Blessed Thistle Enhances Nerve Regeneration

 If you have competent? doctors and hospital they will make sure this gets tested for nerve regeneration in the brain! Maybe by using nanocarriers to get across the blood brain barrier. But then, your competent? doctor already knows about nanocarriers, so you don't need to remind them of it.

Do you prefer your  doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

Blessed Thistle Enhances Nerve Regeneration

Summary: Cnicin, a compound derived from the plant Blessed Thistle, significantly enhances nerve regeneration. The study shows that Cnicin can accelerate the growth of axons, the long fibers of nerve cells, which is crucial for the recovery of nerve function after injury.

This new finding was demonstrated in animal models and human cell cultures, where Cnicin treatment led to rapid improvements in paralysis and neuropathy symptoms. Remarkably, Cnicin can be administered orally, offering a practical advantage over injectable treatments and highlighting its potential for broader clinical application.

Key Facts:

1. Cnicin, extracted from Blessed Thistle, has been shown to speed up axon growth, essential for nerve repair.
2. The compound’s effectiveness was observed in both animal models and human cells, with treated subjects showing quicker recovery from nerve damage.
3. The study emphasizes the need for further clinical trials to determine the optimal dosage, as Cnicin operates within a narrow therapeutic window.

Source: University of Cologne

Blessed thistle (Cnicus benedictus) is a plant in the family Asteraceae and also grows in our climate. For centuries, it has been used as a medicinal herb as an extract or tea, e.g. to aid the digestive system.

Researchers at the Center for Pharmacology of University Hospital Cologne and at the Faculty of Medicine of the University of Cologne have now found a completely novel use for Cnicin under the direction of Dr Philipp Gobrecht and Professor Dr Dietmar Fischer.

Administering a daily dose of Cnicin to mice or rats helped improve paralysis and neuropathy much more quickly. Credit: Neuroscience News

Animal models as well as human cells have shown that Cnicin significantly accelerates axon (nerve fibres) growth. The study ‘Cnicin promotes functional nerve regeneration’ was published in Phytomedicine.

Rapid help for nerves

Regeneration pathways of injured nerves in humans and animals with long axons are accordingly long. This often makes the healing process lengthy and even frequently irreversible because the axons cannot reach their destination on time.

An accelerated regeneration growth rate can, therefore, make a big difference here, ensuring that the fibres reach their original destination on time before irreparable functional deficits can occur.

The researchers demonstrated axon regeneration in animal models and human cells taken from retinae donated by patients. Administering a daily dose of Cnicin to mice or rats helped improve paralysis and neuropathy much more quickly.

Compared to other compounds, Cnicin has one crucial advantage: it can be introduced into the bloodstream orally (by mouth). It does not have to be given by injection.

“The correct dose is very important here, as Cnicin only works within a specific therapeutic window. Doses that are too low or too high are ineffective. This is why further clinical studies on humans are crucial,” said Fischer.

The University of Cologne researchers are currently planning relevant studies. The Center for Pharmacology is researching and developing drugs to repair the damaged nervous system.

Funding: The current study received funding of around 1,200,000 euros from the Federal Ministry of Education and Research within the framework of the project PARREGERON.

About this nerve regeneration and supplements research news

Author: Anna Euteneuer
Source: University of Cologne
Contact: Anna Euteneuer – University of Cologne
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Cnicin promotes functional nerve regeneration” by Dietmar Fischer et al. Phytomedicine

Nano-featured poly (lactide-coco-glycolide)-graphene microribbons as a promising substrate for nerve tissue engineering

What leader in stroke is going to look at this and say? 'We need researchers to find a use for this in stroke recovery.' It will never occur, we have NO LEADERS IN STROKE.  

Of course nothing was done with these earlier posts on this back to July 2012. We have complete and total fucking incompetency in the stroke medical world. And until we get survivors in charge, NOTHING WILL BE ACCOMPLISHED.

• nerve regeneration (7)

 

Nano-featured poly (lactide-coco-glycolide)-graphene microribbons as a promising substrate for nerve tissue engineering

Author links open overlay panelNegar AbbasiAval^abRahmatollahEmadi^aAliValiani^bMahshidKharaziha^a

MohammadKarimipour^cdRezaRahbarghazi^ce

https://doi.org/10.1016/j.compositesb.2019.05.074Get rights and content

Abstract

In this research, nanocomposite poly (lactide-coco-glycolide)-Graphene (PLGA-Gr) microribbons were developed for neural tissue engineering. Moreover, the effects of Gr concentration (0, 0.1, 0.5 and 1 wt %) on the chemical and physical structure, mechanical properties, thermal stability and biological properties were evaluated. Our findings proved that incorporation of graphene nanosheets in the PLGA matrix resulted in the formation of aligned groove-shaped roughness on the surface of microribbons. In addition, Gr nanosheets could significantly promote the electrical conductivity and hydrophilicity of PLGA microribbons. In addition, the tensile strength and elastic modulus of the PLGA-Gr microribbons significantly promoted (upon 2 times and more than 3 times, respectively) compared to PLGA microribbons. The results demonstrated enhanced differentiation rate of SH-SY5Y cells to mature neurons on PLGA-Gr compared to PLGA. In summary, our findings discovered that aligned PLGA-Gr microribbons presented appropriate chemical, physical and mechanical properties to promote neuroblastoma cells. It is anticipated that the offered PLGA scaffolds might have great potential to develop a favorable construct for central nerve regeneration. However, further biological in vivo studies are required to assess the role of PLGA-Gr microribbons on the nerve regeneration.

First-in-class New Neuroprotective and Accelerator of Nerve Regeneration Agent Described

With a bit of innovation I could see this as a possibility for stroke rehab. But nothing will be done because we have shit for brains in our fucking failures of stroke associations.
https://www.alphagalileo.org/ViewItem.aspx?ItemId=182036&CultureCode=en

15 December 2017 Universitat Autònoma de Barcelona

Researchers at the Institute of Neuroscience of the UAB (INc-UAB) have discovered a new pharmacological agent, Neuroheal, which helps to maintain motor neurons alive and accelerates nerve regeneration after traumatic injuries to peripheral nerves. There is currently no drug with these effects being applied in clinical practices.

The research was directed by Caty Casas and included the participation of David Romeo and Xavier Navarro, researchers at the INc-UAB and CIBERNED, and Joaquim Forés of the Hospital Clínic Barcelona.

NeuroHeal was designed to imitate and strengthen neuroprotective mechanisms which naturally command neurons to deal with minor injuries successfully.

The pre-clinical trials indicate that oral administration permits long-lasting maintaining the survival of damaged motor neurons, for at least six months, after peripheral nerve root avulsion, even in cases of delayed surgical reimplantation, as it happens in clinical practices. In addition, the treatment accelerates nerve regeneration, drastically reduces denervation-induced muscular atrophy and increases functional contacts between the nerve and affected muscles.

Researchers at the Institute of Neuroscience of the UAB (INc-UAB) have discovered a new pharmacological agent, Neuroheal, which helps to maintain motor neurons alive and accelerates nerve regeneration after traumatic injuries to peripheral nerves. There is currently no drug with these effects being applied in clinical practices.

“There is currently no pharmacological treatment indicated as an adjuvant therapy to maintain alive a neural population after such a severe injury and until surgical intervention, nor is there any to accelerate nerve regeneration. This new drug acts in both senses”, Caty Casas explains.

Injuries to peripheral nerves are consequence of traffic, work and sportive accidents that can cause nerve sectioning or compression. For example, a digital nerve section or injury in someone who works with dangerous machinery, or a high-energy impact to the shoulder in a motorcycle accident can produce nerve root avulsion in the most vulnerable areas, such as lumbar or brachial roots. The surgical reconstitution may be done days after the accident while the patient is stabilized and diagnosed but during that time, disconnected motor neurons due to nerve traction undergo a fatal and irreparable degenerative process.

In addition, after surgical nerve repairing the surviving motor neurons must regenerate their axons through these same nerves until re-establishing a connection with the muscles they controlled to functional recovering the movements. In this case, it is also a race against time. It can take up to two years for patients to regenerate their nervous circuit. The longer it takes to regenerate, the further muscle atrophy becomes,  hindering a good recovery.

NeuroHeal is a Combination of Two Repurposed Drugs

NeuroHeal is a particular dose combination of two repurposed drugs, Acamprosate and Ribavirin, which are currently used to treat other unrelated diseases. Researchers designed it by using artificial intelligence-based computational tools and systems biology approaches to interpret available biological big data and simulate biological responses to thousands of pharmacological combinations. The combination to conform NeuroHeal presented the best profile amongst all of them. This computational study was conducted thanks to the collaboration with Anaxomics Biotech. 

Researchers have already patented the new drug and hope that it will be used in the near future. “The fact that the two compounds in NeuroHeal are already being used and have demonstrated their pharmacokinetics and safety in humans, allow faster implementation for clinical use”, the researcher concludes.

Attached files

• 
  The analysis of the the spinal cord ventral horn and sciatic nerve (diagram indicating the areas) through confocal microscope clearly demonstrates that in the reimplantation model (RE), animals treated with NeuroHeal (NH) present more motor axonal ramifications (positive ChAT, in red) and more regenerated fibers (positive GAP43, in magenta) than untreated animals.

  ---

• Full bibliographic informationRomeo-Guitart D, Forés J, Navarro X, Casas C. Boosted Regeneration and Reduced Denervated Muscle Atrophy by NeuroHeal in a Pre-clinical Model of Lumbar Root Avulsion with Delayed Reimplantation. Scientific Reports 7, Article number: 12028 (2017). DOI:10.1038/s41598-017-11086-3
  https://www.nature.com/articles/s41598-017-11086-3

Study: Seal oil holds potential to help promote nerve regeneration in patients with Type 1 diabetes

We need nerve regeneration in the brain. Would this help us?
http://www.news-medical.net/news/20170613/Study-Seal-oil-holds-potential-to-help-promote-nerve-regeneration-in-patients-with-Type-1-diabetes.aspx

• Download PDF Copy

June 13, 2017

A research team at the Krembil Neuroscience Centre in Toronto has published a paper that suggests seal oil has the potential to help promote nerve regeneration in patients with Type 1 diabetes.
The study found that patients who ingested an omega-3 supplement derived from seal oil twice a day over a 12-month period reported an increase in corneal nerve fiber length. The paper entitled The effects of omega-3 supplementation on neuropathy in type 1 diabetes was published in the June 2017 issue of Neurology, the medical journal of the American Academy of Neurology.
"Nothing like this has been attempted in humans before," says Dr. Evan Lewis, a neurologist and one of the study's authors. "Results from this trial are a very important step towards a clinical therapy for people with diabetic neuropathy."
Diabetic neuropathy is a form of nerve damage caused by diabetes. Symptoms vary from patient to patient but can include tingling, numbness, loss of sensation, a feeling of burning in the hands and feet, constant pain and difficulty walking. There are currently no therapies available for patients that stop or reverse its effects.
"This study is the first to show that targeted nutritional invention can stop and reverse small fibre damage," says Dr. Vera Bril, head of the division of Neurology in the Department of Medicine, and Medical Director of the Ellen Prosserman Centre for Neuromuscular Diseases at UHN, and the study's principal investigator. Other members of the research team included Dr. Bruce Perkins of the Leadership Sinai Centre for Diabetes as well as Dr. Thomas Wolever and Dr. Richard Bazinet, both of the University of Toronto's Department of Nutritional Sciences.

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The study involved 40 patients and focused primarily on corneal nerve fiber length. Located at the front of the eye, the cornea has the highest density of nerves in the body. Damage to these nerves, or loss of corneal nerve fiber length, is considered a biomarker for the progression of Type 1 diabetes. The study did not measure vision recovery.
Researchers investigated the effects of the omega-3 seal oil supplement on nerve structure and found that patients on average experienced a 29 percent increase in corneal nerve fiber length, which is considered to be representative of small nerve fiber regeneration in other parts of the body.
"These findings suggest that use of this supplement may have the potential to have a regenerative effect," says Dr Lewis. "Our goal was to collect enough data to power a randomized clinical trial and we believe this study lays the groundwork for that to happen."
The next step for the research team will be to conduct a phase three randomized controlled trial involving a larger group of participants.
Funding for this study was provided by Diabetes Canada and the Banting and Best Diabetes Centre.
"The initial results of this research are very promising and Diabetes Canada looks forward to continued study on the impact of omega-3s on nerve regeneration," said Dr. Jan Hux, Chief Science Officer at Diabetes Canada.

Source:

http://www.uhn.ca/corporate/News/PressReleases/Pages/research_suggests_seal_oil_could_help_people_Type1_diabetes.aspx

Unlocking the secrets of nerve regeneration

This sounds like a wonderful candidate for an RFP request to researchers and foundation grant applications to pay for this research. But that would assume we had a stroke leader and strategy.
http://m.medicalxpress.com/news/2016-06-secrets-nerve-regeneration.html
Scientists at Hokkaido University, Japan, found that a glutamate receptor GluD2 was responsible for the regeneration of synapses in the cerebellum.
Hokkaido University researchers investigated what makes a specific nerve cell in the brain regenerate when others do not.
Nerves in the central nervous system of adult mammals do not usually regenerate when injured. The granule cell, a nerve cell located in the cerebellum, is different. When its fibres, called parallel fibres, are cut, rapid regeneration ensues and junctions with other neurons called "synapses" are rebuilt. The precise mechanism for this was unclear.
Researchers at Hokkaido University in Japan, together with colleagues from Sapporo Medical University School of Medicine and Niigata University, investigated the effect of a specific glutamate receptor, called GluD2, on parallel fibre regeneration.
GluD2 is a receptor located at the receiving end of the synapse, where the granule cell parallel fibres meet with another nerve cell type called the Purkinje cell, which is also present in the cerebellum. Nerve impulses pass via chemical mediators from one nerve fibre to another through synapses. The granule cell–Purkinje cell synapse, in particular, is where the regeneration occurs.
The GluD2 receptor is involved in maintaining the synapses between granule cell parallel fibres and Purkinje cell nerve fibres. Shutting down the gene that encodes GluD2 results in a severe reduction in these synapses.
The team investigated the effects of cutting parallel fibres in normal mice and in mice that lack the GluD2 receptor. They examined serial sections of the cerebellum under a microscope, and reconstructed three-dimensional images of parallel fibre synapses on Purkinje cells one, seven and 30 days after the incisions were made.
They found that the cut parallel fibres in normal mice underwent three distinct phases. In the first "degeneration phase", the number of parallel fibres and synapses were halved. In the second "hypertrophy phase", the number of parallel fibres remained the same, but the team observed they had undergone thickening and there was enlargement of their terminals. Interestingly, each terminal tended to make multiple synapses as opposed to a single synapse under normal conditions. In the final "remodeling phase", the number of parallel fibres was recovered and the thickening and enlargement that occurred during the hypertrophic phase were dissolved.
The parallel fibres in mice with no GluD2 receptor remained in the degenerative phase. This, the researchers conclude, indicates that GluD2 plays a "pivotal role" in the regenerative rewiring of parallel fibres.
The major obstacle to regeneration in other nerve fibres is the presence of inhibitory factors in the environment of the adult central nervous system, the researchers write in their study published in the Journal of Neuroscience. These inhibitors increase after injury. Further understanding of the role of GluD2 may allow researchers to unlock the regenerative capacity in the central nervous system.

More information: R. Ichikawa et al. GluD2 Endows Parallel Fiber-Purkinje Cell Synapses with a High Regenerative Capacity, Journal of Neuroscience (2016). DOI: 10.1523/JNEUROSCI.0161-16.2016
Provided by: Hokkaido University

3D multi-channel bi-functionalized silk electrospun conduits for peripheral nerve regeneration

I don't see why your doctor isn't using something like this to reroute nerve signals around your dead brain areas. Or does your doctor have the head up the ass? Hasn't read a research paper since medical school? 

3D multi-channel bi-functionalized silk electrospun conduits for peripheral nerve regeneration

• T.M. Dinis^{a, b, ,} ,
• R. Elia^b,
• G. Vidal^a,
• Q. Dermigny^a,
• C. Denoeud^a,
• D.L. Kaplan^b,
• C. Egles^{a, c},
• F. Marin^a

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DOI: 10.1016/j.jmbbm.2014.09.029

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Abstract

Despite technological advances over the past 25 years, a complete recovery from peripheral nerve injuries remains unsatisfactory today. The autograft is still considered the “gold standard” in clinical practice; however, postoperative complications and limited availability of nerve tissue has motivated the development of alternative approaches. Among them, the development of biomimetic nerve graft substitutes is one of the most promising strategies. In this study, multichanneled silk electrospun conduits bi-functionalized with Nerve Growth Factor (NGF) and Ciliary Neurotropic Factor (CNTF) were fabricated to enhance peripheral nerve regeneration. These bioactive guides consisting of longitudinally oriented channels and aligned nanofibers were designed in order to mimic the fascicular architecture and fibrous extracellular matrix found in native nerve. The simple use of the electrospinning technique followed by a manual manipulation to manufacture these conduits provides tailoring of channel number and diameter size to create perineurium-like structures. Functionalization of the silk fibroin nanofiber did not affect its secondary structure and chemical property. ELISA assays showed the absence of growth factors passive release from the functionalized fibers avoiding the topical accumulation of proteins. Additionally, our biomimetic multichanneled functionalized nerve guides displayed a mechanical behavior comparable to that of rat sciatic nerve with an ultimate peak stress of 4.0±0.6 MPa and a corresponding elongation at failure of 156.8±46.7%. Taken together, our results demonstrate for the first time our ability to design and characterize a bi-functionalized nerve conduit consisting of electrospun nanofibers with multichannel oriented and nanofibers aligned for peripheral regeneration. Our bioactive silk tubes thus represent a new and promising technique towards the creation of a biocompatible nerve guidance conduit.

Nerve Regeneration: Everyone does it, but you

Get your doctor studying this to see how to accomplish this prior to massive research studies. Your doctor would like the Nobel prize in medicine wouldn't s/he?
http://loonylabs.org/2014/08/06/nerve-regeneration/

Efficacy of short-term FK506 administration on accelerating nerve regeneration

Not directly related but brain neurons might be able to use this. So ask your researcher about it.  
http://www.naric.com/research/rehab/record.cfm?search=2&type=all&criteria=J64251&phrase=no&rec=119351
Abstract: Study evaluated the efficacy of short-term FK506 treatment in rat models. The immunosuppressant FK506 (tacrolimus) is an agent that has the ability to accelerate the rate of nerve regeneration and functional recovery. However, the toxic and immunosuppressive properties of FK506 make it undesirable for long-term use. Clinically relevant transection and graft models were evaluated, and walking track analysis (WTA) was used to evaluate functional recovery. FK506 was administered for 5 and 10 days post transection injury and 10 and 20 days post graft injury. Both groups involving a short course were compared with the continuous administration group. In the transection model, FK506 was administered for 5 and 10 days postoperatively. WTA demonstrated that 10 days of FK506 administration was sufficient to reduce functional recovery time by 29 percent compared with negative controls. In the graft model, FK506 was administered for 10 and 20 days postoperatively. Short treatment courses of 10 and 20 days reduced recovery time by 15 and 21 percent, respectively, compared with negative controls. Analysis of blood–nerve barrier (BNB) integrity demonstrated that FK506 facilitated early reconstitution of the BNB. The results of this study indicate that short-term FK506 delivery following nerve injury imparts a significant therapeutic effect.

Efficacy of Short-Term FK506 Administration on Accelerating Nerve Regeneration

I'm not sure  if this is useful for us or not but nerve regeneration sounds like a useful thing for stroke rehab.
 http://nnr.sagepub.com/content/26/6/570.abstract?etoc

Abstract

Background. The slow rate of nerve regeneration following injury can cause extended muscle denervation, leading to irreversible muscle atrophy, fibrosis, and destruction of motor endplates. The immunosuppressant FK506 (tacrolimus) has been shown to accelerate the rate of nerve regeneration and functional recovery. However, the toxic and immunosuppressive properties of FK506 make it undesirable for long-term use. Objective. To take advantage of the regeneration-enhancing effects of FK506 but avoid the potential adverse effects of long-term administration, the current study evaluates and quantifies the efficacy of short-term FK506 treatment in rat models. Methods. Clinically relevant transection and graft models were evaluated, and walking track analysis (WTA) was used to evaluate functional recovery. FK506 was administered for 5 and 10 days post transection injury and 10 and 20 days post graft injury. Both groups involving a short course were compared with the continuous administration group. Results. In the transection model, FK506 was administered for 5 and 10 days postoperatively. WTA demonstrated that 10 days of FK506 administration was sufficient to reduce functional recovery time by 29% compared with negative controls. In the graft model, FK506 was administered for 10 and 20 days postoperatively. Short treatment courses of 10 and 20 days reduced recovery time by 15% and 21%, respectively, compared with negative controls. Analysis of blood–nerve barrier (BNB) integrity demonstrated that FK506 facilitated early reconstitution of the BNB. Conclusions. The results of this study indicate that short-term FK506 delivery following nerve injury imparts a significant therapeutic effect.