Penn study finds hyperbaric oxygen treatments mobilize stem cells

Recovery of injured and diseased tissue the ultimate goal

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According to a study to be published in the American Journal of Physiology-Heart and Circulation Physiology, a typical course of hyperbaric oxygen treatments increases by eight-fold the number of stem cells circulating in a patient’s body. Stem cells, also called progenitor cells are crucial to injury repair. The study currently appears on-line and is scheduled for publication in the April 2006 edition of the American Journal. Stem cells exist in the bone marrow of human beings and animals and are capable of changing their nature to become part of many different organs and tissues. In response to injury, these cells move from the bone marrow to the injured sites, where they differentiate into cells that assist in the healing process. The movement, or mobilization, of stem cells can be triggered by a variety of stimuli – including pharmaceutical agents and hyperbaric oxygen treatments. Where as drugs are associated with a host of side effects, hyperbaric oxygen treatments carry a significantly lower risk of such effects.

“This is the safest way clinically to increase stem cell circulation, far safer than any of the pharmaceutical options,” said Stephen Thom, MD, Ph.D., Professor of Emergency Medicine at the University of Pennsylvania School of Medicine and lead author of the study. “This study provides information on the fundamental mechanisms for hyperbaric oxygen and offers a new theoretical therapeutic option for mobilizing stem cells.”

“We reproduced the observations from humans in animals in order to identify the mechanism for the hyperbaric oxygen effect,” added Thom. “We found that hyperbaric oxygen mobilizes stem/progenitor cells because it increases synthesis of a molecule called nitric oxide in the bone marrow. This synthesis is thought to trigger enzymes that mediate stem/progenitor cell release.”

Hopefully, future study of hyperbaric oxygen’s role in mobilizing stem cells will provide a wide array of treatments for combating injury and disease.

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This article is available on the web at: http://ajpheart.physiology.org/cgi/reprint/00888.2005

PENN Medicine is a $2.7 billion enterprise dedicated to the related missions of medical education, biomedical research, and high-quality patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation’s first medical school) and the University of Pennsylvania Health System.

Penn’s School of Medicine is ranked #2 in the nation for receipt of NIH research funds; and ranked #4 in the nation in U.S. News & World Report’s most recent ranking of top research-oriented medical schools. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.

Penn Health System comprises: its flagship hospital, the Hospital of the University of Pennsylvania, consistently rated one of the nation’s “Honor Roll” hospitals by U.S. News & World Report; Pennsylvania Hospital, the nation’s first hospital; Presbyterian Medical Center; a faculty practice plan; a primary-care provider network; two multispecialty satellite facilities; and home health care and hospice.

http://www.eurekalert.org/pub_releases/2005-12/uops-psf122805.php

Further Evidence that Alzheimer’s Is a Type of Diabetes

Insulin levels drop with progression of Alzheimer’s disease, linked to tangles in brain.

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Researchers at Rhode Island Hospital and Brown Medical School have discovered that insulin and its receptors drop significantly in the brain during the early stages of Alzheimer’s disease, and that levels decline progressively as the disease becomes more severe, leading to further evidence that Alzheimer’s is a new type of diabetes. They also found that acetylcholine deficiency, a hallmark of the disease, is linked directly to the loss of insulin and insulin-like growth factor function in the brain.

The study, published in the November issue of the Journal of Alzheimer’s Disease, is the first to look at insulin levels early in the course of the disease. The authors’ previous work published earlier this year primarily focused on the late stages of Alzheimer’s.

“Insulin disappears early and dramatically in Alzheimer’s disease. And many of the unexplained features of Alzheimer’s, such as cell death and tangles in the brain, appear to be linked to abnormalities in insulin signaling. This demonstrates that the disease is most likely a neuroendocrine disorder, or another type of diabetes,” says senior author Suzanne de la Monte, a neuropathologist at Rhode Island Hospital and a professor of pathology at Brown Medical School in Providence, R.I.

The study analyzed postmortem brain tissue of 45 patients with a diagnosis of either normal aging or different degrees of Alzheimer’s neurodegeneration, termed “Braak Stages.” Researchers analyzed insulin and insulin receptor function in the frontal cortex, a major area affected by Alzheimer’s. They found that with increasing severity of the disease, levels of insulin receptors and the brain’s ability to respond to insulin decreased markedly.

“In the most advanced stage of Alzheimer’s, insulin receptors were nearly 80 percent lower than in a normal brain,” de la Monte says.

Researchers found two parallel abnormalities related to insulin in Alzheimer’s. First, insulin levels decline as the disease progresses. Second, insulin and its related protein IGF-I lose their ability to bind to corresponding cell receptors, creating a resistance to the growth factors and thus causing cells to malfunction and eventually die.

“This has important implications for treatment,” de la Monte says. “If you could target the disease early, you could prevent the further loss of neurons. But you would have to target not just the loss of insulin but the resistance of its receptors in the brain.”

Researchers also offer an explanation for the acetylcholine deficiency that is linked to dementia and has long been recognized as an early abnormality in Alzheimer’s. They found that insulin and IGF-I stimulate the expression of choline acetyltransferase (ChAT), the enzyme responsible for making acetylcholine. This discovery shows a direct link between insulin and IGF-I deficiency and dementia.

“We’re able to show that insulin impairment happens early in the disease. We’re able to show it’s linked to major neurotransmitters responsible for cognition. We’re able to show it’s linked to poor energy metabolism, and it’s linked to abnormalities that contribute to the tangles characteristic of advanced Alzheimer’s disease. This work ties several concepts together, and demonstrates that Alzheimer’s disease is quite possibly a Type three diabetes,” de la Monte says.

Earlier this year, de la Monte and co-authors provided the first evidence that insulin and its related proteins are produced in the brain and that reduced levels of both are linked to the late stages of Alzheimer’s. They surmised that Alzheimer’s is a complex neuroendocrine disease that originates in the central nervous system, raising the possibility of a new type of diabetes.

This study, through the Liver Research Center at Rhode Island Hospital and Brown Medical School, was supported by grants from the National Institute of Alcoholism and Alcohol Abuse, the National Institutes of Health and the Bryan Alzheimer’s Disease Research Center.

Liver research at Brown University

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