Research suggests neural stem cells may regenerate after anti-cancer treatment

Main Category: Cancer / Oncology
Also Included In: Neurology / Neuroscience;  Radiology / Nuclear Medicine
Article Date: 14 Aug 2013 - 1:00 PDT Current ratings for:
Research suggests neural stem cells may regenerate after anti-cancer treatment

Scientists have long believed that healthy brain cells, once damaged by radiation designed to kill brain tumors, cannot regenerate. But new Johns Hopkins research in mice suggests that neural stem cells, the body's source of new brain cells, are resistant to radiation, and can be roused from a hibernation-like state to reproduce and generate new cells able to migrate, replace injured cells and potentially restore lost function.

"Despite being hit hard by radiation, it turns out that neural stem cells are like the special forces, on standby waiting to be activated," says Alfredo Quiñones-Hinojosa, M.D., a professor of neurosurgery at the Johns Hopkins University School of Medicine and leader of a study described online in the journal Stem Cells. "Now we might figure out how to unleash the potential of these stem cells to repair human brain damage."

The findings, Quiñones-Hinojosa adds, may have implications not only for brain cancer patients, but also for people with progressive neurological diseases such as multiple sclerosis (MS) and Parkinson's disease (PD), in which cognitive functions worsen as the brain suffers permanent damage over time.

In Quiñones-Hinojosa's laboratory, the researchers examined the impact of radiation on mouse neural stem cells by testing the rodents' responses to a subsequent brain injury. To do the experiment, the researchers used a device invented and used only at Johns Hopkins that accurately simulates localized radiation used in human cancer therapy. Other techniques, the researchers say, use too much radiation to precisely mimic the clinical experience of brain cancer patients.

In the weeks after radiation, the researchers injected the mice with lysolecithin, a substance that caused brain damage by inducing a demyelinating brain lesion, much like that present in MS. They found that neural stem cells within the irradiated subventricular zone of the brain generated new cells, which rushed to the damaged site to rescue newly injured cells. A month later, the new cells had incorporated into the demyelinated area where new myelin, the protein insulation that protects nerves, was being produced.

"These mice have brain damage, but that doesn't mean it's irreparable," Quiñones-Hinojosa says. "This research is like detective work. We're putting a lot of different clues together. This is another tiny piece of the puzzle. The brain has some innate capabilities to regenerate and we hope there is a way to take advantage of them. If we can let loose this potential in humans, we may be able to help them recover from radiation therapy, strokes, brain trauma, you name it."

His findings may not be all good news, however. Neural stem cells have been linked to brain tumor development, Quiñones-Hinojosa cautions. The radiation resistance his experiments uncovered, he says, could explain why glioblastoma, the deadliest and most aggressive form of brain cancer, is so hard to treat with radiation.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject.

The research was supported by grants from the National Institutes of Health's National Institute of Neurological Disorders and Stroke (RO1 NS070024), the Maryland Stem Cell Research Fund, the Robert Wood Johnson Foundation, the Howard Hughes Medical Institute, the PROMETEO grant, the Red de Terapia Celular (TerCel) from Instituto de Salud Carlos III, and the Consejo Nacional de Ciencia y Tecnología.

Other Johns Hopkins researchers involved in the study include Vivian Capilla-Gonzalez, Ph.D.; Hugo Guerrero-Cazares, M.D., Ph.D.; Janice Bonsu; Oscar Gonzalez-Perez, M.D.; Pragathi Achanta, Ph.D.; John Wong, Ph.D.; and Jose Manuel Garcia-Verdugo, Ph.D.

Johns Hopkins Medicine

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Study suggests average of 3 years of apparent age saved after facial plastic surgery, no consistent improvement in attractiveness

Main Category: Cosmetic Medicine / Plastic Surgery
Article Date: 01 Aug 2013 - 13:00 PDT Current ratings for:
Study suggests average of 3 years of apparent age saved after facial plastic surgery, no consistent improvement in attractiveness

A study suggests that after aesthetic facial plastic surgery the average number of apparent"years saved" (true age minus guessed age) was 3.1 years but there was only an insignificant increase in attractiveness scores, according to a report published by JAMA Facial Plastic Surgery, a JAMA Network publication.

Patients seek out aesthetic facial surgery to look younger and more attractive but there is minimal literature about the effect of the surgery on perceived age and attractiveness, according to the study background.

A. Joshua Zimm, M.D., of the Lenox Hill Hospital and Manhattan Eye, Ear & Throat Institute of North Shore-LIJ Health System, New York, and colleagues quantitatively evaluated the degree of perceived age change and improvement in attractiveness following surgical procedures.

Independent raters examined preoperative and postoperative photographs of 49 patients who underwent aesthetic facial plastic surgery between July 2006 and July 2010 at a private practice in Toronto, Canada. The photographs were shown to 50 blind raters. Patients in the study ranged in age from 42 to 73 years at the time of surgery with an average age of 57 years.

On average, raters estimated their patients' ages to be about 2.1 years younger than their chronological age before surgery and 5.2 years younger than their chronological age after surgery. The average overall years saved following surgery was 3.1 years, according to the results. There also was a small and insignificant increase in attractiveness scores in postprocedural photographs, the results indicate.

"In conclusion, the subjective nature of facial rejuvenation surgery presents a challenge in the assessment of successful results," the study concludes. "Given the limitations of the attractiveness component of this study as described herein, further investigation is warranted to verify these findings."

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JAMA Facial Plast Surg. Published online August 1, 2013. doi:10.1001/jamafacial.2013.268.

JAMA

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Poor dental health may lead to Alzheimer's, study suggests

Main Category: Dentistry
Also Included In: Alzheimer's / Dementia
Article Date: 31 Jul 2013 - 1:00 PDT Current ratings for:
Poor dental health may lead to Alzheimer's, study suggests

People with poor oral hygiene or gum disease may be at a greater risk of developing Alzheimer's disease, a new study led by The University of Central Lancashire (UCLan) School of Medicine and Dentistry suggests.

The research, which has received international collaboration, and led by Professor Stjohn Crean and Dr Sim Singhrao from UCLan, examined brain samples donated by ten patients without dementia and ten patients suffering from dementia. The research demonstrated the presence of products from Porphyromonas gingivalis in brains from patients suffering from dementia. This bacterium is commonly associated with chronic periodontal (gum) disease. These bacteria enter the bloodstream through daily activities such as eating, chewing, tooth brushing but especially following invasive dental treatment, and from there, potentially enter the brain on a regular basis. The researchers propose that every time they reach the brain, the bacteria may trigger immune system responses by already primed brains cells, causing them to release more chemicals that kill neurons. This could be one mechanism that leads to changes in the brain, which is typical of Alzheimer's disease, and could be responsible for causing symptoms such as confusion and deteriorating memory.

The research benefited from donated brain samples, provided by Brains for Dementia Research, a brain donation scheme supported by Alzheimer's Research UK and Alzheimer's Society. Finding P. gingivalis in the brains from dementia sufferers compared to those without dementia is significant as its presence in Alzheimer's diseased brains has not been documented previously and at the same time adds to a growing body of evidence that suggests an association between poor oral health and dementia.

These published research findings from human brain specimens are further supported by recent (as yet unpublished) research from the same group, on periodontal disease, using animal models, which has been carried out in collaboration with the University of Florida. This animal work has confirmed that P. gingivalis in the mouth finds its way to the brain once the periodontal disease becomes established.

Professor Stjohn Crean, Dean of School of Medicine & Dentistry said:

"Whereas previous studies have indicated a link between dementia and other bacteria and viruses such as the Herpes simplex virus type I, this new research indicates a possible association between gum disease and individuals who may be susceptible to developing Alzheimer's disease, if exposed to the appropriate trigger! Research currently underway at UCLan is playing an active role in exploring this link, but it remains to be proven whether poor dental hygiene can lead to dementia in healthy people, which obviously could have significant implications for the population as a whole. It is also likely that these bacteria could make the existing disease condition worse."

Dr. Sim K. Singhrao, Senior Research Fellow at UCLan said: "We are working on the theory that when the brain is repeatedly exposed to bacteria and/or their debris from our gums, subsequent immune responses may lead to nerve cell death and possibly memory loss. Thus, continued visits to dental hygiene professionals throughout one's life may be more important than currently envisaged with inferences for health outside of the mouth only. To help us prove our hypothesis we are hoping to use the Brains for Dementia Research tissue resource to examine brain tissue from people with both intact and compromised memory who have relevant dental records. The future of the research aims to discover if P. gingivalis can be used as a marker, via a simple blood test, to predict the development of Alzhiemer's disease in at risk patients".

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Study suggests role for adenosine in molecular processes involved in epilepsy

Main Category: Epilepsy
Article Date: 29 Jul 2013 - 0:00 PDT Current ratings for:
Study suggests role for adenosine in molecular processes involved in epilepsy

Silk has walked straight off the runway and into the lab. According to a new study published in the Journal of Clinical Investigation, silk implants placed in the brain of laboratory animals and designed to release a specific chemical, adenosine, may help stop the progression of epilepsy. The research was supported by the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute of Biomedical Imaging and Bioengineering (NIBIB), which are part of the National Institutes of Health.

The epilepsies are a group of neurological disorders associated with recurring seizures that tend to become more frequent and severe over time. Adenosine decreases neuronal excitability and helps stop seizures. Earlier studies have suggested abnormally low levels of adenosine may be linked to epilepsy.

Rebecca L. Williams-Karnesky, Ph.D. and her colleagues from Legacy Research Institute, Portland, Ore., Oregon Health and Sciences University (OHSU), Portland, and Tufts University, Boston, looked at long-term effects of an adenosine-releasing silk-implant therapy in rats and examined the role of adenosine in causing epigenetic changes that may be associated with the development of epilepsy.

The investigators argue that adenosine's beneficial effects are due to epigenetic modifications (chemical reactions that change the way genes are turned on or off without altering the DNA code, the letters that make up our genetic background). Specifically, these changes happen when a molecule known as a methyl group blocks a portion of DNA, affecting which genes are accessible and can be turned on. If methyl groups have been taken away (demethylated), genes are more likely to turn on.

The results reported in the paper provided evidence that changing adenosine levels affects DNA methylation in the brain. Specifically, greater amounts of adenosine were associated with lower levels of DNA methylation. The investigators also demonstrate that rats induced to develop epilepsy have higher levels of methylated DNA. Of particular note, epileptic rat brains that had received the adenosine-releasing silk implants exhibited DNA methylation levels close to brains of normal rats and this significantly lessened the worsening of the epilepsy over time.

"We know that there are mutations that are associated with epilepsy. However, there are few people such as Dr. Detlev Boison who are doing this type of work, focusing not just on genetic mutations but how the genes are regulated," said Vicky Whittemore, Ph.D., program director at NINDS.

One mechanism involved in a specific type of epilepsy is an increase in mossy fiber sprouting - the formation of new excitatory circuits in the part of the brain where seizures commonly originate. At the end of the experiment, animals that had been treated with the adenosine-releasing silk implant showed less sprouting than animals that were not given the drug. "Based on our findings that 10 days of adenosine delivery prevented the sprouting of mossy fibers for at least three months in rats, we predict that the benefits of our adenosine therapy may extend even longer. However, this assumption needs to be validated in long-term experiments that go beyond three months," said Dr. Boison, senior author of the paper from Legacy Research Institute and OHSU.

The rats did not receive the implants until they had experienced a number of seizures. The researchers noted that many studies investigating anti-epileptic drugs often test the treatments too early. "If the therapy interferes with the trigger for epilepsy development then the trigger is weakened and subsequent epilepsy is less severe. However, this is not necessarily indicative of a stop in the progression of the disease," said Dr. Boison. They found that the adenosine-releasing silk did not completely abolish seizures in their animal model but reduced them four-fold.

"To avoid interference with the epilepsy-triggering mechanisms, we waited until all animals developed an early stage of epilepsy. In this model, the disease is life-long: seizures become more frequent and worsen with time. Therefore, we challenged ourselves to attempt treatment at a stage where epilepsy had already been established," Dr. Boison continued.

The findings show that the implants are safe to use in rats and suggest that they may one day be used in the clinic. "Adenosine-releasing silk is a biodegradable implant. The release of adenosine occurs for 10 days and then the silk will completely dissolve. This is an ideal set-up for a transient preventative treatment," said Dr. Boison. "Clinical applications could be the prevention of epilepsy following head trauma or the prevention of seizures that often - in about 50 percent of patients - follow conventional epilepsy surgery. In this case, adenosine-releasing silk might be placed into the resection cavity in order to prevent future seizures."

However, before the silk implants are ready for their close-up, future studies will need to determine their optimal use and safety in humans. According to Dr. Boison, "We need to look into the efficacy of different doses of adenosine, the duration of adenosine release, and various time points of intervention."

Future studies also need to demonstrate how long the effects of the adenosine-releasing silk implant will last.

"This work is important because 25-30 percent of people with epilepsy do not have effective therapies. This research may help us to prevent epilepsy in people who suffer some event that places them at risk for the disorder, such as individuals who have experienced head trauma," said Dr. Whittemore.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our epilepsy section for the latest news on this subject.

This study was supported by grants from NINDS (NS061844, NS070359), NIBIB (EB002520), and the U.S. Department of Defense (W81XWH-12-1-0283).

Rebecca L. Williams-Karnesky et al. "Epigenetic changes induced by adenosine augmentation therapy prevent epileptogenesis." J Clin Invest. doi:10.1172/JCI65636, July 25, 2013.

NIH/National Institute of Neurological Disorders and Stroke

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