Posts Tagged Neuroplasticity

[ARTICLE] Update on cell therapy for stroke – Full Text

Abstract

Ischaemic stroke remains a leading cause of death and disability. Current stroke treatment options aim to minimise the damage from a pending stroke during the acute stroke period using intravenous thrombolytics and endovascular thrombectomy; however, there are no currently approved treatment options for reversing neurological damage once a stroke is completed. Preclinical studies suggest that cell therapy may be safe and effective in improving functional outcomes. Several recent clinical trials have reported safety and some improvement in outcomes following cell therapy administration in ischaemic stroke, which are reviewed. Cell therapy may provide a promising new treatment for stroke reducing stroke-related disability. Further investigation is needed to determine specific effects of cell therapy and to optimise cell delivery methods, cell dosing, type of cells used, timing of delivery, infarct size and location of infarct that are likely to benefit from cell therapy.

Introduction

Until recently, intravenous recombinant tissue plasminogen activator was the only proven effective treatment for acute stroke. Endovascular thrombectomy has now been added to our arsenal for acute stroke treatment following the publication of five randomised trials demonstrating highly significant treatment effects favouring endovascular therapy.1–6 Outcome data support advancements in acute stroke care and neurorehabilitation with a significant increase in stroke survivors over time.7 However, despite these advancements, stroke remains a leading cause of long-term disability.8 For patients with residual deficits after stroke, we have no currently approved therapy for restoring function.

Cell therapy is one approach to enhancing recovery after stroke. In animal models, delivery of several different types of stem cells reduce infarct size and improve functional outcomes.9 Clinical trials of cell therapy completed in the 2000s mostly treating small cohorts of patients with chronic stroke demonstrated adequate safety and a suggestion of efficacy with the use of cell therapy. Kondziolka and colleagues used N-Tera 2 cells derived from a lung metastasis of a human testicular germ cell tumour that when treated with retinoic acid generate postmitotic neurons that maintain a fetal neuronal phenotype indefinitely in vitro (LBS neurons). LBS neurons were stereotactically implanted around the stroke bed of chronic subcortical ischaemic stroke. This study demonstrated safety and feasibility of stereotactic cell implantation, although there was no significant improvement in functional outcomes.10 11 Using a similar stereotactic approach implanting cells into the basal ganglia, Savitz and colleagues transplanted LGE cells (fetal porcine striatum-derived cells, Genvec) in five patients. Two patients showed improvements, but two patients experienced adverse effects including delayed worsening of neurological symptoms and seizure resulting in early termination of the study.12 Bang and colleagues reported the safety and feasibility of intravenous infusion of autologous mesenchymal stem cells (MSCs) with no reported adverse effects in five patients treated with intravenous MSCs. Although they reported some initial motor improvements, at 12 months, there was no significant difference in motor scores.13 These early clinical trials mostly focused on chronic subcortical strokes, but more recent trials are now investigating cell therapy for treatment of both cortical and subcortical infarcts. This review discusses the considerations for design of cell therapy trials and summarises the results of more recent studies.

Continue —> Update on cell therapy for stroke | Stroke and Vascular Neurology

Table 1

Summary of recent human cell therapy trials for stroke

Clinical trial/sponsor Age Time after stroke Additional selection criteria Cell type Route Stroke location Patients (n) Safety results Efficacy results
MASTERS/Athersys 18–83 24–48 hours NIHSS 8–20, infarct 5-100cc, premorbid mRS 0–1 Multistem adult-derived stem cell product Intravenous Cortical 129 Similar SAE at 1 year 22(34%) versus 24 (39%) placebo,
Lower mortality—5 deaths (8%) versus 9deaths (15%) in placebo19
No effect on 90-day Global Stroke Recovery Assessment (mRS 0–2, NIHSS increase by 75%, Barthel Index >95) but trend towards improved outcome with earlier delivery of cells19
InveST/Department of Biotechnology, India 18–75 7–29 days NIHSS >7, GCS >8, BI <50, paretic arm or leg stable >48 hours Autologous marrow-derived stem cells Intravenous 120
(58 cell therapy)
61 AE (33%) and eight deaths versus 60 AEs (36%) and five deaths placebo22 No effect on 180-day Barthel Index Score, mRS shift or score >3, NIHSS, change of infarct volume22
RECOVER-Stroke/Aldagen 30–75 13–19 days NIHSS 7–22, mRS >3 ALDHbrautologous marrow-derived stem cells Intracarotid infusion distal to ophthalmic Anterior circulation ± subcortical 29 IA, 19 sham 12 SAE IA, 11 SAE sham; 0 cell-related SAE23 No difference in mRS, Barthel, NIHSS at 90 days or 1 year
PISCES-II/ReNeuron 40–89 2–13 months Paretic arm with NIHSS motor arm score 2–3 CTX0E03 DP allogeneic human fetal neural stem cells Stereotaxic infusion into ipsilateral putamen 21 Pending Pending
Sanbio 18–75 6–60 months NIHSS>7, mRS 3–4, stable symptoms>3 weeks SB623 allogeneic marrow-derived stem cells transiently transfected with plasmid encoding Notch122 Stereotaxic infusion peri-infarct Subcortical ± cortical component24 18 28 SAE, 0 cell-related SAE25 Improved ESS at 6 months (p<0.01) and 12 months (p<0.001)
Improved NIHSS at 6 months (p<0.01) and 12 months(p<0.001)
Improved Fugl-Meyer at 6 months (p<0.001) and 12 months(p<0.001)25
PISCES/ReNeuron >60, male only 6–60 months Persistent hemiparesis, Stable NIHSS over 4 weeks (Pt 2 CTX0E03 DP allogeneic human neural stem cells Stereotaxic infusion into putamen Subcortical 11 16 SAE (in nine patients), 0 cell-related SAE28 Improved NIHSS at 2 years (p=0.002), No change, Barthel Index, MMSE, Ashworth, mRS28 29
  • AE, Adverse Event; ARAT, Action Research Arm Test; BI, Barthel Index; DP, drug product; ESS, European Stroke Scale; IA, intra-arterially; MASTERS, Multistem Administration for Stroke Treatment and Enhanced Recovery Study; MMSE, Mini-Mental Status Examination; mRS, modified Rankin Score; NIHSS, National Institutes of Health Stroke Scale; PISCES, Pilot Investigation of Stem Cells in Stroke; SAE, Serious aAverse Events.

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[Abstract] Supporting Stroke Motor Recovery Through a Mobile Application: A Pilot Study

Abstract

Neuroplasticity and motor learning are promoted with repetitive movement, appropriate challenge, and performance feedback. ARMStrokes, a smartphone application, incorporates these qualities to support motor recovery. Engaging exercises are easily accessible for improved compliance. In a multiple-case, mixed-methods pilot study, the potential of this technology for stroke motor recovery was examined. Exercises calibrated to the participant’s skill level targeted forearm, elbow, and shoulder motions for a 6-wk protocol. Visual, auditory, and vibration feedback promoted self-assessment. Pre- and posttest data from 6 chronic stroke survivors who used the app in different ways (i.e., to measure active or passive motion, to track endurance) demonstrated improvements in accuracy of movements, fatigue, range of motion, and performance of daily activities. Statistically significant changes were not obtained with this pilot study. Further study on the efficacy of this technology is supported.

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Source: Supporting Stroke Motor Recovery Through a Mobile Application: A Pilot Study | American Journal of Occupational Therapy

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[WEB SITE] Spasticity, Motor Recovery, and Neural Plasticity after Stroke – Full Text

Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers. Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for post-stroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the key to promote motor recovery. Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

Introduction

According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).

Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (47). Accumulated evidence from animal (8) and human studies (918) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (2036), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (3738). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.

• Poststroke spasticity and motor recovery are mediated by different mechanisms

• Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)

• Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity

• Possible roles of RS hyperexcitability in motor recovery

• An example of spasticity reduction for facilitation of motor recovery […]

Continue —> Frontiers | Spasticity, Motor Recovery, and Neural Plasticity after Stroke | Neurology

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[ARTICLE] Spasticity, Motor Recovery, and Neural Plasticity after Stroke – Full Text

Abstract

Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers.

Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for poststroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the keys to promote motor recovery.

Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

Introduction

According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).

Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (47). Accumulated evidence from animal (8) and human studies (918) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (2036), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (3738). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.

  • Poststroke spasticity and motor recovery are mediated by different mechanisms
  • Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)
  • Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity
  • Possible roles of RS hyperexcitability in motor recovery
  • An example of spasticity reduction for facilitation of motor recovery

Continue —> Spasticity, Motor Recovery, and Neural Plasticity after Stroke

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[BLOG POST] How to Make New Brain Cells and Improve Brain Function

Scientists used to believe that the brain stopped making new brain cells past a certain age. But that believe changed in the late 1990’s as a result of several studies which were performed on mice at the Salk Institute.

After conducting maze tests, neuroscientist Fred H. Gage and his colleagues examined brain samples collected from mice. What they found challenged long standing believes held about neurogenesis, or the creation of new neurons.

To their astonishment, they discovered that the mice were creating new neurons. Their brains were regenerating themselves.

All of the mice showed evidence of neurogenesis but the brains of the athletic mice showed even more.

 These mice, the ones that scampered on running wheels, were producing two to three times as many new neurons as the mice that didn’t exercise.

The difference between the mice who performed well on the maze tests and those that floundered was exercise.

That’s great for the mice, but what about humans?

To find out if neurogensis occurred in adult humans, Gage and his colleagues obtained brain tissue from deceased cancer patients who had donated their bodies to research. While still living, these people were injected with the same type of compound used on Gage’s mice to detect new neuron growth. When Gage dyed their brain samples, he saw new neurons. Like in the mice study, they found evidence of neurogenesis – the growth of new brain cells.

From the mice study, it appears that those who exercise produce even more new brain cells than those who don’t. Several studies on humans seem to suggest the same thing.

Studies performed at both the University of Illinois at Urbana- Champaign and Columbia University in New York City have shown that exercise benefits brain function. The test subjects were given aerobic exercises such as walking for at least one hour three times a week. After 6 months they showed significant improvements in memory as measured by a word-recall test. Using fMRI scans they also showed increases in blood flow to the hippocampus (part of the brain associated with memory and learning). Scientists suspect that the blood pumping into that part of the brain was helping to produce fresh neurons.

Dr. Patricia A. Boyle and her colleagues of Rush Alzheimer’s Disease Center in Chicago found that the greater a person’s muscle strength, the lower their likelihood of being diagnosed with Alzheimer’s. The same was true for the loss of mental function that often precedes full-blown Alzheimer’s.

Neuroscientist Gage, by the way, exercises just about every day, as do most colleagues in his field. As Scott Small a neurologist at Columbia explains,

 I constantly get asked at cocktail parties what someone can do to protect their mental functioning. I tell them, ‘Put down that glass and go for a run.

So if you want to grow some new brain cells and improve your brain function, go get some exercise!

Source: How to Make New Brain Cells and Improve Brain Function | Online Brain Games Blog

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[WEB SITE] Traumatic Brain Injury Resource Guide – Neuroplasticity

Neuroplasticity

by Lisa Kreber, Ph.D. CBIS
Senior Neuroscientist, Centre for Neuro Skills

What is Neuroplasticity?
Neuronal Firing
How Neuroplasticity Works
Mechanisms of Plasticity
Synaptogenesis
Stem Cells
Modulation of Neurotransmission
Unmasking
Forms of Neuronal Plasticity
Neuronal Remodeling
Depression and Hippocampal Plasticity
Appreciating Plasticity
Ten Principles of Neuroplasticity
Learning, Injury and Recovery

Source: Traumatic Brain Injury Resource Guide – Neuroplasticity

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[ARTICLE] Spasticity, Motor Recovery, and Neural Plasticity after Stroke – Full Text

Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers. Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for post-stroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the key to promote motor recovery. Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

Introduction

According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).

Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (47). Accumulated evidence from animal (8) and human studies (918) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (2036), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (37, 38). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.

• Poststroke spasticity and motor recovery are mediated by different mechanisms

• Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)

• Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity

• Possible roles of RS hyperexcitability in motor recovery

• An example of spasticity reduction for facilitation of motor recovery

Continue —> Frontiers | Spasticity, Motor Recovery, and Neural Plasticity after Stroke | Stroke

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[Abstract] “Genetic Variation and Neuroplasticity: Role in Rehabilitation after Stroke”

Provisional Abstract:

Background and Purpose: Significant inter-individual variability in rehabilitation outcomes exits in many neurologic diagnoses. One factor that may impact response to rehabilitation interventions is genetic variation. Genetic variation refers to the presence of differences in the DNA sequence among a population. Genetic polymorphisms are variations that occur relatively commonly and, while not disease causing, can impact the function of biological systems. The purpose of this article is to describe genetic polymorphisms that may impact neuroplasticity, learning and recovery after stroke.

Summary of Key Points: Genetic polymorphisms for brain-derived neurotrophic factor (BDNF), dopamine, and apolipoprotein E have been shown to impact neuroplasticity and motor learning. Rehabilitation interventions that rely on the molecular and cellular pathways of these factors may be impacted by the presence of the polymorphism. For example, it has been hypothesized that individuals with the BDNF polymorphism may show a decreased response to neuroplasticity based interventions, decreased rate of learning, and overall less recovery after stroke. However, research to date has been limited and additional work is needed to fully understand the role of genetic variation in learning and recovery.

Recommendations for Clinical Practice: Genetic polymorphisms should be considered as possible predictors or covariates in studies that investigate neuroplasticity, motor learning, or motor recovery after stroke. Future predictive models of stroke recovery will likely include a combination of genetic factors and other traditional factors (e.g. age, corticospinal tract integrity) to determine an individual’s expected response to a specific rehabilitation intervention.

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Source: JUST ACCEPTED: “Genetic Variation and Neuroplasticity: Role in Rehabilitation after Stroke”

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[Abstract] Delivering Remote Rehabilitation at Home: An Integrated Physio-Neuro Approach to Effective and User Friendly Wearable Devices – SpringerLink

Abstract

There is a global shortage of manpower and technology in rehabilitation to attend to the five million new patients who are left disabled every year with stroke. Neuroplasticity is increasingly recognized to be a primary mechanism to achieve significant motor recovery. However, most rehabilitation devices either limit themselves to mechanical repetitive movement practice at a limb level or focus only on cognitive tasks. This may result in improvements in impairment but seldom translates into effective limb and hand use in daily activities. This paper presents an easy-to-use, wearable upper limb system, SynPhNe (pronounced like “symphony”), which trains brain and muscle as one system employing neuroplasticity principles. A summary of clinical results with stroke patients is presented. A new, wireless, home-use version of the solution architecture has been proposed, which can make it possible for patients to do guided therapy at home and thus have access to more therapy hours.

Source: Delivering Remote Rehabilitation at Home: An Integrated Physio-Neuro Approach to Effective and User Friendly Wearable Devices | SpringerLink

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[VIDEO] Why Can’t WE Reverse Nerve Damage ? – Reversing Nerve Damage: Central Nervous System Inhibits Cell Regeneration, But Stem Cell Treatment May Help

 

Our nervous system is involved in everything our body does, from maintaining our breath to controlling our muscles. Our nerves are vital to all we do; therefore, nerve pain and damage can heavily influence our quality of life. In Discovery News’ latest video, “Why Can’t We Reverse Nerve Damage?” host Lissette Padilla explains the central nervous system (CNS) has certain proteins that inhibit cell regeneration, because each cell in the nervous system has a unique function on the pathway, like a circuit, and can’t be replaced.

The nervous system can be divided into two sections, with the brain and spinal cord making up the CNS. Nerves are made up of sensory fibers and motor neurons, which comprise the peripheral nervous system. Nerve cells are made up of many parts, but they send signals through threads covered in a protective sheet of myelin. These threads are called axons.

Axons are the long part of the cell that reaches out to neighboring cells to send information down the line. Schwann cells, found only in the peripheral nervous system, are glial cells that produce protective myelin. Schwann cells could potentially clean up damaged nerves, which could make way for healing process to take place and new nerves to be formed.

The problem is these Schwann cells are missing from the CNS. The CNS is comprised of myelin-producing cells called oligodendrocytes. And these cells don’t clean up damaged nerve cells at all, hence the damage problem.

However, research is currently underway to examine the potential success of system cell treatment, where stem cells are injected directly at the injury site. It will still take a few years to see the results of such trials, but since the peripheral nervous system doesn’t have the same blocking proteins that the CNS has, the idea is Schwann cells could help heal the damage.

So it is possible to regrow nerves, albeit slowly. For instance, if you cut a nerve into your shoulder, it could take a year to regrow. By that time, the muscles in your arms could become atrophied. Researchers are working on helping the body heal faster.

Source: Reversing Nerve Damage: Central Nervous System Inhibits Cell Regeneration, But Stem Cell Treatment May Help

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