Dr. Levesque is the first neurosugeon/ neuroscientist that spoke
about this new subject neuroidea
Here is his website:

http://www.neurogeneration.com/

SEEDS

Neurogenesis is now one of the hottest topics in neuroscience.

http://seedmagazine.com/news/2006/02...p?page=all&p=y




The subject of stress has been the single continuous thread running through Gould’s research career. From the brain’s perspective, stress is primarily signaled by an increase in the bloodstream of a class of steroid called glucocorticoids, which put the body on a heightened state of alert. But glucocorticoids can have one nasty side-effect: They are toxic for the brain. When stress becomes chronic, neurons stop investing in themselves. Neurogenesis ceases. Dendrites disappear. The hippocampus, a part of the brain essential for learning and memory, begins withering away.
Gould’s insight was that understanding how stress damages the brain could illuminate the general mechanisms—especially neurogenesis—by which the brain is affected by its environ-mental conditions. For the last several years, she and her post-doc, Mirescu, have been depriving newborn rats of their mother for either 15 minutes or three hours a day. For an infant rat, there is nothing more stressful. Earlier studies had shown that even after these rats become adults, the effects of their developmental deprivation linger: They never learn how to deal with stress. “Normal rats can turn off their glucocorticoid system relatively quickly,” Mirescu says. “They can recover from the stress response. But these deprived rats can’t do that. It’s as if they are missing the ‘off’ switch.”
Gould and Mirescu’s disruption led to a dramatic decrease in neurogenesis in their rats’ adult brains. The temporary trauma of childhood lingered on as a permanent reduction in the number of new cells in the hippocampus. The rat might have forgotten its pain, but its brain never did. “This is a potentially very important topic,” Gould says. “When you look at all these different stress disorders, such as PTSD [post-traumatic stress disorder], what you realize is that some people are more vulnerable. They are at increased risk. This might be one of the reasons why.”
Subsequent experiments have teased out a host of other ways stress can damage the developing brain. For example, if a pregnant rhesus monkey is forced to endure stressful conditions—like being startled by a blaring horn for 10 minutes a day—her children are born with reduced neurogenesis, even if they never actually experience stress once born. This pre-natal trauma, just like trauma endured in infancy, has life-long implications. The offspring of monkeys stressed during pregnancy have smaller hippocampi, suffer from elevated levels of glucocorticoids and display all the classical symptoms of anxiety. Being low in a dominance hierarchy also suppresses neurogenesis. So does living in a bare environment. As a general rule of thumb, a rough life—especially a rough start to life—strongly correlates with lower levels of fresh cells.
Gould’s research inevitably conjures up comparisons to societal problems. And while Gould, like all rigorous bench scientists, prefers to focus on the strictly scientific aspects of her data—she is wary of having it twisted for political purposes—she is also acutely aware of the potential implications of her research.
“Poverty is stress,” she says, with more than a little passion in her voice. “One thing that always strikes me is that when you ask Americans why the poor are poor, they always say it’s because they don’t work hard enough, or don’t want to do better. They act like poverty is a character issue.”
Gould’s work implies that the symptoms of poverty are not simply states of mind; they actually warp the mind. Because neurons are designed to reflect their circumstances, not to rise above them, the monotonous stress of living in a slum literally limits the brain.
In 1989, Gould was a young post-doc working in the lab of Bruce McEwen at Rockefeller University, investigating the effect of stress hormones on rat brains. Chronic stress is devastating to neurons, and Gould’s research focused on the death of cells in the hippocampus. (Rakic’s declaration that there was no such thing as neurogenesis was still entrenched dogma.) While the idea was exciting—stress research was a booming field—the manual labor was brutal. She had to kill her rats at various time points, pluck the tiny brain out of its cranial encasing, cut through the rubbery cortex, slice the hippocampus thinner than a piece of paper, and painstakingly count the dying neurons under a microscope. But while Gould was documenting the brain’s degeneration, she happened upon something inexplicable: evidence that the brain also healed itself. “At first, I assumed I must be counting [the neurons] incorrectly,” Gould said. “There were just too many cells.”
Confused by this anomaly, Gould assumed she was making some simple experimental mistake. She went to the library, hoping to figure out what she was doing wrong. But then, looking through a dusty, 27-year-old science journal buried in the Rockefeller stacks—this was before the Internet—Gould found the explanation she needed, though not the one she was looking for.
Beginning in 1962, a researcher at MIT named Joseph Altman published several papers claiming that adult rats, cats, and guinea pigs all formed new neurons. Although Altman used the same technique that Rakic would later use in monkey brains—the injection of radioactive thymidine—his results were at first ridiculed, then ignored, and soon forgotten.
As a result, the field of neurogenesis vanished before it began. It would be another decade before Michael Kaplan, at the University of New Mexico, would use an electron microscope to image neurons giving birth. Kaplan discovered new neurons everywhere in the mammalian brain, including the cortex. Yet even with this visual evidence, science remained stubbornly devoted to its doctrine. Kaplan remembers Rakic telling him that “Those [cells] may look like neurons in New Mexico, but they don’t in New Haven.” Faced with this debilitating criticism, Kaplan, like Altman before him, abandoned the field of neurogenesis.
The Connecticut Mental Health Center is a drab brick building a mile from the Yale campus. After passing through a metal detector and walking by a few armed guards, a visitor enters a working mental institution. The cramped halls are an uneasy mixture of scientists, social workers and confined patients. The lights are bright and sterile.
Ronald Duman, a professor of Psychiatry and Pharmacology at Yale, has a lab on the third floor, opposite a ward for the mentally ill. His lab is isolated from the rest of the building by a set of locked doors. There is the usual clutter of solutions (most of them just salt buffers), the haphazard stacks of science papers and the soothing hum of refrigerators set well below zero. It is here, in these rooms with a view of New Haven, that Duman is trying to completely change the science of depression and antidepressants.
For the last 40 years, medical science has operated on the understanding that depression is caused by a lack of serotonin, a neurotransmitter that plays a role in just about everything the mind does, thinks or feels. The theory is appealingly simple: sadness is simply a shortage of chemical happiness. The typical antidepressant—like Prozac or Zoloft—works by increasing the brain’s access to serotonin. If depression is a hunger for neurotransmitter, then these little pills fill us up.
Unfortunately, the serotonergic hypothesis is mostly wrong. After all, within hours of swallowing an antidepressant, the brain is flushed with excess serotonin. Yet nothing happens; the patient is no less depressed. Weeks pass drearily by. Finally, after a month or two of this agony, the torpor begins to lift.
But why the delay? If depression is simply a lack of serotonin, shouldn’t the effect of antidepressants be immediate? The paradox of the Prozac lag has been the guiding question of Dr. Ronald Duman’s career. Duman likes to talk with his feet propped up on his desk. He speaks with the quiet confidence of someone whose ideas once seemed far-fetched but are finally being confirmed.


“Even as a graduate student,” Duman says, “I was fascinated by how antidepressants work. I always thought that if I can just figure out their mechanism of action—and identify why there is this time-delay in their effect—then I will have had a productive career.”

When Duman began studying the molecular basis of antidepressants back in the early 90s, the first thing he realized was that the serotonin hypothesis made no sense. A competing theory, which was supposed to explain the Prozaz lag, was that antidepressants increase the number of serotonin receptors. However, that theory was also disproved. “It quickly became clear that serotonin wasn’t the whole story,” Duman says. “Our working hypothesis at the time just wasn’t right.”

But if missing serotonin isn’t the underlying cause of depression, then how do antidepressants work? As millions will attest, Prozac does do something. Duman’s insight, which he began to test gradually, was that a range of antidepressants trigger a molecular pathway that has little, if anything, to do with serotonin. Instead, this chemical cascade leads to an increase in the production of a class of proteins known as trophic factors. Trophic factors make neurons grow. What water and sun do for trees, trophic factors do for brain cells. Depression was like an extended drought: It deprived neurons of the sustenance they need.

http://www.answers.com/topic/parkinsonism

http://www.britannica.com/eb/article...8/parkinsonism

This is probably the most important post to ever have been on this forum and my heartfelt thanks for it. It is so important that I fear that with an ordinary title it will fade away without bein read, so I am going to start a similar thread called "The REAL cause of PD" and offer some reasons for my enthusiasm. Thank you so much for this article CTenaLouise. -Rick

What fascinating reading, CTenaLouise...and Rick, too! I read both your posts and found the information, there, to be one of the most informative...if not THE MOST informative messages that I have ever read, especially as they relate to chronic stress and its inevitable consequences. Rick...extremely interesting in your post...your "take" on the subject... was what you noted about why PD has stymied science for so long...because it lies at the juncture of several disciplines (neurology and endocrinology) whose members do NOT communicate with one another. How frustrating it was to read this when it seems so obvious that the two must work in "sync". If it's so clear to me, why, then, is it not clear to these two disciplines? Or, are they simply "at odds" with each other in this respect...and if so, are those afflicted with PD the "victims", here, of their "arrogance"and unwillingness to work together? Or, have I just misunderstood all of this completely? I have not as yet pursued the sites specifically noted in your posts, but I certainly intend to do so. Suffice it to say that both of you have more than piqued my interest in this subject. Something like this makes it very clear to me...and I hope to you, too...my initial reason for having joined this forum...attempting to learn all I can so that I can be the best possible carepartner to my pwp.

Therese

Hematopoietic cytokines - on the verge of conquering neurology.

Author(s) Tönges L, Schlachetzki JC, Weishaupt JH, Bähr M Institution Deptartment of Neurology, Georg-August-University Göttingen, Faculty of Medicine, S1-Laboratory, Waldweg 33, 37073 Göttingen, Germany. ltoenge@gwdg.de.
Source Curr Mol Med

2007 Mar; 7(2) :157-70.

Two hematopoietic cytokines are currently gaining increasing attention within neurological research. Erythropoietin (EPO) and granulocyte-colony stimulating factor (G-CSF) have long been known for their ability to induce the proliferation of certain populations of hematopoietic lineage cells. However, it has recently been found that EPO, G-CSF, and their respective receptors are also expressed in the human central nervous system (CNS) and may be an important part of the brain's endogenous system of protection. Both hematopoietic cytokines have been shown to have neuroprotective potential in a variety of animal disease models both in vitro and in vivo, through the inhibition of apoptosis, induction of angiogenesis, exertion of anti-inflammatory and neurotrophic effects, as well as by the enhancement of neurogenesis. EPO and G-CSF have been extensively studied in the context of hematological disorders and have recently been successfully applied in the first clinical trials in stroke patients. Intravenous high-dose EPO therapy was associated with an improvement in the clinical outcome and preclinical studies with intravenous high-dose G-CSF therapy have clearly shown that it has considerable neuroprotective potential in the acute, as well as in the chronic phase of stroke. In this review, the current knowledge of the neuroprotective mechanisms of EPO and G-CSF is summarized with regard to in vitro and in vivo data. Focus is placed on the role of EPO in neurological disease models with an emphasis on its influence on functional outcome. New experimental results are assessed in detail and correlated with the findings of recent clinical studies.

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