Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label Thymosin beta 4. Show all posts
Showing posts with label Thymosin beta 4. Show all posts

Wednesday, March 4, 2015

Researchers propose novel new treatment of stroke and other neurological diseases - Thymosin beta-4

What is your doctor doing to start up a clinical trial with this? Does your doctor not have any goals and objectives to improve stroke rehab through research? If not, call your hospital president and ask why they are so incompetent that they don't set useable goals for their doctors to help their patients. 

Researchers propose novel new treatment of stroke and other neurological diseases - Thymosin beta-4


Medicine should reconsider how it treats stroke and other neurological disorders, focusing on the intrinsic abilities of the brain and nervous system to heal themselves rather than the "modest" benefits of clot-busting drugs and other neuroprotective treatments.
Michael Chopp, Ph,D., internationally renowned stroke researcher and scientific director of the Neuroscience Institute at Henry Ford Hospital, and Zhenggang Zhang,M.D., Ph.D., senior scientist at Henry Ford's Department of Neurology, make their case for the change in treatment strategy in an editorial published online in Expert Opinion on Biological Therapy.
The co-authors argue that pharmacologically enhancing the brain's own restorative abilities could benefit not only stroke patients, but those suffering other neurological damage or disease including (TBI), multiple sclerosis (MS) and - that afflicts the elderly, chemotherapy patients and especially diabetics.
Central to their proposal is a new pharmacological agent developed by Dr. Chopp and his colleagues, a synthetic version of a peptide that occurs naturally in humans and other mammals called Thymosin beta-4.
"Pioneering animal studies at Henry Ford have shown Thymosin beta-4 is highly effective for the treatment of in part by increasing the formation of protective myelin around nerve fibers in the central and peripheral nervous systems," says Dr. Chopp.
In their editorial, the authors first detail the limited effectiveness of current standard drug therapy, using (tPA), more commonly known as a "clot buster," to treat neurological disease.
Offering stroke as an example, they cite research showing that only about 5 percent of patients receive tPA, and of those only about 30 percent show significant improvements.
Similar conditions exist for nerve injury after TBI, MS and peripheral neuropathy, the authors write, and for those patients "there is a paucity of therapeutic options."
Among tPA's limitations is that it must be administered within a very short time after stroke to prevent "cascades" of irreversible cell damage.
In contrast, "restorative therapies" such as dosing with Thymosin beta-4 "may be applied well after the onset of injury or the onset of clinical symptoms for degenerative diseases" including and others.
Says Dr. Chopp: "Rather than focusing on destroying clots or other lesions leading to nerve damage, restorative therapies are designed to 'remodel' or rebuild the by stimulating self-healing processes that already exist in the brain, spinal cord and the peripheral nerves connected to them."
"It is therefore time to reconsider how we think about treating neural injury and disease," the authors contend.

Monday, October 15, 2012

Neuroprotective and neurorestorative effects of thymosin β4 treatment following experimental traumatic brain injury

So if there is no evidence based therapy for TBI patients what the hell do you do with them? Get your doctor to get the article, the abstract is worthless.
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2012.06683.x/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false
Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis, and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta 4 (Tβ4) is the major G-actin–sequestering molecule in eukaryotic cells. In addition, Tβ4 has other properties including antiapoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe Tβ4 as a neuroprotective and neurorestorative candidate for treatment of TBI.

Wednesday, February 15, 2012

Researchers Show TB4 Provides Both Neuroprotection and Neurorestoration after Traumatic Brain Injury

Whats good for TBI should be good enough to test for stroke.
http://www.businesswire.com/news/home/20120215005441/en/Researchers-Show-TB4-Neuroprotection-Neurorestoration-Traumatic-Brain
RegeneRx Biopharmaceuticals, Inc. (OTC Bulletin Board: RGRX) (“the Company” or “RegeneRx”) today announced that researchers have shown that Thymosin beta 4 (Tβ4) “provides both neuroprotection and neurorestoration after traumatic brain injury (TBI), indicating that Tβ4 has promising therapeutic potential in patients with TBI.”

“provides both neuroprotection and neurorestoration after traumatic brain injury (TBI), indicating that Tβ4 has promising therapeutic potential in patients with TBI.”

The aims of the study were to test if Tβ4 treatment initiated 6 hours after traumatic brain injury in rats reduces brain damage and improves functional recovery. The rats were divided into two treatment groups and one placebo group. Tβ4 or placebo was systemically administered 6, 24, and 48 hours after injury. Compared with the placebo group, Tβ4 treatment initiated 6 hours post-injury statistically significant improvement of sensorimotor functional recovery and spatial learning, reduced cortical lesion volume and hippocampal cell loss, and enhanced cell proliferation and neurogenesis in the injured brain tissue. The high dose of Tβ4 showed better beneficial effects compared with the low dose treatment.

The research was conducted by Xiong Y, Zhang Y, Mahmood A, Meng Y, Zhang ZG, Morris DC, Chopp MJ in the Department of Neurosurgery at the Henry Ford Hospital System (HFHS) in Detroit, Michigan pursuant to a material transfer agreement between the hospital and RegeneRx Biopharmaceuticals, Inc. and published in Neurosurg., 2012 Feb 10. [Epub ahead of print].

"This preclinical study on the use of Thymosin beta 4 for the treatment of traumatic brain injury adds to the growing body of literature demonstrating the use of Tβ4 in neurological injury. The collective evidence of the neurorestorative properties of Tβ4 in animal models of multiple sclerosis, stroke and traumatic brain injury are compelling and we look forward to evaluating this drug in clinical trials," stated Dr. Dan Morris, Senior Staff Physician, Department of Emergency Medicine at HFHS and one of the investigators in study.

About RegeneRx Biopharmaceuticals, Inc. (www.regenerx.com)

RegeneRx is focused on the development of a novel therapeutic peptide, Thymosin beta 4, or Tβ4, for tissue and organ protection, repair and regeneration. RegeneRx currently has three drug candidates in clinical development and has an extensive worldwide patent portfolio covering its products.

RGN-259 is a sterile, preservative-free topical eye drop for ophthalmic indications. Based on a recently completed Phase 2 clinical trial in patients with dry eye syndrome, RGN-259 was found to show statistically significant improvements in several signs and symptoms of dry eye, as well as positive trends in other outcome measures. We believe the positive results of this Phase 2 exploratory trial reflect RGN-259’s reported mechanisms of action and provide RegeneRx with FDA-approvable endpoints to be targeted in future clinical trials.

RGN-352 is an injectable formulation to treat cardiovascular and central nervous system diseases, as well as other medical indications. RegeneRx is initially targeting RGN-352 for the treatment of patients who have suffered an acute myocardial infarction, or heart attack. Recent pre-clinical efficacy data suggests that RGN-352 may also benefit patients with multiple sclerosis, stroke and traumatic brain injury. RegeneRx has successfully completed a Phase 1 clinical trial with RGN-352 in which the drug candidate was found to be safe and well-tolerated. In 2010, RegeneRx received a $3 million, three-year development grant from the NIH to support the company's acute myocardial infarction program.

Monday, February 13, 2012

Neuroprotective and neurorestorative effects of thymosin β4 treatment initiated 6 hours after traumatic brain injury in rats Laboratory investigation

6 hours later this can be given. So what specifically is this helping with? Ischemic stroke has the cascade of death via glutamate poisoning, excitotoxicity, non-opening of cpilaries. The researchers should find out specifically what this drug is correcting. Further research needed in stroke survivors which will never occur; NO leadership!

Neuroprotective and neurorestorative effects of thymosin β4 treatment initiated 6 hours after traumatic brain injury in rats Laboratory investigation


Abstract

Object

Thymosin β4 (Tβ4) is a regenerative multifunctional peptide. The aim of this study was to test the hypothesis that Tβ4 treatment initiated 6 hours postinjury reduces brain damage and improves functional recovery in rats subjected to traumatic brain injury (TBI).

Methods

Traumatic brain injury was induced by controlled cortical impact over the left parietal cortex in young adult male Wistar rats. The rats were randomly divided into the following groups: 1) saline group (n = 7); 2) 6 mg/kg Tβ4 group (n = 8); and 3) 30 mg/kg Tβ4 group (n = 8). Thymosin β4 or saline was administered intraperitoneally starting at 6 hours postinjury and again at 24 and 48 hours. An additional group of 6 animals underwent surgery without TBI (sham-injury group). Sensorimotor function and spatial learning were assessed using the modified Neurological Severity Score and the Morris water maze test, respectively. Animals were euthanized 35 days after injury, and brain sections were processed to assess lesion volume, hippocampal cell loss, cell proliferation, and neurogenesis after Tβ4 treatment.

Results

Compared with saline administration, Tβ4 treatment initiated 6 hours postinjury significantly improved sensorimotor functional recovery and spatial learning, reduced cortical lesion volume and hippocampal cell loss, and enhanced cell proliferation and neurogenesis in the injured hippocampus. The high dose of Tβ4 showed better beneficial effects compared with the low-dose treatment.

Conclusions

Thymosin β4 treatment initiated 6 hours postinjury provides both neuroprotection and neurorestoration after TBI, indicating that Tβ4 has promising therapeutic potential in patients with TBI. These data warrant further investigation of the optimal dose and therapeutic window of Tβ4 treatment for TBI and the associated underlying mechanisms.