Researchers Prolong Brain Healing Window Post-Stroke

 Do your really think your incompetent? doctor and hospital will get further research going on this? Then you're living in la-la land!

Of course, just to prove the point your incompetent? doctor did nothing with all this earlier IGF-1 research!

Your fuckingly incompetent? doctor DID NOTHING WITH ALL THIS EARLIER RESEARCH! And you still see them?

IGF-1 (21 posts to March 2014)

Researchers Prolong Brain Healing Window Post-Stroke

ZFP384 inhibition prolonged brain repair and improved recovery in stroke models.

Blocking the activity of ZFP384 can prolong the brain’s endogenous repair functions after stroke, report researchers in a collaborative study. They developed an antisense oligonucleotide-based therapy that sustained the reparative activity of microglia by promoting remyelination and neural plasticity, thereby improving functional recovery in mice. Surprisingly, these results were observed even when the treatment began weeks after injury. The findings reveal a promising strategy to extend the brain’s recovery window after stroke, improving long-term outcomes.

Stroke is one of the leading causes of long-term disability worldwide, which often results in impairments in movement, speech, and cognition in patients. While rehabilitation helps patients regain some lost functions, the brain’s natural ability to repair itself often fades within a few months after an injury. This limited period of spontaneous recovery poses a major challenge for patients, often resulting in permanent neurological deficits after the brain’s intrinsic repair capacity declines. Although this loss of reparative ability has been studied extensively, the mechanism behind this loss remains unclear.

To uncover the reason why this happens, a team led by Assistant Professor Jun Tsuyama and Professor Takashi Shichita from the Department of Neuroinflammation and Repair, Institute of Science Tokyo (Science Tokyo), Japan, conducted research in collaboration with researchers from the Tokyo Metropolitan Institute of Medical Science, Kyushu University, Japan, and the University of Freiburg, Germany. Their findings were published in the journal Nature on May 13, 2026.

After a stroke, the brain launches a coordinated repair program that involves several types of cells. Among these, microglia, the brain’s resident immune cells, play a pivotal role. Immediately after an injury, microglia are activated to trigger inflammation, but thereafter, they rapidly transition into a reparative state and produce growth factors, such as insulin-like growth factor 1 (IGF1), which support remyelination, strengthen neural connections, and promote functional recovery. But this only lasts for two months, limiting the brain’s capacity to repair further.

Conversations on Biomarker Use in Multiple Sclerosis Remyelination Research

 Ask your competent? doctor how many miles of myelin need to be fixed post stroke. NO answer, YOU DON'T HAVE A FUNCTIONING STROKE DOCTOR! I expect your stroke doctor to OBJECTIVELY know the damage. Like the number of dead neurons, dead myelinated fibers, dead synapses! Without that knowledge your doctor can never correlate what protocols fix them.

Conversations on Biomarker Use in Multiple Sclerosis Remyelination Research

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Article

June 6, 2025

Author(s):

Ahmed Abdelhak, MD,Isabella Ciccone, MPH

Fact checked by:

Marco Meglio

Conferences|Consortium of Multiple Sclerosis Centers Annual Meeting (CMSC)

Listen

Ahmed Abdelhak, MD, assistant professor of neurology at the UCSF, discussed the evolving landscape of biomarkers in multiple sclerosis and their potential to transform remyelination approaches.

Ahmed Abdelhak, MD

(Credit: UCSF)

Emerging serum and imaging biomarkers are currently aiming to enhance the ability to monitor remyelination in multiple sclerosis (MS). For example, serum neurofilament light chain (NfL) has emerged as a promising biomarker, reflecting neuroaxonal damage and correlating with disease activity and progression. Recent research has shown that elevated serum NfL levels were associated with an increased risk of disability and brain atrophy. Additionally, other serum proteins are being investigated for their roles in neuroinflammation and could contribute to a more complete picture of disease activity in MS.^1,2

Advancements in imaging techniques, particularly MRI, have assisted with the facilitation of identifying remyelinated lesions in vivo.³ Additionally, quantitative susceptibility mapping and myelin water fraction (MWF) imaging have shown promise in distinguishing remyelinated from demyelinated lesions.⁴ These imaging biomarkers, when combined with serum markers, may provide a more comprehensive assessment of remyelination and disease progression for MS. Thus, ongoing research aims to validate these biomarkers and ultimately, integrate them into clinical practice to enhance personalized treatment strategies for patients with MS.

At the 2025 Consortium of Multiple Sclerosis Centers (CMSC) Annual Meeting, held May 28-31, in Phoenix, Arizona, MS expert Ahmed Abdelhak, MD, sat down with NeurologyLive^® to discuss recent advances in biomarkers, such as NFL, that may guide remyelination in MS, based on his presentation given at the meeting.⁵ Abdelhak, assistant professor of neurology at the UCSF, also discussed promising imaging modalities and stressed the need for multimodal biomarker integration in clinical trials. The conversation underscored the broader goal of tailoring therapies based on individual serum proteomic profiles and mechanistic markers to enhance clinical outcomes in MS care.

NeurologyLive: How might emerging serum and imaging biomarkers change the way clinicians monitor remyelination in patients with MS?

Ahmed Abdelhak, MD: That’s such an important question. And as you said, it’s a very exciting topic. You could’ve seen from the other talks in the session that there is immense progress in this field. We are finally starting to see new drugs showing efficacy in inducing remyelination in our patients, which is very important for functional recovery and long-term neuroprotection.

One of the main challenges we’ve been having so far is finding better and more specific ways to monitor outcomes in those trials. One of the things that is very well established—and the group at UCSF, led by Eric Greene, PhD, did immense work on to validate—is visual evoked potential. There is amazing work from Christian Cordano MD, PhD, from our lab, who demonstrated in a very nice way that remyelination really results in changes in visual evoked potential.

So far, this has been integrated into all clinical trials related to remyelination, but we’ve been missing a lot of other markers. Visual evoked potential shows you remyelination only in the visual tract and has some noise at the center level. So one of the main aims, and one of the areas where the field is very interested, is in finding biomarkers that are accessible for many centers and that can be used in many of the upcoming remyelination trials.

Some of those biomarkers originate from serum, and there are also very interesting imaging markers. What we’ve been working on, for example, is trying to study the blood we’ve collected from participants in those remyelination trials in great depth, to find which proteins in the blood change following remyelination. For example, we found that a protein all neurologists are now aware of—NFL—is affected by changes in myelin integrity in this context. In fact, we saw that when you induce remyelination in people with MS, their NFL levels go down.

We did extensive validation of that in animal models and in other cohorts of people with MS. I think we demonstrated in a robust way that if you cause demyelination, NFL levels will go up, and if you remyelinate the axons, NFL levels will be lower. However, as I stressed during the talk, you need the right context to study NFL as a remyelination marker. NFL is heavily influenced by the levels of inflammation we see in our patients—any MS relapses or MRI activity are really impactful. So, in clinical studies looking for remyelination, where you have a very stable patient population, you can use NFL in that context.

In another part of the talk, we also showed new discovery approaches that, by looking at broad proteomic changes in the serum, helped us identify potentially a whole new set of possible remyelination markers. We are now trying to validate these at the tissue level in animal models and in different MS cohorts to define their real clinical context of use.

On the other hand, we have those very promising imaging markers, which have some advantages and disadvantages compared with fluid biomarkers. For example, what we understand from most of the MRI sequences being used now to monitor remyelination is that they might not necessarily have ultimate specificity to reflect only changes happening in myelin. They also reflect changes in axonal integrity and axonal structure, which is one of the limitations.

But on the other hand, you can really use MRI to explore remyelination happening in certain regions in the brain—for example, in the corpus callosum with MWF, or in MS lesions using sequences like MTR. So, I don’t think there’s one optimal marker. Putting all of them together is very important for the next stage of remyelination trials.

What are the most promising biomarkers currently being investigated, and how close are they to routine clinical use?

This is a very exciting field. We have so many possible new markers. I didn’t disclose most of them during the talk, but we talked about NFL in detail. If you look at this panel of markers, you’ll see how extensive the process is of bringing a biomarker from research into the clinical setting.

For example, with NfL, where we have most of data in the field of MS regarding a soluble body fluid marker, we are very close to getting it into the clinic. What we’ve been waiting on is an FDA-approved assay and instrument to run those tests. But we already know a lot about how to use NfL and what an NfL value means in an patient with MS, with our work especially in the context of remyelination.

For other biomarkers, they are at different stages. Some have well-functioning assays but still need further validation to define their clinical context of use. Others are at a very early stage of discovery and assay development. So I’d say we have biomarkers at almost all different stages—some are very close to clinical use, while others still definitely need more work.

The same applies to MRI. It’s probably easier since we’re using clinically available MRI scans, so that part doesn’t need extra validation. But what we do need to validate is what those sequences are actually showing at the tissue level—are they really reflecting what we are expecting? Are they delivering the outcomes we want? If not, there may be a need to develop even more specific sequences. I know this is a topic many groups are actively working on, and there’s a lot of excitement around it as well.

How might these biomarkers help guide treatment decisions or personalize remyelination strategies in practice?

This is actually the topic I’m most focused on now. The beauty of the wide panel of biomarkers we have is that we’re not only looking at the ultimate tissue change—like with NFL, where you see tissue injury—but also at many mechanistic markers and proteins that reflect every individual’s disease state and story.

For example, with the data we showed from the ReBUILD trial (NCT02040298) conducted by Greene, we saw that patients responded to clemastine fumarate in different ways. Some improved a lot, and some improved modestly. Clinically, these patients were quite similar in age and stability. Just looking at the broader clinical picture, you wouldn’t necessarily find a reason why they responded differently. But if you look at their serum proteome, the group that responded very well had a different signature in their blood compared with the group that didn’t respond optimally.

I think that’s really where we want to go with biomarkers in the future—to dissect the disease population and give each group the treatment that works best for them. It’s a long journey, but the fact that we finally have tools that make this possible makes this a very exciting decade for biomarker research.

Any final thoughts you’d like to share on your presentation at CMSC 2025?

I would definitely recommend, as I mentioned in the talk, not to rely on only one biomarker as an outcome parameter in remyelination clinical trials. Let’s leverage the different tools we now have. Let’s find out whether our remyelinating drug really induces functional electrophysiological recovery.

Let’s find out whether it’s really protecting axons. Let’s see where in the brain the changes are happening. And let’s study each patient’s signature related to their remyelination process. I think by leveraging all these tools together, we are getting very close to bringing one of these remyelinating drugs into the clinical setting.

BEYOND NEUROPLASTICITY - tDCS EFFECTS ON INFLAMMATION AND REMYELINATION

Remyelination and axonal integrity are needed post stroke. What are your competent? doctor's EXACT PROTOCOLS TO ACCOMPLISH THAT?  Oh, your doctor doesn't have any? RUN AWAY! Since you don't have a functioning stroke doctor!

 BEYOND NEUROPLASTICITY - tDCS EFFECTS ON INFLAMMATION AND REMYELINATION

 Letizia Leocani 1,2, Silvia Marenna2, Elena Rossi1,2, Valerio Castoldi2, Giancarlo Comi1,3. 1University Vita-Salute San Raffaele, Milan, Italy; 2IRCCS Scientific Institute San Raffaele, Milan, Italy; 3Dep.t of Rehabilitation Sciences, Casa di Cura Igea, Milan, Italy Symposium title Unveiling the Mechanismsof tDCSinNeurorehabilitation: FromProtection to Recovery 

Abstract

Introduction: 

Anodal transcranial direct current stimulation (tDCS) is known to exert neuromodulatory effects on glial cells and neurons, increasing brain activity, promoting plasticity and remyelination. In Multiple Sclerosis, tDCS has provided promising results in relieving several symptoms, from pain and fatigue to sensory, motor and cognitive deficits. However, tDCS may modulate other mechanisms that can impact directly disease activity and its clinical impact, e.g. inflammation and remyelination. 

Methods: 

With the aim of exploring these effects we use pre-clinical models of autoimmune demyelination (autoimmune encephalomyelitis EAE) and of toxic demyelination with little inflammation (cuprizone intoxication) we used non-invasive visual (VEP) evoked potentials to monitor nervous conduction along the visual pathways during the course of the two diseases and pre and post treatment. 

 Results: 

Anodal, cathodal or sham tDCS were applied daily for 5 consecutive days after which brain and optic nerves were collected for histology. VEPs were significantly delayed in both models prior and after sham tDCS, while cathodal tDCS significantly prevented the development of VEPs latency delay when administered prior to the development of EAE and anodal tDCS significantly improved VEPs delay when administered after the development of cuprizone-related demyelination. In both models, tDCS led to increased myelin or paranodal integrity, reduced axonal loss and reduced expression of inflammatory microglia/macrophages.. 

 Conclusions: 

tDCS is associated with significant improvement or preservation of nervous conduction, reduced inflammation and remyelination and axonal integrity. These findings prompt further work exploring the possibility to use neuromodulation as a disease-modifying treatment of Multiple Sclerosis, beyond its recognized beneficial effects on neural plasticity. 

 Research Category and Technology and Methods Basic Research: 9. Transcranial Direct Current Stimulation (tDCS) Keywords tDCS, Multiple Sclerosis, Inflammation, remyelination http://dx.doi.org/10.1016/j.brs.2024.12.439

Pregnancy Hormone Estriol May Reverse Myelin Damage in Multiple Sclerosis

Now we just need to know if stroke causes myelin damage. WHOM will answer that fuckingly simple question? With NO stroke leadership, nothing ever gets solved in stroke.  You're screwed along with your children and grandchildren when they have strokes.

Pregnancy Hormone Estriol May Reverse Myelin Damage in Multiple Sclerosis

Summary: Treating a mouse model of multiple sclerosis (MS) with the pregnancy hormone estriol could reverse myelin breakdown in the brain’s cortex, a primary area affected in MS.

MS results in inflammation that damage the myelin coating around nerve fibers in the brain’s cortex, leading to disability worsening. Current MS treatments only target inflammation and can’t repair myelin damage.

However, the new study found that estriol not only prevented brain atrophy but also induced remyelination, suggesting it could repair MS-induced damage.

Key Facts:

1. Estriol, a type of estrogen hormone produced in pregnancy, has previously been found to reduce brain atrophy and improve cognitive function in MS patients.
2. The research is a major advancement as cortical atrophy in MS patients is associated with permanent worsening of disability, such as cognitive decline, visual impairment, weakness, and sensory loss.
3. This UCLA-led study is the first to demonstrate that estriol treatment can induce remyelination in the cortex, indicating it can potentially repair, rather than merely slow down, the destruction of myelin.

Source: UCLA

Treating a mouse model of multiple sclerosis with the pregnancy hormone estriol reversed the breakdown of myelin in the brain’s cortex, a key region affected in multiple sclerosis, according to a new UCLA Health study published in Laboratory Investigation.

In multiple sclerosis, inflammation spurs the immune system to strip away the protective myelin coating around nerve fibers in the brain’s cortex, hampering electrical signals sent and received by the brain.

Atrophy of the cortex in MS patients is associated with permanent worsening of disability, such as cognitive decline, visual impairment, weakness and sensory loss.

This is the first study to identify a treatment that could repair myelin in the cortex, undoing some of the damage caused by MS. Credit: Neuroscience News

No currently available treatments for MS can repair damage to myelin. Instead, these treatments target inflammation to reduce symptom flare-ups and new nerve tissue scarring.

Remyelinating strategies: What can be learned from normal brain development

Do we need this after a stroke? Have we demyelinated neurons in the brain? What does your doctor know about this and what is the protocol to fix it?  

And we have this research already, just needs testing humans:

Compound Created To Help Reconstruct Myelin in Multiple SclerosisDecember 2019

And this:

Gallic and vanillic acid suppress inflammation and promote myelination in an in vitro mouse model of neurodegeneration December 2018

The latest here:

Remyelinating strategies: What can be learned from normal brain development

Author links open overlay panelJohnShelestakMuhammadIrfanTara M.DeSilva

https://doi.org/10.1016/j.coph.2022.102290Get rights and content

Under a Creative Commons license

Open access

Abstract

Multiple sclerosis (MS) is a neuroinflammatory demyelinating and neurodegenerative disease of the central nervous system (CNS). Immunomodulatory therapies are effective in reducing relapses, however, there is no remedy for progressive disease emphasizing the need for regenerative strategies. Chronic demyelination causes axonal injury and loss which is a key component of neurodegeneration and permanent disability in MS. New oligodendrocyte progenitor cells (OPCs) proliferate in response to inflammatory demyelination representing the potential for remyelination to protect axons and preserve neuronal function. The majority of remyelinating therapies have targeted intrinsic signaling processes in oligodendrocytes to promote differentiation or utilized methods for transplantation of oligodendrocytes. Here, we discuss specific roles of microglia in contributing to normal myelin development and the significance of these functions for remyelinating strategies.

Axonal Regulation of Central Nervous System Myelination: Structure and Function

I have never been able to figure out if demyelination occurs during stroke. Ask your doctor and get the protocol to remyelinate if needed.
http://journals.sagepub.com/doi/abs/10.1177/1073858417703030

Anna Klingseisen, David A. Lyons

First Published April 11, 2017 Review Article

Download PDF	Article information

Abstract

Approximately half of the human brain consists of myelinated axons. Central nervous system (CNS) myelin is made by oligodendrocytes and is essential for nervous system formation, health, and function. Once thought simply as a static insulator that facilitated rapid impulse conduction, myelin is now known to be made and remodeled in to adult life. Oligodendrocytes have a remarkable capacity to differentiate by default, but many aspects of their development can be influenced by axons. However, how axons and oligodendrocytes interact and cooperate to regulate myelination in the CNS remains unclear. Here, we review recent advances in our understanding of how such interactions generate the complexity of myelination known to exist in vivo. We highlight intriguing results that indicate that the cross-sectional size of an axon alone may regulate myelination to a surprising degree. We also review new studies, which have highlighted diversity in the myelination of axons of different neuronal subtypes and circuits, and structure-function relationships, which suggest that myelinated axons can be exquisitely fine-tuned to mediate precise conduction needs. We also discuss recent advances in our understanding of how neuronal activity regulates CNS myelination, and aim to provide an integrated overview of how axon-oligodendrocyte interactions sculpt neuronal circuit structure and function.

Effect of glial cells on remyelination after spinal cord injury

Do we need this after a stroke? Have we demyelinated neurons in the brain? What does your doctor know about this and what is the protocol to fix it?  Scream at your doctor if you have to get her attention about actually fixing you up to 100% recovery. 

Effect of glial cells on remyelination after spinal cord injury

Hai-feng Wang¹, Xing-kai Liu², Rui Li³, Ping Zhang², Ze Chu⁴, Chun-li Wang², Hua-rui Liu², Jun Qi², Guo-yue Lv², Guang-yi Wang², Bin Liu M.D. ⁵, Yan Li⁶, Yuan-yi Wang M.D. ^7
1 Department of Neurosurgery, First Hospital of Jilin University, Changchun, Jilin Province, China
² Department of Hepatobiliary and Pancreas Surgery, First Hospital of Jilin University, Changchun, Jilin Province, China
³ Hand & Foot Surgery and Reparative & Reconstruction Surgery Center, Second Hospital of Jilin University, Changchun, Jilin Province, China
⁴ Department of Emergency, First Hospital of Jilin University, Changchun, Jilin Province, China
⁵ Department of Cardiology, First Hospital of Jilin University, Changchun, Jilin Province, China
⁶ Department of Surgery, School of Medicine, University of Louisville, Louisville, KY, USA
⁷ Department of Orthopedics, First Hospital of Jilin University, Changchun, Jilin Province, China

Date of Acceptance	14-Sep-2017
Date of Web Publication	10-Nov-2017

Correspondence Address:
Bin Liu
Department of Cardiology, First Hospital of Jilin University, Changchun, Jilin Province
China
Yuan-yi Wang
Department of Orthopedics, First Hospital of Jilin University, Changchun, Jilin Province
China

Source of Support: This work was supported by the National Natural Science Foundation of China, No. 81601957., Conflict of Interest: None

DOI: 10.4103/1673-5374.217354

Abstract

Remyelination plays a key role in functional recovery of axons after spinal cord injury. Glial cells are the most abundant cells in the central nervous system. When spinal cord injury occurs, many glial cells at the lesion site are immediately activated, and different cells differentially affect inflammatory reactions after injury. In this review, we aim to discuss the core role of oligodendrocyte precursor cells and crosstalk with the rest of glia and their subcategories in the remyelination process. Activated astrocytes influence proliferation, differentiation, and maturation of oligodendrocyte precursor cells, while activated microglia alter remyelination by regulating the inflammatory reaction after spinal cord injury. Understanding the interaction between oligodendrocyte precursor cells and the rest of glia is necessary when designing a therapeutic plan of remyelination after spinal cord injury.

Study shows how brain begins repairs after 'silent strokes'

My doctor told me I must have had a number of these small white matter strokes. Of course he never showed my any of my scans so he could have been pulling stuff out of thin air. 
http://m.medicalxpress.com/news/2016-12-brain-silent.html

New, functional brain cells replace those destroyed by stroke in animals. Here, cells are in various stages of maturity: immature cells are green, more mature cells are red and fully mature cells are orange. Credit: University of California, Los Angeles

UCLA researchers have shown that the brain can be repaired—and brain function can be recovered—after a stroke in animals. The discovery could have important implications for treating a mind-robbing condition known as a white matter stroke, a major cause of dementia.
White matter stroke is a type of ischemic stroke, in which a blood vessel carrying oxygen to the brain is blocked. Unlike large artery blockages or transient ischemic attacks, individual white matter strokes, which occur in tiny blood vessels deep within the brain, typically go unnoticed but accumulate over time. They accelerate Alzheimer's disease due to damage done to areas of the brain involved in memory, planning, walking and problem-solving.
"Despite how common and devastating white matter stroke is there has been little understanding of how the brain responds and if it can recover," said Dr. Thomas Carmichael, senior author of the study and a professor of neurology at the David Geffen School of Medicine at UCLA. "By studying the mechanisms and limitations of brain repair in this type of stroke, we will be able to identify new therapies to prevent disease progression and enhance recovery."
In a five-year study, Carmichael's team looked at white matter strokes in animals and found that the brain initiated repair by sending replacement cells to the site, but then the process stalled. The team had a short list of molecular suspects from previous research that they thought might be responsible. Researchers identified a molecular receptor as the likely culprit in stalling the repair; when they blocked the receptor, the animals began to recover from the stroke.
"White matter stroke is an important clinical target for the development of new therapies," Carmichael said.
Annually in the United States, about 795,000 suffer a stroke, resulting in nearly 130,000 deaths. Multiply the number of strokes by six, and you'll have an estimate of the number of strokes that are "silent," in that they do not produce symptoms that lead to hospitalization. Most of these silent strokes are white matter strokes.
The paper was published in the electronic edition of the Proceedings of the National Academy of Sciences.

More information: Elif G. Sozmen et al. Nogo receptor blockade overcomes remyelination failure after white matter stroke and stimulates functional recovery in aged mice, Proceedings of the National Academy of Sciences (2016). DOI: 10.1073/pnas.1615322113
Provided by: University of California, Los Angeles

Programming Hippocampal Neural Stem/Progenitor Cells into Oligodendrocytes Enhances Remyelination in the Adult Brain after Injury

Do we need this after a stroke? Have we demyelinated neurons? What does your doctor know about this and what is the protocol to fix it?
http://www.sciencedirect.com/science/article/pii/S2211124715005501

• Simon M.G. Braun^{1, 2, 5},
• Gregor-Alexander Pilz^{1, 2},
• Raquel A.C. Machado¹,
• Jonathan Moss³,
• Burkhard Becher^{2, 4},
• Nicolas Toni³,
• Sebastian Jessberger^{1, 2, ,}

Under a Creative Commons license

 Show more

doi:10.1016/j.celrep.2015.05.024

Get rights and content

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Highlights

•

Programming hippocampal NSPCs into oligodendrocytes follows developmental programs

•

Programming NSPCs into oligodendrocytes enhances remyelination after injury

•

Induced oligodendrocytes mature and myelinate, as shown at a single-cell level

•

Proof of concept for targeting hippocampal NSPCs for glial brain repair is provided

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Summary

Demyelinating diseases are characterized by a loss of oligodendrocytes leading to axonal degeneration and impaired brain function. Current strategies used for the treatment of demyelinating disease such as multiple sclerosis largely rely on modulation of the immune system. Only limited treatment options are available for treating the later stages of the disease, and these treatments require regenerative therapies to ameliorate the consequences of oligodendrocyte loss and axonal impairment. Directed differentiation of adult hippocampal neural stem/progenitor cells (NSPCs) into oligodendrocytes may represent an endogenous source of glial cells for cell-replacement strategies aiming to treat demyelinating disease. Here, we show that Ascl1-mediated conversion of hippocampal NSPCs into mature oligodendrocytes enhances remyelination in a diphtheria-toxin (DT)-inducible, genetic model for demyelination. These findings highlight the potential of targeting hippocampal NSPCs for the treatment of demyelinated lesions in the adult brain.

Erythropoietin Amplifies Stroke-Induced Oligodendrogenesis in the Rat

I like the last lines, they would have helped me tremendously. But this might require the knowledge of what white matter damage you have vs. gray matter damage.

Erythropoietin Amplifies Stroke-Induced Oligodendrogenesis in the Rat

Background

Erythropoietin (EPO), a hematopoietic cytokine, enhances neurogenesis and angiogenesis during stroke recovery. In the present study, we examined the effect of EPO on oligodendrogenesis in a rat model of embolic focal cerebral ischemia.

Methodology and Principal Findings

Recombinant human EPO (rhEPO) at a dose of 5,000 U/kg (n = 18) or saline (n = 18) was intraperitoneally(In mammals, the serous membrane lining the cavity of the abdomen and that is folded over the viscera.) administered daily for 7 days starting 24 h after stroke onset. Treatment with rhEPO augmented actively proliferating oligodendrocyte progenitor cells (OPCs) measured by NG2 immunoreactive cells within the peri-infarct white matter and the subventricular zone (SVZ), but did not protect against loss of myelinating oligodendrocytes measured by cyclic nucleotide phosphodiesterase (CNPase) positive cells 7 days after stroke. However, 28 and 42 days after stroke, treatment with rhEPO significantly increased myelinating oligodendrocytes and myelinated axons within the peri-infarct white matter. Using lentivirus to label subventricular zone (SVZ) neural progenitor cells, we found that in addition to the OPCs generated in the peri-infarct white matter, SVZ neural progenitor cells contributed to rhEPO-increased OPCs in the peri-infarct area. Using bromodeoxyuridine (BrdU) for birth-dating cells, we demonstrated that myelinating oligodendrocytes observed 28 days after stroke were derived from OPCs. Furthermore, rhEPO significantly improved neurological outcome 6 weeks after stroke. In vitro, rhEPO increased differentiation of adult SVZ neural progenitor cells into oligodendrocytes and enhanced immature oligodendrocyte cell proliferation.

Conclusions

Our in vivo and in vitro data indicate that EPO amplifies stroke-induced oligodendrogenesis that could facilitate axonal re-myelination and lead to functional recovery after stroke.