[lou_lou]

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.

[lou_lou]

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

[lou_lou]

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

[reverett123]

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

[Virginia Therese]

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

[lou_lou]

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.

Language english

[lou_lou]

Dopamine and adult neurogenesis
Andreas Borta and Günter U. HöglingerExperimental Neurology, Philipps University, Marburg, Germany
Address correspondence and reprint requests to Günter U. Höglinger, Experimental Neurology, Philipps University, D-35033 Marburg, Germany. E-mail: guenter.hoeglinger@med.uni-marburg.de
: BrdU, 5-bromo-2'deoxyuridine; EGFR, epidermal growth factor receptor; NeuN, neuronal nuclear antigen; 6-OHDA, 6-hydroxydopamine; 7-OH-DPAT, 7-hydroxy-N,N-di-n-propyl-2-aminotetralin; PD, Parkinson's disease; PSA-NCAM, polysialic neural cell adhesion molecule; SGZ, subgranular zone; SVZ, subventricular zone; TH, tyrosine hydroxylase.
Abstract

Dopamine is an important neurotransmitter implicated in the regulation of mood, motivation and movement. We have reviewed here recent data suggesting that dopamine, in addition to being a neurotransmitter, also plays a role in the regulation of endogenous neurogenesis in the adult mammalian brain. In addition, we approach a highly controversial question: can the adult human brain use neurogenesis to replace the dopaminergic neurones in the substantia nigra that are lost in Parkinson's disease?


PDF -
http://www.blackwell-synergy.com/act...9.2006.04241.x

Dopamine and adult neurogenesis
Andreas Borta and Gu¨nter U. Ho¨glinger
Experimental Neurology, Philipps University, Marburg, Germany
Abstract
Dopamine is an important neurotransmitter implicated in the
regulation of mood, motivation and movement. We have reviewed
here recent data suggesting that dopamine, in addition
to being a neurotransmitter, also plays a role in the regulation
of endogenous neurogenesis in the adult mammalian brain. In
addition, we approach a highly controversial question: can the
adult human brain use neurogenesis to replace the dopaminergic
neurones in the substantia nigra that are lost in Parkinson’s
disease?

The recent discovery that the adult mammalian brain has the
potential to generate new neurones and to integrate them into
existing circuits has caused a shift in our understanding of
how the central nervous system functions in health and
disease (Alvarez-Buylla and Lim 2004). It has been consistently
demonstrated, in two distinct areas of the forebrain,
that mature cells in all neural lineages, including neurones,
are generated throughout adulthood. Neuroblasts born in the
adult subventricular zone (SVZ), subadjacent to the ependyma
lining the lateral ventricles, migrate along the rostral
migratory stream to the olfactory bulb, where they become
interneurones. Neuroblasts born in the adult subgranular
zone (SGZ) of the dentate gyrus migrate into the adjacent
granular layer, where they become granular neurones. The
constitutive neurogenesis that occurs in the SVZ and SGZ is
thought to be of functional importance in olfaction, mood
regulation and memory processes (Nilsson et al. 1999;
Santarelli et al. 2003; Enwere et al. 2004; Kempermann
et al. 2004). The factors that govern the generation, migration,
differentiation, integration and survival of new neuroblasts
in the SVZ and SGZ include diffusible molecules such
as neurotransmitters (Hagg 2005; Lledo and Saghatelyan
2005). It is therefore conceivable that an alteration in brain
neurotransmitter levels, as occurs in neurodegenerative
diseases, would affect adult neurogenesis in the SVZ and
SGZ with yet unknown functional consequences. Inversely,
the discovery of adult neurogenesis has raised the hope that
the SVZ and SGZ, or other regions of the adult brain, might
still have the capacity to generate neuroblasts that can replace
the neurones lost through disease.
Parkinson’s disease (PD) has received much attention in
recent years with regard to adult neurogenesis, as the
degenerative process is relatively selective for the dopaminergic
nigrostriatal projection. We have evaluated the published
evidence indicating that (i) dopamine plays a role in
the regulation of constitutive neurogenesis in the adult brain,
and that (ii) adult neurogenesis can repair the damaged
nigrostriatal dopaminergic system.
Dopaminergic control of adult neurogenesis
The neurotransmitter dopamine contributes to the ontogenesis
of the mammalian brain by regulating neural precursor
cell proliferation. Dopamine (Voorn et al. 1988; Ohtani et al.
2003) and its receptors (Lidow and Rakic 1995; Diaz et al.
1997) appear early during embryonic development in the
highly proliferative germinal zones of the brain. Dopamine
receptors are classified as either D1-like (D1 and D5) or D2-
like (D2, D3 and D4), according to structural homologies and
shared second messenger cascades. Dopamine receptors,
particularly of the D3 type, are abundantly expressed during
brain development in the germinative neuroepithelial zones
actively involved in neurogenesis in most basal forebrain
Received August 6, 2006; revised manuscript received September 5,
2006; accepted September 13, 2006.
Address correspondence and reprint requests to Gu¨nter U. Ho¨glinger,
Experimental Neurology, Philipps University, D-35033 Marburg,
Germany. E-mail: guenter.hoeglinger@med.uni-marburg.de
Abbreviations used: BrdU, 5-bromo-2¢deoxyuridine; EGFR, epidermal
growth factor receptor; NeuN, neuronal nuclear antigen; 6-OHDA,
6-hydroxydopamine; 7-OH-DPAT, 7-hydroxy-N,N-di-n-propyl-2-amiaminotetralin;
PD, Parkinson’s disease; PSA-NCAM, polysialic neural cell
adhesion molecule; SGZ, subgranular zone; SVZ, subventricular zone;
TH, tyrosine hydroxylase.

Keywords: adult neurogenesis, dopamine, Parkinson’s disease,
substantia nigra, subventricular zone.
J. Neurochem. (2007) 100, 587–595.

http://tinyurl.com/2hafca

[lou_lou]

Neuroplasticity: The Secret’s in the Stem Cell


Time was, we were taught that brain cells were irreplaceable. While we could grow new skin cells or lining cells for the gastrointestinal tract, brain cells were all created before birth. Then we learned that stroke victims regained function best when they were returned to activity quickly after the stroke -- and that gave us the first clue that the brain might be able to regenerate. Before, we let the stroke victim rest and get out of bed when and if they felt they were able. Many times, they were never able to walk again. Now stroke victims go to special rehabilitation centers where they are more-or-less forced to walk long before they think they can. We’ve learned that recovery from stroke is much more complete this way.

A stroke results from damaged brain tissue. Most often a clot blocks a major brain artery, and within minutes the brain tissue sustained by that artery begins to die. (Sometimes the damage results from bleeding; the symptoms are often similar, the medication quite different; the benefit from rapid return to activity the same.) Once that particular chunk of brain dies, that’s it. It’s not coming back. But the brain tissue just next to it can take over its function. We call this neuroplasticity, meaning that the adjacent tissue remodels itself to take over the function of the destroyed tissue. How is this possible?

Researchers have found that the brain contains stem cells. Stems cells have the ability to divide and form themselves into other, specialized cells. For example, at conception, the ovum can be considered a stem cell; it will divide and the daughters will differentiate themselves into kidney cells, skin cells, blood cells, brain cells, and all the other tissues of the body. The bone marrow of an adult contains stem cells, which have no other purpose than to divide and provide daughter cells that become red blood cells and all the different kinds of white blood cells. A careful search of the brain has, in recent years, uncovered stem cells that can, when encouraged, divide and change into neurons and glial cells.

Neurotrophins Enable the Birth of New Cells

While we have but recently discovered that the brain can grow new cells, we’ve known for some time that the synapses that connect cells form new connections and lose old ones all our lives. This is part of the process of learning, be it physical, mental, or emotional, and it occurs through the mediation of brain-tissue growth factors called neurotrophins (“trophin” from a Greek word meaning birth). These neurotrophins are produced as a result of brain activity and have a more important role in certain areas of the brain, including the frontal cortex and hippocampus.

One of the better known among the many different neurotrophins is brain derived neurotrophic factor (BDNF). It contributes not just to the synaptic reconnections, but also to neurogenesis, the growth of new cells. . BDNF helps us form our brain after birth and as we grow3. BDNF is critically important to the hippocampus. Perhaps it shouldn't be a surprise that levels of BDNF are low in people with Alzheimer’s

Summary: Your Wonderful Brain


Your brain is subject to damage through the normal slings and arrows of time. In most cases, it has the ability to repair itself if you take good care of it. This month we’ve look specifically at the brain’s ability to form new cells that will replace those that have been damaged. This is good news and a good reason not to give up and accept dimming memory and abilities as a part of life. When you exercise your mind and your body, you give your brain what it needs to form new cells and new synapses. Sure, and you’re not likely to be the exception to the general rule that we all return to dust, but you can make the best of what you are given. My wish for you is that you can be that sharp, snappy, respected elder, still loved and valued by your friends and family.

http://www.rienstraclinic.com/newsle...007Jan.html#03

[lou_lou]

Science - and those that study science realize the only contant in this world is change.
We need to open our hearts and minds to change -

example: as we age we are prone to get stuck in a rut, yet-
We have seen such rapid technology change, yet change is very hard.
1980's
we used to have rotary dial phones while I was in high school the phones were buttons! then we were freed from the connections of the cord to the wall, now we are free from the walls, and we overly multi-tasking with cell phones -driving! stimuli everywhere!
children are extremely impatient, as they scream at their high speed internet connections - I remember 10 years ago -computers were very slow, and we are calling for new words to be used to catch up with the technology,
we called, the old fashioned way of mailing -snail mail...

we are advancing - that is what we do -we build on the old views -and continue to transform our world, we can take a flight and find how fast we can get to Paris!
Now the Medical concepts must change, and the pharmaceutical companies
aren't actually keeping up? they are not curing us!?
they are still giving us palliative medicine -perhaps they want us addicted because they are addicted to "Money", and if we were getting well,
their pockets would not have that much power in them -they do not
want real change.
they are poisoning us with palliative meds, they theory is off!
the masses think - they should cure us!
and they can -

then I have been forced to look at cancer treatments again!! still the same old crapola!
chemo and radiation!!

My oldest sister was just given a complete hysterectomy, she has cancer,
and like my grandmother who died in 1973, in the last chance to live chemo days.

they found my dear dear sister, after that major surgery just 12 days ago! are going to give my big sister radiation and then put her on freakin' chemo!
then AMGEN will arrive on the scene like the good guys with Black hats,
will come in with the Neupogen to save her from dying from anemia -
lack of red blood cells!

my grandma died in 1973 -by unsafe huge chemo dose -
my mom died in 1988 - little by little chemo poisoning -her cancer metatisized
my family is now praying for my sister in 2007!!!
the chemo is past its expiration date, the good minds of the scientific world are crying out CHANGE!!
and big pharma is stuffing cotton in their ears, the tweaking of bad medicine?

AMGEN is guilty -they own a patent on a glial derrived neutrophic factor - GDNF! and we/ our PD friends, were getting out of wheel chairs
and they pulled the plugs... but they -AMGEN inc. and the likes of them - need to be put in prison.

Something must change drastically - and it must start with opening our
minds and hearts
so we can change this global chemical trial that we are on ,
anyone knows we that take a pill that we have never taken before, just because
a doctor gives it to us, are we safe? our children are watching us - show them something great while we can

are we/ me [ are we just puppets, they tell us a nice tall tale, and we buy it?]

children learn by example




sincerely,
tena




Neurogenesis - Changing your mind:

During most of the 20th century,

leading scientists theorized that brain cells didn’t divide like other cells in the body. It was generally understood that neurons could not be added to the brain after earliest childhood. A respected proponent of this theory was Pasko Rakic, chairman of the Neurobiology Department at Yale University, whose research in the early 1980s concluded that no new neurons were being formed in the brains of adult primates.

However, in light of recent research, many neuroscientists (including Rakic) have had, shall we say, a change of mind.

“I think the fact that there are so many neurons that are produced . . . suggests that they must play some important function, because it wouldn’t make sense for the brain to expend so much energy to make these new cells if they’re not going to be used.”

—Elizabeth Gould at the 2002 Annual Convention of the American Psychological Association, quoted in APA's Monitor on Psychology, November 2002



By studying the detrimental effects of chronic stress on the brains of rats and primates, Princeton University psychology professor Elizabeth Gould has observed inexplicable evidence of the brain’s capacity to heal itself by the creation of new neurons—a process called neurogenesis.

Gould has demonstrated that the brain’s mechanisms are affected by its surroundings. Jonah Lehrer, highlighting Gould’s work in an article for the February-March 2006 issue of Seed magazine titled “The Reinvention of the Self,” uses the term “environ-mental conditions.” He describes Gould’s discoveries: “The structure of our brain, from the details of our dendrites to the density of our hippocampus, is incredibly influenced by our surroundings. Put a primate under stressful conditions, and its brain begins to starve. It stops creating new cells. The cells it already has retreat inwards. The mind is disfigured.”

If the brain structure is hurt by stressful or negative “environ-mental” conditions, can its functions be helped, even healed, by positive “environ-mental” forces? As Lehrer points out, the social implications of this cutting-edge study of neurogenesis are enormous.

THE SCIENCE OF DEPRESSION

Ronald Duman, professor of psychiatry and pharmacology at Yale University and an expert on depression, studies the molecular and cellular changes caused by stress as well as by the use of antidepressants. In a 2001 report published in the Journal of Pharmacology and Experimental Therapeutics, he, too, concluded that “decreased rates of cell proliferation are seen in response to stress.” He also noted that “drugs, as well as hormones and growth factors, can regulate the rate of cell proliferation.”

But he questioned whether a shortage of serotonin is the root cause of depression—an assumption that underlies the science behind antidepressant drugs. In an article titled “Antidepressants and Neuroplasticity” in the June 2002 issue of the journal Bipolar Disorders, Duman and colleague Carrol D’Sa proposed that, based on their studies, the reason antidepressants work is not because they cause a surge in serotonin (which should, but doesn’t, result in an immediate lessening of the symptoms of depression) but because they promote the production of trophic factors, proteins that lead to neurogenesis. In other words, by encouraging new cell growth, the drugs enhance the brain’s plasticity, or ability to adapt and thus cope.

Duman’s research is causing a change in the way neuroscience views depression. It has also led to further studies linking neurogenesis, depression and stress. In one study, Gould and her team deprived newborn rats of their mothers for either 15 minutes or three hours a day, placing a high level of stress on the infant rodents. Of those who were separated for the longer period, they reported: “Our results suggest that early adverse experience inhibits structural plasticity . . . and diminishes the ability of the hippocampus to respond to stress in adulthood” (Nature Neuroscience, August 2004). In other words, the rats never recovered their ability to deal with high levels of stress—in this case the early absence of their mother. Chronic stress debilitates dendrites, inhibits cell production and causes atrophy of the hippocampus, a part of the brain essential for learning and memory and also implicated in mood disorders, whereas access to a nurturing adult contributed directly to the development of healthy brain structure and function.

Lehrer remarks that “neurogenesis is an optimistic idea.” But Gould’s team, having demonstrated that deprivation and stress have negative and long-lasting consequences, is now showing that “the brain, like skin, can heal itself.” Lehrer goes on to note that Gould is “finding hopeful antidotes to neurogenesis-inhibiting injuries. ‘My hunch is that a lot of these abnormalities [caused by stress] can be fixed in adulthood,’ she says. ‘I think that there’s a lot of evidence for the resiliency of the brain.’”

MAKING THE CONNECTION

In another study, Gould and her coworkers studied the brains of adult marmosets. Some of the animals were housed in large enclosures that featured natural vegetation and encouraged foraging. Others were kept in standard laboratory cages. When the team compared the brains of animals from each group, they reported finding “dramatic differences in structural plasticity.” The marmosets that were used to the more complex environments were found not only to have more connections between neurons but also to experience a higher rate of neurogenesis than the ones that were kept in stark lab cages. When the caged animals were transferred from their bleak environment to the more natural, enriched setting, they responded with changes in their brain chemistry: the rate of new cell growth in their brains increased.

Much remains to be discovered as researchers continue their studies in this fascinating field. But if various kinds of deprivation can be shown to cause deterioration in the dendrites of the brain, wouldn’t an environment that is enriched by kindness, caring and love also contribute to the construction or regeneration of a healthy brain?

Are we not discovering that we can literally change our minds? Neuroscience may be stumbling across some spiritual truths; the positive power of love and concern that the Creator God intended us to experience and exemplify could actually regenerate the human brain.

Consider in addition that the Hebrew Scriptures and Apostolic Writings are replete with calls for individuals to repent of their harmful attitudes and actions. Do repentant people experience both physical and spiritual benefits from changing their ways?

That certainly appears to be Paul’s message when he writes in Romans 12:2
that we should “be transformed by the renewing of [our] mind”!

THOMAS E. FITZPATRICK
thomas.fitzpatrick@visionjournal.org
__________________