[Neuroscience] Re: Depression, behavior, and Neurobiology

Peter F 19eimc_minus19 at ozemail.com.au
Thu May 25 03:33:38 EST 2006


"Dr. Wayne Simon" <wayne.simon at comcast.net> wrote in message 
news:hdednVl4u8jB1-jZnZ2dneKdnZydnZ2d at comcast.com...
>
> "John H." <j_hasenkam at yahoo.com.au> wrote in message 
> news:1148529304.803506.85760 at u72g2000cwu.googlegroups.com...
>> No-one, except the scientologists, is denying the value of drugs. I
>> explicitly stated that the drugs are important as a treatment but that
>> the problem is the over riding emphasis on drugs; though this too is
>> now changing. As to my stated concerns regarding the use of
>> antidepressants in children, I do think that psychiatry has a case to
>> answer here. I am not suggesting children should be denied access to
>> the same but much greater prudence and a more creative approach to
>> treating depression children is required. Indeed, given the research on
>> the potential long term problems I am surprised that at the frequency
>> of treating childhood depression with antidepressants. As you stated
>> many years ago Doc: benefits and costs: there is a long term risk but
>> the short term risk is also substantial. The trouble with that though
>> is the simple fact that the vast majority of clinicians have little
>> awareness of the long term problems that may arise. Methinks they
>> prefer not to dwell upon the same.
>>
>> As  to causative matters, it would do the mental health profession the
>> world of public image good if it refrained from grasping at straws that
>> will eventually be used to light bonfires upon which to roast
>> psychiatry. This is one reason why the scientologists are attracting
>> attention. Don't worry Doc, here in Australia at least we dismiss those
>> sorts, though I'm not sure of the situation in the USA.
>>
>>
>> John
>
> I respectfully have to disagree.

Seems to me more like a disrespectful prejudiced misread of John's
post.

> I think more people are attracted to the pseudo-science of folks like el 
> ron hubbard, because they are not fully educated in the sciences and are 
> easily swayed by arguments that appear to be scientific and logical but 
> are truly loaded with flaws.

Can arrogant ignorance and lopsided logic be a symptoms of an
AEVASIVE (~ an in dEPTh alternative to "neurotic") mindset in action?

To answer my own question: I know it can!

Immunity to neurosis can only be guaranteed to
people who happen to have gotten their entire
spectrum of primal needs sufficiently fulfilled - IOW people who have
acquired a state of near enough maximal ALQholism.

> The attractiveness and simplicity of some of these alternatives seem to be 
> implicit if one believes that the well represented illogical trains of 
> thought.

"So much for illogica ltrans of thought".

<snip>

Here are two relevant reports from one and the same
instance of cutting edge of science.

DEPRESSION can be treated in a variety of ways, but it is possible that all 
treatments do the same thing in the brain. Now there could be a way to find 
out exactly what's happening there, opening up the potential for 
comparisons.
Prozac, one of the most common drug treatments for depression, acts by 
stimulating the growth of new neurons in the hippocampus. Grigori Enikolopov 
and his team from Cold Spring Harbor Laboratory in New York wanted to narrow 
down which steps in neurogenesis the drug was influencing. So they created 
mice with nuclei in their nerve cells that glow green during neurogenesis, 
making it easy to count and compare the number of developing neurons.
By tracking other factors associated with different stages of neurogenesis, 
Enikolopov's team found that only one step was actually influenced by 
Prozac: amplifying the neural progenitor cell, just downstream of the stem 
cell (Proceedings of the National Academy of Sciences, DOI: 
10.1073/pnas.0601992103).
Now the researchers are testing a range of treatments - from different drugs 
to deep brain stimulation - to see if they influence the same step in neuron 
development. But mice simply aren't cut out for testing one of the common 
treatment for depression. In psychotherapy, "the mice run under the couch", 
Enikolopov says.
>From issue 2552 of New Scientist magazine, 20 May 2006, page 22
=======

22:00 15 May 2006
NewScientist.com news service
Jessica Marshall

A new mouse model may help explain exactly what happens in the brain in 
response to antidepressants like Prozac. The research may hold huge 
potential for understanding and screening new treatments for depression. And 
the wide variety of existing treatments may have more in common than was 
previously thought, the researchers suggest.
Prozac (fluoxetine), one of the most common drug treatments for depression, 
acts by stimulating the growth of new neurons in the brain's hippocampus. 
Grigori Enikolopov and his team from Cold Spring Harbor Laboratory in New 
York, US, wanted to narrow down which steps in this growth process, called 
neurogenesis, Prozac was influencing.
So the team engineered mice with nuclei in their nerve cells that glow green 
during neurogenesis. This made it easy to count and compare the number of 
developing neurons. By tracking other factors associated with different 
stages of neurogenesis, Enikolopov's team found that only one step was 
influenced by Prozac.
The drug did not promote neuron growth by stimulating stem cells, but rather 
by stimulating the division of cells just "downstream" of the stem cell, 
called amplifying neural progenitor cells, which have already committed to 
becoming neurons.
Tailored treatments
Now the researchers are testing a range of treatments - from different drugs 
to deep brain stimulation - to see if they influence the same step in neuron 
development.
If these different treatments are all acting on the same step, that would 
provide a precise target for development of new therapies, Enikolopov says, 
and potential therapies could be screened more quickly.
But if different therapies target different steps in neurogenesis, that 
could make different treatments appropriate under different conditions, he 
suggests. For example, Parkinson's disease is associated with depression. 
Doctors may be better off treating such patients with an antidepressant drug 
that acts downstream of the step where Parkinson's attacks, in order for the 
treatment to have an effect.
In either case, Enikolopov asks: "How is the generation of new neurons 
translated into improved mood? That is the most critical and unanswered 
question."
The team is also testing mice pups treated with Prozac to see if 
neurogenesis responds the same way in juveniles as in adults. They hope this 
may shed light on concerns over whether Prozac is appropriate to give to 
children.
Journal reference: Proceedings of the National Academy of Sciences (DOI: 
10.1073/pnas.0601992103)
 




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