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Scientists discover the brain has ability to repair itself
Neuroscientists at Auckland (N.Z.) University and the Carlsson Institute for Neuroscience in Sweden have found a cell pathway providing new evidence that the brain may be able to repair itself, according to the results of an eight-year study.

The research may yield new information for fighting Parkinson's disease, Alzheimer's and preventing strokes.

What you need to know - Conventional View
  • The research suggests that the brain generates new stem cells, an important revelation.
  • The stem cells divide and convert themselves into other types of cell, which allow them to move to areas of the brain containing destroyed and damaged cells.
  • Humans have a cellular pathway that cells use to get to areas of the brain that need new cells, suggesting it repairs itself.
  • The cellular pathways had previously been seen with rats.
  • The research was conducted in part by using donated human brains and utilizing MRIs.
  • The study will be published February 2007 week as the cover story in the journal Science.
  • "The challenge is to understand what makes these cells divide and migrate down the pathway. How can we increase that; how can we help stimulate the cells to travel to areas of brain damage. We know that in a rat, if it has the equivalent of Parkinson's disease or stroke, cells leave this pathway to go to areas of damage. The pathway in humans probably has the same facility," said Dr. Richard Faull, one of the study's lead researchers.
What you need to know - Alternative View
  • The human body is a self-repairing mechanism, and conventional medicine has for a long time grossly underestimated the ability of the brain to repair itself.
  • Alzheimer's disease is often a reversible condition that can be cured with detoxification protocols(Healing Bath, Nutritive Body Lotion and Detox Patches), nutritional therapies (Memoregain), daily superfoods (Etherium’s LifeSource Superfood) consumption and diligent avoidance of brain-damaging chemicals such as aspartame.
  • "The more science looks closely at the human body, the more it will realize that the drugs and surgery approach to treatment is irrelevant to genuine health. The only way to achieve health is to support the body's own natural healing and regenerative processes."
Bottom line
  • The brain is a self-repairing organ and does not simply degenerate over time.
Stress significantly hastens progression of Alzheimer's disease

Stress hormones appear to rapidly exacerbate the formation of brain lesions that are the hallmarks of Alzheimer's disease, according to researchers at UC Irvine. The findings suggest that managing stress and reducing certain medications prescribed for the elderly could slow down the progression of this devastating disease.

In a study with genetically modified mice, Frank LaFerla, professor of neurobiology and behaviour, and a team of UCI researchers found that when young animals were injected for just seven days with dexamethasone, a glucocorticoid similar to the body's stress hormones, the levels of the protein beta-amyloid in the brain increased by 60 percent. When beta-amyloid production increases and these protein fragments aggregate, they form plaques, one of the two hallmark brain lesions of Alzheimer's disease. The scientists also found that the levels of another protein, tau, also increased. Tau accumulation eventually leads to the formation of tangles, the other signature lesion of Alzheimer's. The findings appear in this week's issue of the Journal of Neuroscience.

"It is remarkable that these stress hormones can have such a significant effect in such a short period of time," LaFerla said. "Although we have known for some time that higher levels of stress hormones are seen in individuals in the early stages of Alzheimer's, this is the first time we have seen how these hormones play such a direct role in exacerbating the underlying pathology of the disease."

The researchers injected four-month-old transgenic mice with levels of dexamethasone similar to the level of hormones that would be seen in humans under stress. At this young age, there would be little formation of plaques and tangles in the brains of the mice. After one week, the scientists found that the level of beta-amyloid in the brains of the animals compared to what is seen in the brains of untreated eight- to nine-month-old mice, demonstrating the profound consequence of glucocorticoid exposure. When dexamethasone was given to 13-month-old mice that already had some plaque and tangle pathology, the hormone again significantly worsened the plaque lesions in the brain and led to increased accumulation of the tau protein. "Although we expected that this drug, which, like the stress hormone cortisol, activates glucocorticoid receptors, might have some effect on plaques and tangles, it was surprising to find that such large increases were induced in relatively young mice," said James L. McGaugh, research professor of neurobiology and behavior and co-author of the paper.

The increased accumulation of beta-amyloid and tau appears to work in a "feedback loop" to hasten the progression of Alzheimer's. The researchers found that the higher levels of beta-amyloid and tau led to an increase in the levels of the stress hormones, which would come back to the brain and speed up the formation of more plaques and tangles.

According to the researchers, these findings have profound implications for how to treat the elderly who suffer from Alzheimer's disease.

"This study suggests that not only is stress management an important factor in treating Alzheimer's disease, but that physicians should pay close attention to the pharmaceutical products they prescribe for their elderly patients," said Kim Green, a postdoctoral researcher in neurobiology and behaviour and first author of the paper. "Some medications prescribed for the elderly for various conditions contain glucocorticoids. These drugs may be leading to accelerated cognitive decline in patients in the early stages of Alzheimer's."

Alzheimer's disease is a progressive neurodegenerative disorder that affects 4.5 million to 5 million adults in the United States. If no effective therapies are developed, it is estimated that 13 million Americans will be afflicted with the disease by 2050. In recent years, LaFerla has been at the forefront of Alzheimer's research. He and other members of his research team developed the transgenic mice used in this study, which are now a model for studying Alzheimer's around the world. Earlier this year, he announced work on a new compound that not only relieves the cognitive symptoms of Alzheimer's disease, but also reduces the plaques and tangles in the brain.

References on all articles:
www.Newstarget.com

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  • accelerates neuron growth and repair – trauma/damage to the brain
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