“Latest Stem Cells News”

For years, researchers seeking new therapies for traumatic brain injury have been tantalized by the results of animal experiments with stem cells. In numerous studies, stem cell implantation has substantially improved brain function in experimental animals with brain trauma. But just how these improvements occur has remained a mystery.

Now, an important part of this puzzle has been pieced together by researchers at the University of Texas Medical Branch at Galveston. In experiments with both laboratory rats and an apparatus that enabled them to simulate the impact of trauma on human neurons, they identified key molecular mechanisms by which implanted human neural stem cells — stem cells that are in the process of developing into neurons but have not yet taken their final form — aid recovery from traumatic axonal injury.

A significant component of traumatic brain injury, traumatic axonal injury involves damage to axons and dendrites, the filaments that extend out from the bodies of the neurons. The damage continues after the initial trauma, since the axons and dendrites respond to injury by withdrawing back to the bodies of the neurons.

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Neuron transplants have repaired brain circuitry and substantially normalized function in mice with a brain disorder, an advance indicating that key areas of the mammalian brain are more reparable than was widely believed.

Collaborators from Harvard University, Massachusetts General Hospital (MGH), Beth Israel Deaconess Medical Center (BIDMC) and Harvard Medical School (HMS) transplanted normally functioning embryonic neurons at a carefully selected stage of their development into the hypothalamus of mice unable to respond to leptin, a hormone that regulates metabolism and controls body weight. These mutant mice usually become morbidly obese, but the neuron transplants repaired defective brain circuits, enabling them to respond to leptin and thus experience substantially less weight gain.

Repair at the cellular-level of the hypothalamus — a critical and complex region of the brain that regulates phenomena such as hunger, metabolism, body temperature, and basic behaviors such as sex and aggression — indicates the possibility of new therapeutic approaches to even higher-level conditions such as spinal cord injury, autism, epilepsy, ALS  (Lou Gehrig’s disease), Parkinson’s disease, and Huntington’s disease.

“There are only two areas of the brain that are known to normally undergo ongoing large-scale neuronal replacement during adulthood on a cellular level — so-called ‘neurogenesis,’ or the birth of new neurons — the olfactory bulb and the subregion of the hippocampus called the dentate gyrus, with emerging evidence of lower level ongoing neurogenesis in the hypothalamus,” said Jeffrey Macklis, Harvard University professor of stem cell and regenerative biology and HMS professor of neurology at MGH, and one of three corresponding authors on the paper. “The neurons that are added during adulthood in both regions are generally smallish and are thought to act a bit like volume controls over specific signaling.  Here we’ve rewired a high-level system of brain circuitry that does not naturally experience neurogenesis, and this restored substantially normal function.”

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A novel pathway of stem cell activity in human brain that represents potential targets of brain injuries affecting newborns has been identified by researchers at Barrow Neurological Institute at St. Joseph’s Hospital and Medical Center. The recent study, which raises new questions of how the brain evolves, is published in the current issue of Nature, one of the world’s most cited scientific journals.

Nader Sanai, MD, director of Barrow’s Brain Tumor Research Center, led this study, which is the first developmental study of human neural stem cells in a region of the brain called the subventricular zone, the tissue structure in which brain stem cells reside. Also participating in the study were researchers from University of California San Francisco and the University of Valencia in Spain.

The findings revealed that there is a pathway of young migrating neurons targeting the prefrontal cortex of the human brain in the first few months of life. After the first year of life, the subventricular zone of the brain slows down, tapering production of new brain cells by the time a child is 18-months and then to nearly zero by age two. This revelation settles conflicting prior reports that suggested that human neural stem cell cells remain highly active into adulthood.

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Scientists in the US have made a major breakthrough that has the potential for people with brain damage, caused by epilepsy or Parkinson’s for example, to use their own brain stem cells as a treatment.

Steven Roper of the University of Florida discovered that stem cells from the human brain that were transplanted into the brains of newborn rats matured and were able to function just like native rat cells.

The researchers found that the adult stem cells had the ability to turn into all types of brain tissue in the rats, including the neocortex, which deals with higher processing, and the hippocampus, involved in memory and spatial awareness.

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Scientists have identified a way of prompting nerve system repair in multiple sclerosis (MS).

Studies on rats by Cambridge and Edinburgh University researchers identified how to help stem cells in the brain regenerate myelin sheath, needed to protect nerve fibres.
MS charities said the “exciting” Nature Neuroscience work offered hope of restoring physical functions.

But they cautioned it would be some years before treatments were developed.
MS is caused by a defect in the body’s immune system, which turns in on itself, and attacks the fatty myelin sheath.

It is thought to affect around 100,000 people in the UK.
Around 85% have the relapsing/remitting form of the condition, in which “flare-ups” which cause disability, are followed by a recovery of a level of the lost physical function.

In this form of MS, there does appear to be some natural myelin repair.
However, around 10% of people are diagnosed with a progressive form of MS, where the decline continues without any periods of remission.

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U.S. researchers have found that a supplemental protein may help restore impaired mobility of people who suffer from a stroke.
Naturally occurring in humans, the protein has proved to work well in restoring motor function in rats after a stroke, according to two new studies by researchers at the University of California, Irvine (UCI).
The researchers hope that the protein will also help humans.

Administered directly to the brain, the protein restores 99 percent of lost movement; if it’s given through the nose, 70 percent of lost movement is regained. Untreated rats improve by only 30 percent.

Report of the Brain Tumor Progress Review Group (SuDoc HE 20.3502:B 73/10)

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