Category Archives: Stem Cell Videos

The process researchers use to generate induced pluripotent stem cells (iPSCs)-a special type of stem cell that can be made in the lab from any type of adult cell-is time consuming and inefficient. To speed things up, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) turned to kinase inhibitors.

These chemical compounds block the activity of kinases, enzymes responsible for many aspects of cellular communication, survival, and growth.

As they outline in a paper published September 25 in Nature Communications, the team found several kinase inhibitors that, when added to starter cells, help generate many more iPSCs than the standard method.

This new capability will likely speed up research in many fields, better enabling scientists around the world to study human disease and develop new treatments.

"Generating iPSCs depends on the regulation of communication networks within cells," explained Tariq Rana, Ph.D., program director in Sanford-Burnham's Sanford Children's Health Research Center and senior author of the study.

"So, when you start manipulating which genes are turned on or off in cells to create pluripotent stem cells, you are probably activating a large number of kinases. Since many of these active kinases are likely inhibiting the conversion to iPSCs, it made sense to us that adding inhibitors might lower the barrier."

According to Tony Hunter, Ph.D., professor in the Molecular and Cell Biology Laboratory at the Salk Institute for Biological Studies and director of the Salk Institute Cancer Center, "The identification of small molecules that improve the efficiency of generating iPSCs is an important step forward in being able to use these cells therapeutically.

"Tariq Rana's exciting new work has uncovered a class of protein kinase inhibitors that override the normal barriers to efficient iPSC formation, and these inhibitors should prove useful in generating iPSCs from new sources for experimental and ultimately therapeutic purposes." Hunter, a kinase expert, was not involved in this study.

The promise of iPSCs At the moment, the only treatment option available to many heart failure patients is a heart transplant. Looking for a better alternative, many researchers are coaxing stem cells into new heart muscle.

In Alzheimer's disease, researchers are also interested in stem cells, using them to reproduce a person's own malfunctioning brain cells in a dish, where they can be used to test therapeutic drugs.

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Making it easier to make stem cells

---Implications for treating muscular dystrophy and other muscle wasting diseases

Newswise Working with mice, Johns Hopkins researchers have solved a key part of a muscle regeneration mystery plaguing scientists for years, adding strong support to the theory that muscle mass can be built without a complete, fully functional supply of muscle stem cells.

This is good news for those with muscular dystrophy and other muscle wasting disorders that involve diminished stem cell function, says Se-Jin Lee, M.D., Ph.D., lead author of a report on the research in the August issue of the Proceedings of the National Academy of Sciences, and professor of molecular biology and genetics at the Johns Hopkins University School of Medicine.

Muscle stem cells, known as satellite cells, reside next to muscle fibers and are usually dormant in adult mammals, including humans. After exercise or injury, they are stimulated to divide and fuse, either with themselves or with nearby muscle fibers, to increase or replace muscle mass. In muscle wasting disorders, like muscular dystrophy, muscle degeneration initially activates satellite cells to regenerate lost tissue, but eventually the renewal cycle is exhausted and the balance tips in favor of degeneration, the researchers explain.

Muscle maintenance and growth under healthy, non-injury conditions have been more of a mystery, including the role of myostatin, a protein secreted from muscle cells to stop muscle growth. Blocking myostatin function in normal mice causes them to bulk up by 25 to 50 percent. What is not known is which cells receive and react to the myostatin signal. Current suspects include satellite cells and muscle cells themselves.

In this latest study, researchers used three approaches to figure out whether satellite cells are required for myostatin activity. They first looked at specially bred mice with severe defects in either satellite cell function or number. When they used drugs or genetic engineering to block myostatin function in both types of mice, muscle mass still increased significantly compared to that seen in mice with normal satellite cell function, suggesting that myostatin is able to act, at least partially, without full satellite cell function.

Second, the researchers guessed that if myostatin directly inhibits the growth of satellite cells, their numbers should increase in the absence of myostatin. The researchers marked the satellite cells with a permanent dye and then blocked myostatin activity with a drug. Mouse muscle mass increased significantly as expected, but the satellite cells did not increase in number, nor were they found fusing with muscle fibers at a higher rate. According to Lee, these results strongly suggest that myostatin does not suppress satellite cell proliferation.

Third, to further confirm their theory that myostatin acts primarily through muscle cells and not satellite cells, the team engineered mice with muscle cells lacking a protein receptor that binds to myostatin. If satellite cells harbor most of the myostatin receptors, removal of receptors in muscle cells should not alter myostatin activity, and should result in muscles of normal girth. Instead, what the researchers saw was a moderate, but statistically significant, increase in muscle mass. The evidence once again, they said, suggested that muscle cells are themselves important receivers of myostatin signals.

Lee notes that, since the results give no evidence that satellite cells are of primary importance to the myostatin pathway, even patients with low muscle mass due to compromised satellite cell function may be able to rebuild some of their muscle tone through drug therapy that blocks myostatin activity.

Everybody loses muscle mass as they age, and the most popular explanation is that this occurs as a result of satellite cell loss. If you block the myostatin pathway, can you increase muscle mass, mobility and independence for our aging population? asks Lee. Our results in mice suggest that, indeed, this strategy may be a way to get around the satellite cell problem.

Originally posted here:
Hopkins Researchers Solve Key Part of Old Mystery in Generating Muscle Mass

Newswise Researchers at Moffitt Cancer Center have discovered that the micro ribonucleic acid miR-214 plays a critical role in regulating ovarian cancer stem cell properties. This knowledge, said the researchers, could pave the way for a therapeutic target for ovarian cancer.

The study appears in a recent issue of the The Journal of Biological Chemistry.

According to the studys lead author, Jin Q. Cheng, Ph.D., M.D., senior member of the Molecular Oncology Department and Molecular Oncology and Drug Discovery Program at Moffitt, certain miRNAs can cause therapeutic resistance and cancer metastasis by regulating multiple gene targets. Previous work has shown that one microRNA miR-214 is elevated in cancer. In ovarian cancer, up-regulated miR-214 has been associated with late-stage and high-grade tumors. In past research, miR-214 has also been associated with resistance to the chemotherapy drug cisplatin, but the role played by miR-214 in cancer stem cells had not been determined.

Evidence suggests that cancer stem cells are responsible for cancer initiation, progression, metastasis, chemoresistance and relapse, Cheng said. Data are emerging to support the role of both miRNAs and transcription factor p53 in cancer stem cell regulation.

Their current study found that miR-214 regulates ovarian cancer stem cell properties by direct repression of p53, which led to induction of a stem cell transcription factor (Nanog). The researchers demonstrated that p53 mediated miR-214-induced Nanog in ovarian cancer stem cells and also induced chemoresistance.

It is plausible that miR-214 has an important influence on stem cells through its capacity to modulate p53, explained Cheng. Our study demonstrates direct evidence that miR-214 plays a critical role in maintaining ovarian cancer stem cells.

Given that knowledge, the researchers concluded that miR-214 is a potential therapeutic target for treating ovarian cancer.

The research was supported in part by the National Cancer Institute, part of the National Institutes of Health (grant numbers CA135328 and CA114343) and the U.S. Army (W81XWH-11-1-0223).

About Moffitt Cancer Center Located in Tampa, Moffitt is one of only 41 National Cancer Institute-designated Comprehensive Cancer Centers, a distinction that recognizes Moffitts excellence in research, its contributions to clinical trials, prevention and cancer control. Since 1999, Moffitt has been listed in U.S. News & World Report as one of Americas Best Hospitals for cancer. With more than 4,200 employees, Moffitt has an economic impact on the state of nearly $2 billion. For more information, visit MOFFITT.org, and follow the Moffitt momentum on Facebook, twitter and YouTube.

Media release by Florida Science Communications

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Researchers Find Possible Molecular Key to Regulation of Ovarian Cancer Stem Cells

Thursday, September 27, 2012

ROCHESTER, Minn. Mayo Clinic researchers have found a way to detect and eliminate potentially troublemaking stem cells to make stem cell therapy safer. Induced Pluripotent Stem cells, also known as iPS cells, are bioengineered from adult tissues to have properties of embryonic stem cells, which have the unlimited capacity to differentiate and grow into any desired types of cells, such as skin, brain, lung and heart cells. However, during the differentiation process, some residual pluripotent or embryonic-like cells may remain and cause them to grow into tumors.

MULTIMEDIA ALERT: Video resources, including an interview with Dr. Nelson will be available for journalists at the Mayo Clinic News Network.

"Pluripotent stem cells show great promise in the field of regenerative medicine; however, the risk of uncontrolled cell growth will continue to prevent their use as a therapeutic treatment," says Timothy Nelson, M.D., Ph.D., lead author on the study, which appears in the October issue of STEM CELLS Translational Medicine.

Using mouse models, Mayo scientists overcame this drawback by pretreated stem cells with a chemotherapeutic agent that selectively damages the DNA of the stem cells, efficiently killing the tumor-forming cells. The contaminated cells died off, and the chemotherapy didn't affect the healthy cells, Dr. Nelson says.

"The goal of creating new therapies is twofold: to improve disease outcome with stem cell-based regenerative medicine while also ensuring safety. This research outlines a strategy to make stem cell therapies safer for our patients while preserving their therapeutic efficacy, thereby removing a barrier to translation of these treatments to the clinic," says co-author Alyson Smith, Ph.D.

Stem cell therapies continue to be refined and improved. Researchers are finding that stem cells may be more versatile than originally thought, which means they may be able to treat a wider variety of diseases, injuries and congenital anomalies. Stem cell therapy is an emerging regenerative strategy being studied at Mayo Clinic.

"By harnessing the potential of regenerative medicine, we'll be able to provide more definitive solutions to patients," says Andre Terzic, M.D., Ph.D., co-author and director of Mayo Clinic's Center for Regenerative Medicine.

Other members of the Mayo research team included Clifford Folmes, Ph.D., Katherine Hartjes, Natalie Nelson and Saji Oommen, Ph.D. The research was supported by the Todd and Karen Wanek Family Program for Hypoplastic Left Heart Syndrome, National Institutes of Health New Innovator Award OD007015-01, and a Mayo Clinic Center for Regenerative Medicine accelerated research grant.

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Mayo Clinic Finds Way to Weed Out Problem Stem Cells, Making Therapy Safer

Scientists find new way to up safety factor of stem cell therapy by causing contaminated cells to purge themselves.

Pluripotent stem cells show great potential in treating various debilitating diseases, but at a risk: during the process of reprogramming the cells so they will grow (differentiate) into the desired tissue, some of their DNA may be damaged causing them to develop into tumors. Researchers have been scrambling to find a way to overcome this huge drawback to an otherwise highly promising therapeutic candidate.

Now, researchers at the Mayo Clinic in Rochester, Minnesota, think they might have found an answer. Reporting in the October issue of STEM CELLS Translational Medicine, they detail a low-cost, highly-effective way to detect and then purge at-risk cells during an early stage in the differentiation process.

Strategies to improve the safety of stem cell therapy have generally focused on separating or depleting damaged cells after the cells have differentiated. However, while this method was able to diminish the number of tumors formed as well as significantly reduce their size, the technical burdens and cost of specialized reagents and equipment needed to do so remain a challenge for widespread clinical applications, says lead investigator Timothy J. Nelson, M.D., Ph.D. He directs the cell biology group within the clinics Regenerative Strategies team.

Instead, the Mayo team turned to a relatively simple protocol that involves pre-treating cultured stem cells with a genotoxin an agent that sniffs out gene mutations or chromosomes changes in contaminated cells and kills them after first priming the cells through the up-regulation of Puma protein, which can be activated to send a series of signals leading to cell suicide. They tested their theory using stem cells taken from a mouse model.

The results showed that not only did the contaminated cells die off, At the same time, it didnt affect the remaining healthy cells capability to differentiate nor did it have any negative consequence on their genomic stability, Nelson says. And it worked on stem cells derived from both natural and bioengineered sources.

This novel strategy, based on innate mechanisms of pluripotent stem cells, is primed for high-throughput and cost-effective clinical translation.

The potential for tumor formation has been a significant drawback to therapeutic use of certain cell populations, said Anthony Atala, M.D., Editor of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine. The strategy outlined in this manuscript shows promise for avoiding the risk of uncontrolled cell growth upon transplantation.

STEM CELLS Translational Medicine

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Tumorogenic stem cells purged

September 26, 2012

Connie K. Ho for redOrbit.com Your Universe Online

Scientists from the La Jolla, California-based Sanford-Burnham Medical Research Institute recently discovered kinase inhibitors, which could help facilitate the production of stem cells in the laboratory as well as increase the amount of cells for projects related to disease research and drug development.

Researchers were initially interested in quickening the process utilized in the production of induced pluripotent stem cells (iPSCs), a special group of stem cells that can be derived from any kind of an adult cell in the laboratory. iPSCs have been used to produce cells of all types, including cells from the brain, heart and muscles.

The team of investigators found that kinase inhibitors could limit the activity of kinase, enzymes that assist in cellular communication, growth and survival. When they combined starter cells along with kinase inhibitors, they discovered that they could produce more iPSCs than the method that has been used in the past by scientists.

Generating iPSCs depends on the regulation of communication networks within cells, remarked the studys senior author Tariq Rana, program director in Sanford-Burnhams Childrens Health Research Center, in a prepared statement. So, when you start manipulating which genes are turned on or off in cells to create pluripotent stem cells, you are probably activating a large number of kinases. Since many of these active kinases are likely inhibiting the conversion to iPSCs, it made sense to us that adding inhibitors might lower the barrier.

The scientists focused on identifying kinase inhibitors with a group of over 240 chemical compounds that limited kinase. The compounds were each added to the cell and many of the kinase inhibitors generated more iPSCs than the untreated cells. They found that the more powerful inhibitors focused on kinases AurkA, P38, and PI3K. Team members from Ranas laboratory collaborated with staff members from Stanford-Burnhams bioinformatics, animal modeling, genomics and histology core facilities to confirm the findings of the study.

We found that manipulating the activity of these kinases can substantially increase cellular reprogramming efficiency, continued Rana in the statement. But whats more, weve also provided new insights into the molecular mechanism of reprogramming and revealed new functions for these kinases. We hope these findings will encourage further efforts to screen for small molecules that might prove useful in iPSC-based therapies.

With this new finding, researchers will be able to create new treatments and examine human disease. For example, researchers can use stem cells in Alzheimers disease studies in reproducing malfunctioning brain cells from an individual. These cells can then be observed in therapeutic drug testing.

The identification of small molecules that improve the efficiency of generating iPSCs is an important step forward in being able to use these cells therapeutically. Tariq Ranas exciting new work has uncovered a class of protein kinase inhibitors that override the normal barriers to efficient iPSC formation, and these inhibitors should prove useful in generating iPSCs from new sources for experimental and ultimately therapeutic purposes, Tony Hunter, a professor in the Molecular and Cell Biology Laboratory at the Salk Institute for Biological Studies and director of the Salk Institute Cancer Center, and unaffiliated with the study, said in the statement.

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Kinase Inhibitors Quicken Stem Cell Production Process

ScienceDaily (Sep. 26, 2012) Is aging inevitable? What factors make older tissues in the human body less able to maintain and repair themselves, as in the weakening and shrinkage of aging muscles in humans? A new study from Massachusetts General Hospital (MGH) investigators and collaborators at King's College London describes the mechanism behind impaired muscle repair during aging and a strategy that may help rejuvenate aging tissue by manipulating the environment in which muscle stem cells reside.

The report will appear in the journal Nature and has received advance online release.

Rare muscle stem cells are located inside each skeletal muscle of the body. Also called satellite cells, due to their position on the surface of the muscle fibers they serve and protect, these cells are essential to maintaining the capacity of muscles to regenerate. Satellite cells are able to generate new, differentiated muscle cells while keeping their identity as stem cells, retaining the ability to maintain and repair muscle tissue. Normally in a resting or dormant state, satellite cells respond rapidly to repair injured tissues. The current study finds that aging muscle stem cells lose their ability to maintain a dormant state, so that when called upon to repair injured muscle, they are unable to mount an adequate response.

Andrew Brack, PhD, of the MGH Center for Regenerative Medicine, senior and corresponding author of the Nature paper, says, "Just as it is important for athletes to build recovery time into their training schedules, stem cells also need time to recuperate, but we found that aged stem cells recuperate less often. We were surprised to find that the events prior to muscle regeneration had a major influence on regenerative potential. That makes sense to us as humans, in terms of the need to sleep and to eat a healthy diet, but that the need to rest also plays out at the level of stem cells is quite remarkable." An assistant professor of Medicine at Harvard Medical School, Brack is also a principal faculty member at the Harvard Stem Cell Institute.

In a series of experiments in mice, the authors found that a developmental protein called fibroblast growth factor-2 (FGF2) is elevated in the aging muscle stem cell microenvironment and drives stem cells out of the dormant state. Satellite cells that are forced to replicate lose the ability to maintain their identity as stem cells, reducing the stem cell population. The authors also found that blocking the age-related increase in FGF signaling both in aged satellite cells or in the cellular microenvironment protected against stem cell loss, maintained stem cell renewal during aging and dramatically improved the ability of aged muscle tissue to repair itself. Lead author Joe Chakkalakal, PhD, a research fellow in Brack's lab, says, "This work highlights the usefulness of targeting the aged stem cell or its environment to protect stem cells and the tissues they serve from the effects of aging."

Noting that FGF2 is known for laying the foundation for muscle development, Brack adds, "At present we don't know why this developmental factor is re-expressed in the aged stem cell environment. It appears that what was beneficial for the development of muscle becomes detrimental during aging. After this proof-of-principle study, we are beginning to ask whether the lessons we have learned can be translated to improving the health of the ever-growing aged human population."

Additional co-authors of the Nature paper are Kieran Jones and Albert Basson, PhD, King's College London. The study was supported by funds from the National Institutes of Health, Harvard Stem Cell Institute, and the Biotechnology and Biological Sciences Research Council of the U.K.

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Inadequate cellular rest may explain effects of aging on muscles

Sept. 26, 2012

Stem cells are biological building blocks, the starting point of human life. But without proper direction, they're not very useful when it comes to treating disease.

"If we just take stem cells and inject them into you, they will simply become a cancerous tumor," says Randy Ashton, a University of Wisconsin-Madison assistant professor of biomedical engineering.

Ashton

Working in the Wisconsin Institute for Discovery, Ashton is seeking to instruct the development of human stem cells in the lab by using the molecules cells already use to communicate with one another.

"We are trying to understand how particular tissues arise in development," says Ashton. "Then, using human pluripotent stem cells, we can replicate the signals that allow those structures to develop in order to create tissues that would be therapeutic for different degenerative diseases and disorders."

For several years, Ashton has worked with two cellular communication molecules sonic hedgehog and ephrin ligands that factor into how a stem cell determines which blueprint to work from when it is differentiating into a specific cell type. In a paper co-authored by Ashton, Anthony Conway and other former colleagues at the University of California, Berkeley, and published on Sept. 16 in Nature Neuroscience, Ashton explains the role that ephrin ligands play in creating the proper circumstances for adult neurogenesis, the process by which stem cells can become neurons.

"Basically, a stem cell can 'sense' what's in its environment, and then it makes a decision to determine whether it's going to become a muscle cell or a brain cell," says Ashton.

Deeper understanding of stem cell instruction could yield deeper understanding of the origins of specific diseases.

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The language of stem cells, decoded

IRVINE, CA--(Marketwire - Sep 26, 2012) - Stem cell researchers are literally on the brink of developing new treatments for some of the world's most devastating diseases.Each of us is standing at the intersection of real, tangible progress and limitless possibility. We have the opportunity to help transform medicine by supporting stem cell research online.

On October 3, scientists, researchers and supporters will celebrate International Stem Cell Awareness Day. A new interactive website, http://www.StemCellsOfferHope.com, has been launched to share easily digestible factoids and colorful stem cell imagery within social networks.It also features banners and graphics for bloggers to post information and links to share with their community of followers, family and friends on Facebook, Twitter and Pinterest.Bloggers are encouraged to help drive visitors to this website through the use of entries and social media posts.

"This is a critical and historic time for stem cell research," said Peter Donovan, Ph.D., director, Sue & Bill Gross Stem Cell Research Center, UC Irvine. "The act of simply raising awareness about this research is one of the best things people can do to help accelerate the process."

Researchers have been working diligently to unlock the potential of stem cells and have made significant strides since the discovery of a method to grow and duplicate human stem cells less than 15 years ago. Their efforts to develop cures for conditions such as Alzheimer's disease, multiple sclerosis, macular degeneration, Huntington's disease, Parkinson's disease, as well as traumatic brain injuries and paralysis caused by spinal cord injuries are moving forward at a rapid pace.

For more information visit http://www.stemcellsofferhope.com.

About the Sue & Bill Gross Stem Cell Research Center, UC Irvine: The Sue & Bill Gross Stem Cell Research Center, UC Irvine is one of the largest most technologically advanced stem cell research facilities in the world. The center was established in 2010 in part through a $10 million gift from Bill Gross, founder and co-chief investment officer of international investment firm PIMCO, and his wife Sue. For more than 40 years, its team of scientists and multiple research and graduate assistants have worked to unlock the potential of stem cells for treating and curing an estimated 70 major diseases and disorders. The research center has devised new methods for growing stems cells that are 100 percent more effective than previous techniques. Other advances have led to the world's first clinical trial of a human neural stem cell-based therapy for chronic spinal cord injury and the first FDA-approved clinical trial using human embryonic stem cells. The embryonic stem cells are produced from embryos donated for research purposes during fertility treatments. These cells would otherwise be destroyed. For more information, visit stemcell.uci.edu.

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Educate, Inform & Inspire Global Awareness by Sharing 'Stem Cells Offer Hope'

SEOUL, South Korea, Sept. 26, 2012 /PRNewswire/ --In the first study of its kind, researchers at Korea's leading university and the RNL Bio Stem Cell Technology Institute announced this week the results of a study that suggests an astounding possibility: adult stem cells may not only have a positive effect on those suffering from Alzheimer's disease, theycanprevent the disease.Using fat-derived adultstem cells from humans [scientific term:adMSCs, orhuman, adipose-derived mesenchymal stem cells], researchers were able to cause Alzheimer's disease brains in animal models to regenerate. The researchers, for the first time in history, used stem cells toidentify the mechanism that is key to treatment of Alzheimer's disease, and demonstrated how to achieve efficacy as well as prevention of the symptoms of Alzheimer's with adult stem cells, a "holy grail" of biomedical scientists for decades.

Alzheimer's disease, the most common form of dementia (loss of brain function), is the 6th leading cause of death, and affects 1 in 8 people -- more than breast cancer. As of 2010, there were 35.6 million people with Alzheimer's disease in the world, but this number is expected to double every 20 years. It is estimated that the total cost of Alzheimer's is US $604 billion worldwide, with 70% of this cost in the US and Europe. To put that in perspective, Alzheimer's care costs more than the revenues of Wal-Mart (US$414 billion) and Exxon Mobil (US$311 billion), according to the British World Alzheimer's Report of ADI. The cost of Alzheimer's is at the top of health economists' list of the disorders of aging that could topple nations' entire economies, and that regularly ruin not only the lives of patients but of their relatives.

According to the results of this first major study, Alzheimer's may soon be a preventable disease, or even a thing of the past. Equally important, the safety human administration of the kind of adult stem cells used in this experiment has been established in multiple articles and government-approved clinical trials.

THE RESEARCH:

The study was jointly led by Seoul National University Professor Yoo-Hun Suh and RNL Bio Stem Cell Technology Institute (SCTI) director Dr. Jeong-Chan Ra.

The researchers and their teams injected stem cells into mice genetically designed to have the core symptoms and physiology of Alzheimer's disease. They were able to identify that these human stem cells, derived from adipose tissue, behave in a very special way when injected into the tail vein of mice subjects. The cells migrated through the blood brain barrier, thought by many to be impossible for adult stem cells to cross, and went into the brain. In fact,fluorescent labeled cells were monitored for distribution in subjects and the team identified that the infused cells migrated throughout the bodiesincluding brainexcept the olfactory organ, and therefore confirmed that IV infused stem cell can reach to the brain across the blood brain barrier.

The team infused human adipose stem cells intravenously in Alzheimer model mice multiple times two weeks apart from three month to 10 month.Once there, the mice who received cells improved in every relevant way: ability to learn, ability to remember, and neuropathological signs. More important, for the first time ever, Alzheimer model mice showed the mediation of IL-10, which is known for anti-inflammation and neurological protection.

The team also found that stem cell restored special learning ability from Alzheimer model subjects with great reduction of neuropathy lesions.This was found using tests used for Alzheimer's disease: behavioral assessment. In assessment it was found, amazingly, that stem cells' therapeutic effect on Alzheimer's disease was tremendous. This was also found in pathological analysis. The key though was prevention: the scientists showed that stem cells, when infused into Alzheimer's mice, decreased beta amyloid and APP-CT, known to cause brain cell destruction, leading to dementia and Alzheimer's disease. In the lab it was clear that stem cells increased neprilysin, which hydrolyzes toxic proteins. No other compound or treatment has ever suggested so strongly the potential to prevent, as well as stop, this epidemic of incurable dementia sweeping across suffering patients and their families.

Stopping Alzheimer's disease, let alone preventing it, is the focus of thousands of researchers worldwide. Speaking of their breakthrough discovery,Professor Yoo-Hun Suh, who led the study, said, "It is a ground breaking discovery that such a simple method as IV injection of the safest autologous adipose stem cells, without causing any immune rejection, or any ethical issues, opened a new door to conquering Alzheimer's disease, one of the most horrible, expensive and incurablediseases of our time." Joining him, leader of the RNL Bio Stem Cell Technology InstituteDr. Jeong-Chan Ra said, "It has never been more clear that it is an ethical imperative for governments to provide patients with incurable diseases with their right to participate not only in studies like this but in therapies with such obvious potential, once they have been tested as many times for safety as has our technology." Both scientists stressed that the real breakthrough in their complex research is the prevention of the onset of symptoms.

Specifically, stem cells grafted in the brain, in another part of the study, were identified to induce cell division and neuro differentiation of endogenous neuro progenitor cells around the hippocampus and its surrounding cells and increase in great deal the stability of dendrites and synapses. Stem cell also contributed various anti-inflammatory and neuro growth factors, especially increased the expression of IL-10. This again suppressed apoptosis of brain neurons, the prevention effect against Alzheimer's disease.

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Study Shows Stem Cells May Prevent And Cure Alzheimer's