MagLab MRI machine provides in-depth analysis of strokes
New research conducted at the Florida State University-based National High Magnetic Field Laboratory has revealed a new, innovative way to classify the severity of a stroke, aid in diagnosis and evaluate potential treatments.
“Stroke affects millions of adults and children worldwide,” said Sam Grant, MagLab researcher and associate professor of chemical and biomedical engineering at the FAMU-FSU College of Engineering. “This research offers a new technique for the chemical analysis of metabolites during stroke and a means of evaluating dynamic changes in cell processes and size in living tissue.”
The research is detailed in two papers, “Metabolic properties in stroked rats revealed by relaxation-enhanced magnetic resonance spectroscopy at ultrahigh fields,” in Nature Communications and “Metabolic T1 dynamics and longitudinal relaxation enhancement in vivo at ultrahigh magnetic fields on ischemia” in the Journal of Cerebral Blood Flow and Metabolism.
The new technique is a way of narrowly applying energy to the metabolites of a specimen exposed to a very high magnetic field. Metabolites are the biological compounds used in the chemical process of breaking down food or other chemicals into energy and producing new materials.
By selectively “exciting” these metabolites and analyzing their distribution and confinement in brain tissue, the research team can investigate the metabolic microenvironment and tell whether cells were shrinking or expanding, a critical tool to understanding the severity of stroke, Grant said.
That information could help medical professionals better treat patients.
“Strokes cause an interruption of blood and oxygen to flow to the brain,” explained Jens Rosenberg, another MagLab researcher and one of Grant’s co-authors. “Through this research, we can see how neurons and other neural cells respond to the disruption of blood flow after stroke and use that information to better understand the full impacts of stroke.”
The MagLab’s flagship 900 MHz Ultra Widebore NMR magnet system was a critical component to the research. Utilizing this powerful magnet, the research team, which included scientists from the Champaulimod Center in Portugal and the Weizmann Institute of Science in Israel, were able to acquire localized chemical signatures of metabolites from 125-microliter volumes within the brain with high sensitivity and fidelity in six seconds.
Typical MRIs at hospitals or doctor’s offices measure around 1.5 – 3 tesla (the unit of magnetic field strength), while the 900 MHz measures a whopping 21.1 tesla, providing at least seven times the sensitivity.
“This very high field coupled with the RF pulse sequence design by our collaborators and homebuilt RF probes offer a unique non-invasive way of evaluating stroke evolution and potential treatments,” Rosenberg said.
The team also sees exciting possibilities to use this technique to further investigate debilitating diseases.
“By evaluating spectral regions previously undetectable, we hope to fingerprint certain diseases, like ischemic stroke, so that we can identify new characteristics that are specific to pathological conditions at the metabolic level in vivo,” Grant said. “There is a lot of work to be done to identify these dynamic changes and decide when and how our treatments can be most effective.”
Further research on metabolites using this technique could also be used for analysis of neurological disorders such as dementia, schizophrenia, Lou Gehrig’s, Parkinson’s, Alzheimer’s and Huntington’s diseases.
(Image credit)
Filed under stroke metabolites MRS brain tissue neurological disorders neuroscience science
Mechanism that repairs brain after stroke discovered
A previously unknown mechanism through which the brain produces new nerve cells after a stroke has been discovered at Lund University and Karolinska Institutet in Sweden. The findings have been published in the journal
Science.
A stroke is caused by a blood clot blocking a blood vessel in the brain, which leads to an interruption of blood flow and therefore a shortage of oxygen. Many nerve cells die, resulting in motor, sensory and cognitive problems.
The researchers have shown that following an induced stroke in mice, support cells, so-called astrocytes, start to form nerve cells in the injured part of the brain. Using genetic methods to map the fate of the cells, the scientists could demonstrate that astrocytes in this area formed immature nerve cells, which then developed into mature nerve cells.
”This is the first time that astrocytes have been shown to have the capacity to start a process that leads to the generation of new nerve cells after a stroke”, says Zaal Kokaia, Professor of Experimental Medical Research at Lund University.
The scientists could also identify the signalling mechanism that regulates the conversion of the astrocytes to nerve cells. In a healthy brain, this signalling mechanism is active and inhibits the conversion, and, consequently, the astrocytes do not generate nerve cells. Following a stroke, the signalling mechanism is suppressed and astrocytes can start the process of generating new cells.
”Interestingly, even when we blocked the signalling mechanism in mice not subjected to a stroke, the astrocytes formed new nerve cells”, says Zaal Kokaia.
“This indicates that it is not only a stroke that can activate the latent process in astrocytes. Therefore, the mechanism is a potentially useful target for the production of new nerve cells, when replacing dead cells following other brain diseases or damage.”
The new nerve cells were found to form specialized contacts with other cells. It remains to be shown whether the nerve cells are functional and to what extent they contribute to the spontaneous recovery that is observed in a majority of experimental animals and patients after a stroke.
A decade ago, Kokaia’s and Lindvall’s research group was the first to show that stroke leads to the formation of new nerve cells from the adult brain’s own neural stem cells. The new findings further underscore that when the adult brain suffers a major blow such as a stroke, it makes a strong effort to repair itself using a variety of mechanisms.
The major advancement with the new study is that it demonstrates for the first time that self-repair in the adult brain involves astrocytes entering a process by which they change their identity to nerve cells.
”One of the major tasks now is to explore whether astrocytes are also converted to neurons in the human brain following damage or disease. Interestingly, it is known that in the healthy human brain, new nerve cells are formed in the striatum. The new data raise the possibility that some of these nerve cells derive from local astrocytes. If the new mechanism also operates in the human brain and can be potentiated, this could become of clinical importance not only for stroke patients, but also for replacing neurons which have died, thus restoring function in patients with other disorders such as Parkinson’s disease and Huntington’s disease”, says Olle Lindvall, Senior Professor of Neurology.
Filed under stroke nerve cells astrocytes neurogenesis neuroscience science
A mini-stroke may not cause lasting physical damage, but it could increase your risk of developing post-traumatic stress disorder (PTSD), a small, new study suggests.
Almost one-third of patients who suffered a mini-stroke — known as a transient ischemic attack (TIA) — developed symptoms of PTSD, including depression, anxiety and reduced quality of life, the researchers said.
"At the moment, a TIA is seen by doctors as a fairly benign disorder," said study co-author Kathrin Utz, a researcher in the department of neurology at the University of Erlangen-Nuremberg in Germany.
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Filed under stroke PTSD transient ischemic attack depression anxiety neuroscience science
Identification of a protein that may increase the currently short therapeutic window in stroke
A new study published in the prestigious publication The EMBO Journal shows that the mitochondrial protein Mfn2 may be a future therapeutic target for neuronal death reduction in the late phases of an ischemic stroke. The study has been coordinated by Dr Francesc Soriano, Ramón y Cajal researcher at the Department of Cell Biology of the University of Barcelona (UB) and member of the Research Group Celltec UB. The study, funded by the Fundació La Marató de TV3, is part of the PhD thesis developed by Àlex Martorell Riera (UB), first author of the article. Experts Antonio Zorzano and Manuel Palacín, from the Department of Biochemistry and Molecular Biology of UB and the Institute for Research in Biomedicine (IRB Barcelona), and Jesús Pérez Clausell and Manuel Reina, from the Department of Cell Biology of UB, also collaborated in the study.
When blood flow is blocked in the brain
According to the World Health Organization (WHO), strokes are the second leading cause of death in the world. A stroke occurs when a blood vessel is blocked interrupting blood flow in the brain. Ictus damage is progressive: it begins some minutes after the attack. Recommended treatment consists in restoring blood flow to the brain, but it must be done during the first four hours after the stroke.
According to researcher Francesc Soriano, “one of the main causes of brain death in ictus events is glutamate increase; glutamate is the main excitatory neurotransmitter in the central nervous system. Glutamate extracellular concentrations remain low due to the activity of membrane transporters, which require energy to work”.
When blood flow is blocked, energy levels are reduced in the affected area. This phenomenon leads glutamate transporters to work inversely, so glutamate is expelled to the extracellular space. Glutamate activates its receptors —particularly, the N-methyl-D-aspartate receptor (NMDA)— on neurons’ surface, a process that triggers an excessive flux of calcium, the activation of a series of reactions and neuronal death, in a process known as excitotoxicity. “Many of these excitotoxic cascades —points out Soriano— converge on the mitochondrion, an organelle which plays a major role not only in energy production, but also in apoptosis”.
New therapeutic strategies against ischemic ictus
Specifically, Mfn2 is a mitochondrial protein involved in the regulation of organelles’ morphology and function. The team led by Dr Francesc Soriano has just discovered that the reduction in Mfn2 protein levels occurs four hours after the initiation of the excitotoxic process in in vitro and in vivo animal models.
In vivo experiments proved that if Mfn2 reduction is stopped, delayed excitotoxic cell death is blocked. The research team from the Department of Cell Biology of UB found that the Mfn2 reduction is triggered by a genetic transcription mechanism (DNA is transcribed into RNA molecules). UB experts also discovered that MEF2 is the transcription factor involved in this process. Authors affirm that these findings are essential to find a strategy to reverse Mfn2 reduction.
Currently, the team led by Dr Francesc Soriano are researching on brain damage in excitotoxic conditions in animal models where the gene Mfn2 has been removed. The main objective is to design therapeutic strategic in order to reduce damage.
Filed under stroke Mfn2 glutamate excitotoxicity cell death neuroscience science
Patients who were treated with a statin in the hospital after suffering from a hemorrhagic stroke were significantly more likely to survive than those who were not, according to a study published today in JAMA Neurology. This study was conducted by the same researchers who recently discovered that the use of cholesterol-lowering statins can improve survival in victims of ischemic stroke.
Ischemic stroke is caused by a constriction or obstruction of a blood vessel that blocks blood from reaching areas of the brain, while hemorrhagic stroke, also known as intracerebral hemorrhage, is bleeding in the brain.
“Some previous research has suggested that treating patients with statins after they suffer hemorrhagic stroke may increase their long-term risk of continued bleeding,” said lead author Alexander Flint, MD, PhD, of the Kaiser Permanente Department of Neuroscience in Redwood City, Calif. “Yet the findings of our study suggest that stopping statin treatments for these patients may carry substantial risks.”
The study included 3,481 individuals who were admitted to any of 20 Kaiser Permanente hospitals in Northern California with a hemorrhagic stroke over a 10-year period. Researchers looked at patient survival and discharge 30 days after the stroke.
Patients treated with a statin while in the hospital were more likely to be alive 30 days after suffering a hemorrhagic stroke than those who were not treated with a statin — 81.6 percent versus 61.3 percent. Patients treated with a statin while in the hospital were also more likely to be discharged to home or an acute rehabilitation facility than those who were not — 51.1 percent compared to 35.0 percent.
Patients whose statin therapy was discontinued — that is, patients taking a statin as an outpatient prior to experiencing a hemorrhagic stroke who did not receive a statin as an inpatient — had a mortality rate of 57.8 percent compared with a mortality rate of 18.9 percent for patients using a statin before and during hospitalization.
The researchers concluded that statin use is strongly associated with improved outcomes after hemorrhagic stroke, and that discontinuing statin use is strongly associated with worsened outcomes after hemorrhagic stroke.
(Source: share.kaiserpermanente.org)
Filed under stroke statin intracerebral hemorrhage neuroscience science
Increased risk of stroke in people with cognitive impairment
People with cognitive impairment are significantly more likely to have a stroke, with a 39% increased risk, than people with normal cognitive function, according to a new study published in CMAJ (Canadian Medical Association Journal).
"Given the projected substantial rise in the number of older people around the world, prevalence rates of cognitive impairment and stroke are expected to soar over the next several decades, especially in high-income countries," writes Dr. Bruce Ovbiagele, Chair of the Department of Neurology, Medical University of South Carolina, Charleston, South Carolina, with coauthors.
Cognitive impairment and stroke are major contributors to disability, and stroke is the second leading cause of death world-wide. Although stroke is linked to the development and worsening of cognitive impairment, it is not known whether the reverse is true. Previous studies that have looked at the link between cognitive impairment and subsequent stroke have been inconsistent in their findings.
The study in CMAJ, by researchers in the United States, Taiwan and South Korea, analyzed data from 18 studies of 121 879 people with cognitive impairment, of whom 7799 later had strokes. Most of the included studies were conducted in North America or Europe.
The researchers observed a significantly higher rate of stroke in people with cognitive impairment than in people with normal cognitive function.
"We found that the risk of future stroke was 39% higher among patients with cognitive impairment at baseline than among those with normal cognitive function at baseline," write the authors. "This risk increased to 64% when a broadly adopted definition of cognitive impairment was used."
Blockage of blood vessels in the brain (brain infarcts), atherosclerosis, inflammation and other vascular conditions are associated with a higher risk of stroke and cognitive impairment and may contribute to the increased risk.
"Cognitive impairment should be more broadly recognized as a possible early clinical manifestation of cerebral infarction, so that timely management of vascular risk factors can be instituted to potentially prevent future stroke events and to avoid further deterioration of cognitive health," conclude the authors.
Filed under stroke cognitive impairment cognitive function neuroscience science
A new study suggests that colds and other minor infections may temporarily increase stroke risk in children. The study found that the risk of stroke was increased only within a three-day period between a child’s visit to the doctor for signs of infection and having the stroke.
The study was led by researchers at UCSF Benioff Children’s Hospital San Francisco in collaboration with the Kaiser Permanente Division of Research.
“These findings suggest that infection has a powerful but short-lived effect on stroke risk,” said senior author Heather Fullerton, MD, a pediatric vascular neurologist and medical director of the Pediatric Brain Center at UCSF Benioff Children’s Hospital San Francisco.
“We’ve seen this increase in stroke risk from infection in adults, but until now, an association has not been studied in children.”
Strokes are extremely rare in children, affecting just five out of 100,000 kids per year. “The infections are acting as a trigger in children who are likely predisposed to stroke,” said Fullerton. “Infection prevention is key for kids who are at risk for stroke, and we should make sure those kids are getting vaccinated against whatever infections – such as flu - that they can.”
The study appears in the August 20, 2014, online issue of Neurology.
In the study, researchers reviewed a Kaiser Permanente database of 2.5 million children and identified 102 children who had an ischemic stroke – a stroke that occurs as a result of an obstruction within a blood vessel supplying blood to the brain - without a major infection such as meningitis or sepsis. The researchers then compared them with 306 children without stroke. Medical records for the group of children who had a stroke were reviewed for minor infections up to two years before their strokes.
The study found that the risk of stroke was increased only within a three-day time frame, which the researchers say represents a period of acute inflammation. As an infection resolves, the inflammation decreases, as does the stroke risk.
A total of 10 of the 102 children who had a stroke had a doctor visit for an infection within three days of the stroke, or 9.8 percent, while only two of the 306 control participants, or 0.7 percent, had an infection during the same time period.
The children who had strokes were 12 times more likely to have had an infection within the previous three days than the children without strokes. The total number of infections over a two-year period was not associated with increased stroke risk. About 80 percent of the minor infections identified by the researchers were upper respiratory.
“It’s important the public does the things we can to prevent infection, like vaccinations, good hand washing and covering your mouth when you sneeze in order to protect all children, but it’s especially important to help prevent stroke in someone who is otherwise predisposed,” said Fullerton.
(Source: ucsf.edu)
Filed under children stroke arterial ischemic stroke infections neuroscience science
When investigators at the Stanford University School of Medicine applied light-driven stimulation to nerve cells in the brains of mice that had suffered strokes several days earlier, the mice showed significantly greater recovery in motor ability than mice that had experienced strokes but whose brains weren’t stimulated.
These findings, published online Aug. 18 in Proceedings of the National Academy of Sciences, could help identify important brain circuits involved in stroke recovery and usher in new clinical therapies for stroke, including the placement of electrical brain-stimulating devices similar to those used for treating Parkinson’s disease, chronic pain and epilepsy. The findings also highlight the neuroscientific strides made possible by a powerful research technique known as optogenetics.
Stroke, with 15 million new victims per year worldwide, is the planet’s second-largest cause of death, according to Gary Steinberg, MD, PhD, professor and chair of neurosurgery and the study’s senior author. In the United States, stroke is the largest single cause of neurologic disability, accounting for about 800,000 new cases each year — more than one per minute — and exacting an annual tab of about $75 billion in medical costs and lost productivity.
The only approved drug for stroke in the United States is an injectable medication called tissue plasminogen activator, or tPA. If infused within a few hours of the stroke, tPA can limit the extent of stroke damage. But no more than 5 percent of patients actually benefit from it, largely because by the time they arrive at a medical center the damage is already done. No pharmacological therapy has been shown to enhance recovery from stroke from that point on.
Enhancing recovery
But in this study — the first to use a light-driven stimulation technology called optogenetics to enhance stroke recovery in mice — the stimulations promoted recovery even when initiated five days after stroke occurred.
“In this study, we found that direct stimulation of a particular set of nerve cells in the brain — nerve cells in the motor cortex — was able to substantially enhance recovery,” said Steinberg, the Bernard and Ronni Lacroute-William Randolph Hearst Professor in Neurosurgery and Neurosciences.
About seven of every eight strokes are ischemic: They occur when a blood clot cuts off oxygen flow to one or another part of the brain, destroying tissue and leaving weakness, paralysis and sensory, cognitive and speech deficits in its wake. While some degree of recovery is possible — this varies greatly among patients depending on many factors, notably age — it’s seldom complete, and typically grinds to a halt by three months after the stroke has occurred.
Animal studies have indicated that electrical stimulation of the brain can improve recovery from stroke. However, “existing brain-stimulation techniques activate all cell types in the stimulation area, which not only makes it difficult to study but can cause unwanted side effects,” said the study’s lead author, Michelle Cheng, PhD, a research associate in Steinberg’s lab.
For the new study, the Stanford investigators deployed optogenetics, a technology pioneered by co-author Karl Deisseroth, MD, PhD, professor of psychiatry and behavioral sciences and of bioengineering. Optogenetics involves expressing a light-sensitive protein in specifically targeted brain cells. Upon exposure to light of the right wavelength, this light-sensitive protein is activated and causes the cell to fire.
Steinberg’s team selectively expressed this protein in the brain’s primary motor cortex, which is involved in regulating motor functions. Nerve cells within this cortical layer send outputs to many other brain regions, including its counterpart in the brain’s opposite hemisphere. Using an optical fiber implanted in that region, the researchers were able to stimulate the primary motor cortex near where the stroke had occurred, and then monitor biochemical changes and blood flow there as well as in other brain areas with which this region was in communication. “We wanted to find out whether activating these nerve cells alone can contribute to recovery,” Steinberg said.
Walking farther
By several behavioral, blood flow and biochemical measures, the answer two weeks later was a strong yes. On one test of motor coordination, balance and muscular strength, the mice had to walk the length of a horizontal beam rotating on its axis, like a rotisserie spit. Stroke-impaired mice whose primary motor cortex was optogenetically stimulated did significantly better in how far they could walk along the beam without falling off and in the speed of their transit, compared with their unstimulated counterparts.
The same treatment, applied to mice that had not suffered a stroke but whose brains had been similarly genetically altered and then stimulated just as stroke-affected mice’s brains were, had no effect on either the distance they travelled along the rotating beam before falling off or how fast they walked. This suggests it was stimulation-induced repair of stroke damage, not the stimulation itself, yielding the improved motor ability.
Stroke-affected mice whose brains were optogenetically stimulated also regained substantially more of their lost weight than unstimulated, stroke-affected mice. Furthermore, stimulated post-stroke mice showed enhanced blood flow in their brain compared with unstimulated post-stroke mice.
In addition, substances called growth factors, produced naturally in the brain, were more abundant in key regions on both sides of the brain in optogenetically stimulated, stroke-affected mice than in their unstimulated counterparts. Likewise, certain brain regions of these optogenetically stimulated, post-stroke mice showed increased levels of proteins associated with heightened ability of nerve cells to alter their structural features in response to experience — for example, practice and learning. (Optogenetic stimulation of the brains of non-stroke mice produced no such effects.)
Steinberg said his lab is following up to determine whether the improvement is sustained in the long term. “We’re also looking to see if optogenetically stimulating other brain regions after a stroke might be equally or more effective,” he said. “The goal is to identify the precise circuits that would be most amenable to interventions in the human brain, post-stroke, so that we can take this approach into clinical trials.”
(Source: med.stanford.edu)
Filed under stroke optogenetics channelrhodopsin motor cortex animal model neuroscience science
Kessler stroke researchers and colleagues have identified an association between over-optimistic estimation of one’s own ability to take medications accurately, and memory loss among stroke survivors. Results indicate that assessing patients for their ability to estimate medication skills accurately may predict memory disorder. The article, “Stroke survivors over-estimate their medication self-administration ability (MSA), predicting memory loss,” was epublished ahead of print on May 28 by Brain Injury. The authors are AM Barrett, MD, and J Masmela of Kessler Foundation, Elizabeth E Galletta of Hunter College, Jun Zhang of St. Charles Hospital, Port Jefferson, NY, and Uri Adler, MD, of Kessler Institute for Rehabilitation.
Researchers compared 24 stroke survivors with 17 controls, using the Hopkins Medication Schedule to assess MSA, the Geriatric Depression Scale to assess mood, and the Hopkins Verbal Test and Mini-Mental State Examination to assess memory. Results showed that stroke survivors over-estimated their MSA in comparison to controls. Over-estimation of MSA correlated strongly with verbal memory deficit.
Strategies that enhance adherence to medication are a public health priority. “Few studies, however, have looked at cognitive factors that may interfere with MSA,” commented Dr. Barrett. “While some stroke survivors have obvious cognitive deficits, many people are not aware that stroke survivors can be intelligent and high functioning, but still have trouble with thinking that can cause errors in medication self-management. These individuals may not realize their own deficits, a condition called cognitive anosognosia. Screening stroke survivors for MSA may be a useful approach to identifying memory deficits that hinder rehabilitation and community participation and contribute to poor outcomes.”
Larger studies of left and right stroke survivors need to be conducted in the community and rehabilitation settings in order to determine the underlying mechanisms for both over-estimation and under-estimation of self-performance.
(Source: kesslerfoundation.org)
Filed under stroke rehabilitation memory anosognosia neuroscience science
(Image caption: MRI scans showing brain damage in the stroke patients before treatment. Source: Stem Cells Translational Medicine.)
Stem cells show promise for stroke in pilot study
A stroke therapy using stem cells extracted from patients’ bone marrow has shown promising results in the first trial of its kind in humans.
Five patients received the treatment in a pilot study conducted by doctors at Imperial College Healthcare NHS Trust and scientists at Imperial College London.
The therapy was found to be safe, and all the patients showed improvements in clinical measures of disability.
The findings are published in the journal Stem Cells Translational Medicine. It is the first UK human trial of a stem cell treatment for acute stroke to be published.
The therapy uses a type of cell called CD34+ cells, a set of stem cells in the bone marrow that give rise to blood cells and blood vessel lining cells. Previous research has shown that treatment using these cells can significantly improve recovery from stroke in animals. Rather than developing into brain cells themselves, the cells are thought to release chemicals that trigger the growth of new brain tissue and new blood vessels in the area damaged by stroke.
The patients were treated within seven days of a severe stroke, in contrast to several other stem cell trials, most of which have treated patients after six months or later. The Imperial researchers believe early treatment may improve the chances of a better recovery.
A bone marrow sample was taken from each patient. The CD34+ cells were isolated from the sample and then infused into an artery that supplies the brain. No previous trial has selectively used CD34+ cells, so early after the stroke, until now.
Although the trial was mainly designed to assess the safety and tolerability of the treatment, the patients all showed improvements in their condition in clinical tests over a six-month follow-up period.
Four out of five patients had the most severe type of stroke: only four per cent of people who experience this kind of stroke are expected to be alive and independent six months later. In the trial, all four of these patients were alive and three were independent after six months.
Dr Soma Banerjee, a lead author and Consultant in Stroke Medicine at Imperial College Healthcare NHS Trust, said: “This study showed that the treatment appears to be safe and that it’s feasible to treat patients early when they might be more likely to benefit. The improvements we saw in these patients are very encouraging, but it’s too early to draw definitive conclusions about the effectiveness of the therapy. We need to do more tests to work out the best dose and timescale for treatment before starting larger trials.”
Over 150,000 people have a stroke in England every year. Survivors can be affected by a wide range of mental and physical symptoms, and many never recover their independence.
Stem cell therapy is seen as an exciting new potential avenue of treatment for stroke, but its exact role is yet to be clearly defined.
Dr Paul Bentley, also a lead author of the study, from the Department of Medicine at Imperial College London, said: “This is the first trial to isolate stem cells from human bone marrow and inject them directly into the damaged brain area using keyhole techniques. Our group are currently looking at new brain scanning techniques to monitor the effects of cells once they have been injected.”
Professor Nagy Habib, Principal Investigator of the study, from the Department of Surgery and Cancer at Imperial College London, said: “These are early but exciting data worth pursuing. Scientific evidence from our lab further supports the clinical findings and our aim is to develop a drug, based on the factors secreted by stem cells, that could be stored in the hospital pharmacy so that it is administered to the patient immediately following the diagnosis of stroke in the emergency room. This may diminish the minimum time to therapy and therefore optimise outcome. Now the hard work starts to raise funds for this exciting research.”
Filed under stem cells stroke CD34+ brain tissue medicine neuroscience science
