on medical scans, the team's model recreates the exact shape and structure of an individual patient's blood vessels using 3D printing. To create the models, they first use a patient’s existing CT scans to 3D print a plastic replica of their carotid artery, including any narrowing caused by atherosclerosis. Next, the inside of this plastic structure is coated with collagen, and then cells that line the carotid artery get layered on top. Blood is passed through the replica artery, mimicking the speed and pressure of blood flow in the body.

Neurophysiologist reveals the 1 exercise they’d never skip for brain health

 You got this from your competent? doctor way back in 2024, right?

5 Exercises We Hate, and Why You Should Do Them Anyway March 2024 

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!

The latest here:

Neurophysiologist reveals the 1 exercise they’d never skip for brain health

As Alzheimer’s disease and other forms of dementia continue to rise, many people are looking for ways to protect their brain health as they age. One neurophysiologist believes one physical exercise may stand above the rest when it comes to the brain.

In a recent episode of The Diary of a CEO podcast, neurophysiologist Louisa Nicola, whose mission is to “end Alzheimer’s disease,” according to her profile on Instagram @ louisanicola_, was asked which single exercise she would choose if she could do only one for the rest of her life to protect her brain. Her answer? The deadlift.

Nicola argued that the exercise engages nearly the entire body. “If done correctly, the deadlift can use almost every muscle in your body,” she said, listing muscles including the erector spinae (deep back muscles extending from the pelvis to the base of the skull), glutes, quadriceps, serratus anterior (a muscle on the side of the chest), and calves. Recruiting so many muscle groups at once, the movement would also be comparable to a barbell squat, she said.

She also suggested that lifting heavier weights places greater demands on the brain. “I want both men and women lifting heavy because…think of your brain as real estate,” Nicola said. “There’s real estate in your brain reserved for lifting heavy.”

According to Nicola, moving heavier loads requires more neural resources, resulting in a greater “neural drive” that she believes benefits the brain.

The discussion comes amid growing concern over dementia worldwide. Alzheimer’s disease is the most common cause of dementia, a condition characterized by progressive declines in memory, thinking, and everyday functioning. Alzheimer’s disease is responsible for around 60 to 80 percent of dementia cases, according to the Alzheimer’s Association.

While experts continue to search for treatments and preventive strategies, physical activity is increasingly recognized as one of the most important modifiable lifestyle factors associated with healthy aging and reduced dementia risk.

Physicians who spoke to Newsweek noted that while the deadlift is beneficial for brain health, no single exercise has been proven to prevent Alzheimer’s disease.

Neurophysiologist Reveals the 1 Exercise They’d Never Skip for Brain Health

Nuances on Deadlifts and Benefits for the Brain

Dr. Joanna Fong-Isariyawongse, a triple board-certified neurologist, sleep specialist, and epileptologist, told Newsweek that there’s “some nuance” to the idea that one exercise is best or that heavier lifting is always better.

Research suggests different forms of exercise support different aspects of brain health, she explained. Resistance training appears particularly helpful for overall cognition; aerobic activities, such as brisk walking, benefit memory, while balance-focused exercises, such as tai chi, have performed well in recent studies involving older adults, she noted.

“So, rather than one single exercise, a combination tends to offer the broadest protection,” Fong-Isariyawongse said.

Dr. Sergio Guiteau, a board-certified family medicine and sports medicine physician, told Newsweek that there is currently no evidence directly linking heavier weightlifting to greater neuroprotection or lower dementia rates.

“What we do know is that resistance training, as well as any activity or exercise that challenges balance, coordination, and learning, will decrease dementia risk more than just trying to maximize weight on a deadlift,” Guiteau said.

Dr. Parth Bhavsar, a board-certified family medicine physician and founder of TeleDirectMD, emphasized that brain protection depends on much more than lifting heavier weights. He told Newsweek that factors including consistency, technique, cardiovascular fitness, sleep quality, blood pressure control, insulin sensitivity, and avoiding injuries all contribute to long-term brain health.

Bhavsar noted: “If a person can perform deadlifts safely, it is one of the best strength exercises. However, the best brain-protective exercise is an exercise that you will be able to perform safely, progressively, and consistently,” and “heavy lifting can be a part of it.”

Deadlift Alternatives That Can Be Just as Effective

The experts stressed that people do not need to perform heavy deadlifts to gain potential brain benefits.

“The encouraging part is that none of this requires deadlifting heavy,” Fong-Isariyawongse said. Machine weights, resistance bands, bodyweight exercises, walking, and tai chi all appear to provide meaningful brain-health benefits while carrying a lower risk of injury.

Bhavsar listed numerous alternatives, including trap-bar deadlifts, kettlebell deadlifts from an elevated surface, Romanian deadlifts with light dumbbells, sit-to-stand exercises, goblet squats, step-ups, leg presses, farmer carries, resistance-band rows, and sled pushes or pulls.

Dr. Mariam Zakhary, a physician specializing in physical medicine, rehabilitation, and sports medicine from the Ikon Recovery Center, told Newsweek: “Deadlifts are a great compound exercise due to their ability to recruit multiple large muscle groups and the fact that they challenge coordination, balance, force generation, and motor function.”

However, she added that people can obtain similar functional benefits through sit-to-stand movements, chair squats, step-ups, resistance-band exercises, low-weight hip hinges, and supervised machine-based strength training.

Guiteau likewise highlighted squats, step-ups, and resistance-band exercises as adaptable options, particularly for people with mobility limitations or prior injuries.

The Most Important Factor for Brain Health

The experts largely agreed on one key point when it comes to exercise and brain health—consistency matters more than any single exercise.

Bhavsar noted that physical inactivity is identified as a modifiable dementia risk factor in the 2024 Lancet commission report on dementia prevention. He also pointed to recommendations from the United States Centers for Disease Control and Prevention (CDC) and World Health Organization (WHO) encouraging regular physical activity to help reduce the risk of cognitive decline.

Zakhary agreed that “consistency is key,” noting that “the most beneficial form of exercise will be the one that safely challenges both your cardiovascular system and your musculoskeletal system and allows you to sustain the exercise over time.”

Fong-Isariyawongse added that physical activity is only part of the equation. Learning a language, playing an instrument, or mastering another new skill can also produce measurable changes in brain connectivity and volume.

Taken together, the experts suggest that while the deadlift may be an excellent strength exercise for many people, the strongest evidence supports a broader approach, rather than any single movement alone.

Do you have a tip on a health or science story that Newsweek should be covering? Do you have a question about the brain? Let us know via life@newsweek.com.

Contact Newsweek editors on this story: Charlotte Nisbet and Gray R. Thomas

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Study reveals a previously unknown ability of the brain to repair itself

Repeating the reporting on this since repetition may be the only way to get thru the thick heads in your stroke hospitals! Print this out and slap your doctor with it, asking when s/he will initiate research in humans to prove this out!

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!

 Study reveals a previously unknown ability of the brain to repair itself

The brain evidently can regenerate itself better than previously assumed after injuries or certain autoimmune diseases. Using a mouse model, researchers at the University of Zurich have demonstrated that special supporting and nourishing cells repopulate damaged areas of the brain by initially sending only newly formed cell nuclei there.

Glial cells are supporting and nourishing cells in the brain. Star-shaped glial cells called astrocytes are vital to the functioning of neurons. They supply the nerve cells with nutrients, help to regulate blood flow and keep brain tissue healthy. It had long been assumed that when astrocytes are lost – as happens, for instance, in brain injuries or autoimmune diseases such as rare neuromyelitis optica spectrum disorder, in which the body's own antibodies destroy these cells – the adult brain cannot fully replace them.

Regenerative astrocytes repair damaged tissue

A new study by co-lead authors Marina Herwerth and Matthias Wyss from the Institute of Pharmacology and Toxicology at the University of Zurich (UZH) has now overturned that assumption: their research team headed by Bruno Weber discovered a specialized group of "regenerative" astrocytes in the brains of living mice that step in on the perimeter of the damaged area of the brain to rebuild the cells.

The findings of our study reveal a previously unknown ability of the adult brain to repair itself. They point toward new ways of supporting recovery from ailments involving the loss of astrocytes."

Bruno Weber, University of Zurich

Only cell nuclei migrate

The researchers used two-photon microscopy to observe the brains of living mice in real time over a period of several weeks and mapped which genes switch on in which areas of the brain. This way they were able to identify the special astrocytes that take care of rebuilding injured tissue. But those cells don't just divide, they also perform a remarkable feat: "they send the newly formed nuclei of their daughter cells gliding across long distances to repopulate the damaged area of the brain and knit the astrocyte network back together," Weber explains.

Starting points for targeted regeneration

The discovery of how adult brain cell nuclei migrate through the long star-shaped extensions of astrocytes to injured tissue expands comprehension of how the brain organizes and regenerates itself after certain injuries. If those mechanisms can be selectively activated, that could help to more effectively repair damaged brain tissue, restore astrocyte networks and thus improve recovery after certain brain disorders. "We were able to identify numerous genes and signaling pathways that are temporarily activated during repair. They could serve as starting points in the future for influencing post-disease and -injury regeneration processes," Weber stresses.

Source:

University of Zurich

Journal reference:

Herwerth, M., et al. (2026). Focal astrocyte loss reveals nuclear translocation during lesion repopulation. Nature Neuroscience. DOI: 10.1038/s41593-026-02354-5. https://www.nature.com/articles/s41593-026-02354-5

Regenerative Astrocytes Repair Brain Damage

 How long will it take for your competent? doctor/hospital to get human testing going for stroke? NEVER?

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!

Your stroke medical 'professionals' have been creating protocols on astrocytes for over a decade, right!

• astrocytes (123 posts to June 2011)

Regenerative Astrocytes Repair Brain Damage

Summary: Researchers discovered a previously unknown mechanism through which the adult mammalian brain repairs itself following focal injuries or autoimmune damage. Using two-photon microscopy and longitudinal gene mapping in living mouse models, researchers identified a specialized population of “regenerative” astrocytes capable of repopulating damaged brain regions.

Rather than relying solely on classical cell body division at the site of injury, these specialized astrocytes situated along the lesion perimeter send newly formed daughter cell nuclei gliding long distances through their star-shaped cellular extensions. These migrating cell nuclei repopulate the depleted lesion zone, re-establishing functional astrocyte networks.

This discovery overturns long-held assumptions regarding the limited regenerative capacity of adult glial networks, revealing molecular signaling pathways that could serve as therapeutic targets for traumatic brain injury and autoimmune conditions such as neuromyelitis optica spectrum disorder (NMOSD).

Key Facts

• Overturning Dogma on Glial Regeneration: Demonstrates that the adult central nervous system possesses a previously unrecognized capability to replace lost astrocytes and restore damaged tissue architecture.
• Mechanism of Long-Distance Nuclear Migration: Specialized regenerative astrocytes remain at the lesion boundary and send newly generated cell nuclei gliding across long astrocytic extensions into the depleted injury core.
• Rebuilding Functional Glial Networks: Astrocytes perform vital homeostatic functions, including nutrient supply to neurons, blood flow regulation via end-feet, and extracellular ion balance, making their network reconstruction essential for neuronal survival.
• Targeted Clinical Applications: Holds therapeutic relevance for neurotraumatic brain injuries and rare autoimmune conditions like neuromyelitis optica spectrum disorder (NMOSD), where autoantibodies selectively destroy astrocytes.
• Molecular Targets for Therapeutics: The team identified specific genes and signaling pathways temporarily activated during nuclear migration, providing potential targets for pharmacological interventions to accelerate brain repair.

Source: University of Zurich

The brain evidently can regenerate itself better than previously assumed after injuries or certain autoimmune diseases. Using a mouse model, researchers at the University of Zurich have demonstrated that special supporting and nourishing cells repopulate damaged areas of the brain by initially sending only newly formed cell nuclei there.

Glial cells are supporting and nourishing cells in the brain. Star-shaped glial cells called astrocytes are vital to the functioning of neurons. They supply the nerve cells with nutrients, help to regulate blood flow and keep brain tissue healthy.

It had long been assumed that when astrocytes are lost – as happens, for instance, in brain injuries or autoimmune diseases such as rare neuromyelitis optica spectrum disorder, in which the body’s own antibodies destroy these cells – the adult brain cannot fully replace them.

The image on the left shows a brain lesion (diameter: just under 0.5 mm). Around the perimeter of the lesion, the newly discovered “regenerative” astrocytes begin to seal the defect by forming long cellular extensions (shown in red). Newly formed cell nuclei (shown in blue) migrate along the cellular extensions toward the damaged area. Unaltered astrocytes (shown in green) surround the lesion area. The image on the right shows an enlargement of the marked area in the left image. Credit: Institute of Pharmacology and Toxicology, University of Zurich

Regenerative astrocytes repair damaged tissue

A new study by co-lead authors Marina Herwerth and Matthias Wyss from the Institute of Pharmacology and Toxicology at the University of Zurich (UZH) has now overturned that assumption: their research team headed by Bruno Weber discovered a specialized group of “regenerative” astrocytes in the brains of living mice that step in on the perimeter of the damaged area of the brain to rebuild the cells.

“The findings of our study reveal a previously unknown ability of the adult brain to repair itself. They point toward new ways of supporting recovery from ailments involving the loss of astrocytes,” Weber says.

Only cell nuclei migrate

The researchers used two-photon microscopy to observe the brains of living mice in real time over a period of several weeks and mapped which genes switch on in which areas of the brain. This way they were able to identify the special astrocytes that take care of rebuilding injured tissue. But those cells don’t just divide, they also perform a remarkable feat: “they send the newly formed nuclei of their daughter cells gliding across long distances to repopulate the damaged area of the brain and knit the astrocyte network back together,” Weber explains.

Starting points for targeted regeneration

The discovery of how adult brain cell nuclei migrate through the long star-shaped extensions of astrocytes to injured tissue expands comprehension of how the brain organizes and regenerates itself after certain injuries. If those mechanisms can be selectively activated, that could help to more effectively repair damaged brain tissue, restore astrocyte networks and thus improve recovery after certain brain disorders.

“We were able to identify numerous genes and signaling pathways that are temporarily activated during repair. They could serve as starting points in the future for influencing post-disease and -injury regeneration processes,” Weber stresses.

Key Questions Answered:

Q: How do “regenerative” astrocytes differ from standard cell division during tissue repair?

A: Instead of whole cells migrating or simply dividing locally, these specialized astrocytes remain at the perimeter of the damaged area. They divide and send the newly formed nuclei of their daughter cells gliding long distances through their extended cellular processes directly into the injured zone to rebuild the network.

Q: What conditions cause the loss of astrocytes in the adult brain?

A: Astrocytes are lost during traumatic brain injuries, strokes, and specific neuroinflammatory or autoimmune conditions, most notably Neuromyelitis Optica Spectrum Disorder (NMOSD), where the body’s immune system produces autoantibodies that target and destroy astrocytes.

Q: How was this nuclear migration observed in real time?

A: Researchers at the University of Zurich used in vivo two-photon microscopy in living mouse models over several weeks. This allowed them to track living cells, observe nuclear movement through astrocytic branches, and map corresponding gene expression changes as the tissue repaired itself.

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: Kurt Bodenmueller
Source: University of Zurich
Contact: Kurt Bodenmueller – University of Zurich
Image: The image is credited to Institute of Pharmacology and Toxicology, University of ZurichOriginal Research: Open access.

“Focal astrocyte loss reveals nuclear translocation during lesion repopulation” by Marina Herwerth, Matthias T. Wyss, Nicola B. Schmid, Anna Lasne, Jacqueline Condrau, Luca Ravotto, José María Mateos Melero, Andres Kaech, Gustav Bredell, Carolina Thomas, Rachel Kim, Petra Kukanja, Vladyslav L. Korobeynyk, Christine Stadelmann, Thomas Misgeld, Jeffrey L. Bennett, Sebastian Jessberger, Aiman S. Saab, Shane A. Liddelow & Bruno Weber. Nature Neuroscience
DOI:10.1038/s41593-026-02354-5