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Topic: RE: virus: Does it hurt to be smart? (Read 1038 times) |
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Blunderov
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RE: virus: Does it hurt to be smart?
« on: 2005-06-20 03:38:41 » |
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[Blunderov] Research into ampakines continues apace. As always, the
promise of control over the unseen is an almost irresistible sell. As
can readily be imagined the promise has not gone unnoticed by glass bead
gamers:
<q> CAN A BRAIN PILL MAKE YOU A BETTER CHESS PLAYER?
Natrol (NASDAQ:NTOL) and the US Chess Federation will present the
brainSpeed Human Chess Challenge, a regulation match where two
world-famous Grandmasters control a gigantic chessboard featuring human
being as the chess pieces, on June, 11, 2005
In a twist on tradition, Chess masters and fans at the 2005 US Chess
Federation National Open will get a sneak preview of Natrol (R)
brainSpeed (tm), the new cognitive health supplement designed to help
improve mental agility, promote attention and maintain memory.
This innovative nutritional product which helps you think faster, hits
the
chess world, June 11, 2005 at the famed Riviera Hotel grand ballroom
when two world-famous Chess Grandmasters control a gigantic chessboard
featuring human beings as chess pieces!
Natrol (R) BrainSpeed (tm) has been developed to take chess players to
the next level by targeting the cholinergic system, the key to mental
processing speed - by helping to accelerate reaction time, improve
decision making velocity and promote mental acuity.
The human chess pieces will also issue brainspeeding tickets to
attendees, inviting them to take the brainSpeedometer online test to
measure their current mental agility. This test establishes a
brainSpeed benchmark for attention, memory and mental performance and
then allows people to track their progress as they use the product. The
product will also be made available for sales during the Open before its
official retail launch in August.</q>
[Blunderov]I think any conclusions drawn from comparisons to such a
'benchmark' must be unclear. The more one does IQ tests the better one
becomes at them. Some further enquiry produced more food for thought
though.
http://nootropics.com/acetylcholine/
'Nicotine has been found to improve memory performance in a variety of
tests, including the radial-arm maze. This improvement, together with
the consistent finding of a decline in cortical nicotinic receptor
concentration in Alzheimer's patients, has fueled the search for novel
nicotinic ligands with therapeutic potential.'
[Blunderov]Doctors don't brute this information abroad much (probably
they consider the info to be dangerous to the child like minds of
non-doctors) but yes, smoking prevents Alzheimers disease. Feel free to
take it up as a hobby in your 60's.
http://nootropics.com/ampakines/cx614.html
In sum, these results extend prior evidence that ampakines are effective
in enhancing synaptic responses, most likely by slowing deactivation,
and that their effects are exerted through sites that are only in part
shared with other modulators.
http://nootropics.com/neurogenesis/stemcell.html
Plasticity is an essential characteristic of the brain: it is part of
how the brain functions and is continuous while the brain interacts with
the outer world. The state of activation and the level of activity of
the entire organism affect the brain's plastic response. Brain
plasticity has many substrates, ranging from synapses to neurites and
entire cells. The production of new neurons is part of plasticity even
in the adult and old brain, but under normal conditions neurogenesis
only occurs in two privileged regions of the adult brain: hippocampus
and olfactory system. At least in the hippocampus, physical activity
stimulates neurogenesis by acting on the proliferation of neuronal stem
cells. More specific functions such as learning may be able to recruit
new neurons from the pool of cells with neurogenic potential. In a
broader context neuronal stem cells can likely be found throughout the
brain. Therefore, novel approaches to neuroregeneration will, when most
effective, make use of the activity-related effects on neuronal stem
cells in the adult brain to activate these stem cells in a targeted
manner to enhance brain function.
http://nootropics.com/neurogenesis/stemcell.html
Plasticity is an essential characteristic of the brain: it is part of
how the brain functions and is continuous while the brain interacts with
the outer world. The state of activation and the level of activity of
the entire organism affect the brain's plastic response. Brain
plasticity has many substrates, ranging from synapses to neurites and
entire cells. The production of new neurons is part of plasticity even
in the adult and old brain, but under normal conditions neurogenesis
only occurs in two privileged regions of the adult brain: hippocampus
and olfactory system. At least in the hippocampus, physical activity
stimulates neurogenesis by acting on the proliferation of neuronal stem
cells. More specific functions such as learning may be able to recruit
new neurons from the pool of cells with neurogenic potential. In a
broader context neuronal stem cells can likely be found throughout the
brain. Therefore, novel approaches to neuroregeneration will, when most
effective, make use of the activity-related effects on neuronal stem
cells in the adult brain to activate these stem cells in a targeted
manner to enhance brain function.
http://nootropics.com/neurogenesis/exercise.html
It is remarkable that neurons are able to survive and function for a
century or more in many persons that age successfully. A better
understanding of the molecular signaling mechanisms that permit such
cell survival and synaptic plasticity may therefore lead to the
development of new preventative and therapeutic strategies for
age-related neurodegenerative disorders. We all know that overeating and
lack of exercise are risk factors for many different age-related
diseases including cardiovascular disease, diabetes and cancers. Our
recent studies have shown that dietary restriction (reduced calorie
intake) can increase the resistance of neurons in the brain to
dysfunction and death in experimental models of Alzheimer's disease,
Parkinson's disease, Huntington's disease and stroke. The mechanism
underlying the beneficial effects of dietary restriction involves
stimulation of the expression of 'stress proteins' and neurotrophic
factors. The neurotrophic factors induced by dietary restriction may
protect neurons by inducing the production of proteins that suppress
oxyradical production, stabilize cellular calcium homeostasis and
inhibit apoptotic biochemical cascades. Interestingly, dietary
restriction also increases numbers of newly-generated neural cells in
the adult brain suggesting that this dietary manipulation can increase
the brain's capacity for plasticity and self-repair. Work in other
laboratories suggests that physical and intellectual activity can
similarly increase neurotrophic factor production and neurogenesis.
Collectively, the available data suggest the that dietary restriction,
and physical and mental activity, may reduce both the incidence and
severity of neurodegenerative disorders in humans. A better
understanding of the cellular and molecular mechanisms underlying these
effects of diet and behavior on the brain is also leading to novel
therapeutic agents that mimick the beneficial effects of dietary
restriction and exercise.
[Blunderov]Now this would be the ultimate Western pill! '...mimick the
beneficial effects of dietary restriction and exercise.' Run Forest,
run! (And pass the popcorn.)
http://nootropics.com/smartdrugs/brainviagra.html
Other small biotechs and big drug firms, including Merck, Johnson &
Johnson and GlaxoSmithKline, also are in pursuit. The prize is a stake
in what will be one of the next huge global drug markets.
The first users will be the four million Americans with Alzheimer's
disease, but ultimately the market may be far larger. Several million
people have so-called mild cognitive impairment, and Pfizer and J&J now
are testing whether this can be treated by their already-approved
Alzheimer's drugs, Aricept and Reminyl.
The market ratchets up quickly from there. Depending on their mechanism
of action, memory drugs might work in the treatment of millions of
people with head trauma, Down's syndrome or mental retardation. Patients
recovering from severe strokes may one day ingest memory drugs while
getting cognitive therapy to relearn basic motor skills and speech. Some
new drugs may even block bad memories
The big score: treating 76 million middle-aged folks who aren't demented
but may welcome a way to reverse the frustrating forgetfulness that
comes with age. "People in the industry are thinking about it. It would
be a huge market, but the drugs would have to be very safe," says
Novartis research chief Paul Herrling. Adds James McGaugh, a
neuroscientist at the University of California, Irvine: "Drug companies
won't tell you this, but they are really gunning for the market of
nonimpaired people--the 44-year-old salesman trying to remember the
names of his customers."
http://nootropics.com/smartmice/smartpain.html
It hurts to be smart. That's one conclusion from the latest study of
so-called Doogie mice - "smart" rodents that are genetically engineered
to have enhanced memory and learning skills.
Along with those extra IQ points, researchers have found, comes an added
sensitivity to pain.
The new work offers a sobering lesson about the difficulty of enhancing
certain brain functions without simultaneously taking a toll on others.
It might temper any momentum to engineering genetic enhancements into
people. Doogie mice, named after the main character in the television
show Doogie Howser, MD, made a big splash when they were introduced to
the world in September 1999.
Having been endowed with extra copies of a gene involved in memory
formation, the animals outperformed their normal counterparts on a
variety of tasks.
They were better at recognising objects they had seen before, remembered
painful experiences longer and recalled with greater accuracy the
location of submerged platforms in milky water.
Some scientists sniffed at the suggestion that the mice were brainy,
noting intelligence was much more than a collection of four or five
mental skills.
Nonetheless, the work was the first to show that, by adding a few extra
copies of a single gene to an embryo, researchers improved an animal's
performance on a range of memory and learning tasks.
Some suggested drugs designed to mimic the gene's effects might help
Alzheimer's patients. The new work hints it won't be that easy.
Min Zhou and his colleagues at Washington University School of Medicine
in St Louis assessed how Doogie mice responded to tissue damage and
inflammation.
They suspected that pain caused by those types of injury might be
controlled by the same "NR2B receptor" Doogie mice are overendowed with
and that gives them their superior memories.
NR2B receptors are proteins that act as "coincidence detectors" in the
brain. They recognise, for example, when a certain sound is linked to
the arrival of food and help consolidate such coincidences into learnt
associations.
The researchers subjected the mice to stimuli that caused either
short-term or long-term pain.
They heated the animals' tails, poked their foot pads with stiff fibres
and injected their paws with irritating solutions. Then they used
neurological tests to see how the animals' brains responded and tracked
their behavior.
Those tests indicated that, compared with normal mice, Doogie mice were
equally sensitive to short-term pain. But chronic inflammatory pain,
such as that caused by the injected irritants, lasted longer in Doogie
mice.
"Our results suggest that a genetic manipulation conferring enhanced
cognitive abilities may also provide unintended traits, such as
increased susceptibility to persistent pain," the team reports in
yesterday's issue of the journal Nature Neuroscience.
[Blunderov]As I darkly opined in a previous post, 'be careful of what
you wish for. You may just get it'.
Best Regards.
---
To unsubscribe from the Virus list go to <http://www.lucifer.com/cgi-bin/virus-l>
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Blunderov
Archon
Gender:
Posts: 3160
Reputation: 8.90
Rate Blunderov
"We think in generalities, we live in details"
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RE: virus: Does it hurt to be smart?
« Reply #1 on: 2005-06-28 04:00:36 » |
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[Blunderov] Research into ampakines continues apace. This has not gone
unnoticed by glass bead gamers:
<q> CAN A BRAIN PILL MAKE YOU A BETTER CHESS PLAYER?
Natrol (NASDAQ:NTOL) and the US Chess Federation will present the
brainSpeed Human Chess Challenge, a regulation match where two
world-famous Grandmasters control a gigantic chessboard featuring human
being as the chess pieces, on June, 11, 2005
In a twist on tradition, Chess masters and fans at the 2005 US Chess
Federation National Open will get a sneak preview of Natrol (R)
brainSpeed (tm), the new cognitive health supplement designed to help
improve mental agility, promote attention and maintain memory.
This innovative nutritional product which helps you think faster, hits
the
chess world, June 11, 2005 at the famed Riviera Hotel grand ballroom
when two world-famous Chess Grandmasters control a gigantic chessboard
featuring human beings as chess pieces!
Natrol (R) BrainSpeed (tm) has been developed to take chess players to
the next level by targeting the cholinergic system, the key to mental
processing speed - by helping to accelerate reaction time, improve
decision making velocity and promote mental acuity.
The human chess pieces will also issue brainspeeding tickets to
attendees, inviting them to take the brainSpeedometer online test to
measure their current mental agility. This test establishes a
brainSpeed benchmark for attention, memory and mental performance and
then allows people to track their progress as they use the product. The
product will also be made available for sales during the Open before its
official retail launch in August.</q>
[Blunderov]I think any conclusions drawn from comparisons to such a
'benchmark' must be unclear. The more one does IQ tests the better one
becomes at them. Some further enquiry produced more food for thought
though.
http://nootropics.com/acetylcholine/
'Nicotine has been found to improve memory performance in a variety of
tests, including the radial-arm maze. This improvement, together with
the consistent finding of a decline in cortical nicotinic receptor
concentration in Alzheimer's patients, has fueled the search for novel
nicotinic ligands with therapeutic potential.'
[Blunderov]Doctors don't brute this information abroad much (probably
they consider the info to be dangerous to the child-like minds of
non-doctors) but yes, smoking prevents Alzheimers disease. Feel free to
take it up as a hobby in your 60's.
http://nootropics.com/ampakines/cx614.html
In sum, these results extend prior evidence that ampakines are effective
in enhancing synaptic responses, most likely by slowing deactivation,
and that their effects are exerted through sites that are only in part
shared with other modulators.
http://nootropics.com/neurogenesis/stemcell.html
Plasticity is an essential characteristic of the brain: it is part of
how the brain functions and is continuous while the brain interacts with
the outer world. The state of activation and the level of activity of
the entire organism affect the brain's plastic response. Brain
plasticity has many substrates, ranging from synapses to neurites and
entire cells. The production of new neurons is part of plasticity even
in the adult and old brain, but under normal conditions neurogenesis
only occurs in two privileged regions of the adult brain: hippocampus
and olfactory system. At least in the hippocampus, physical activity
stimulates neurogenesis by acting on the proliferation of neuronal stem
cells. More specific functions such as learning may be able to recruit
new neurons from the pool of cells with neurogenic potential. In a
broader context neuronal stem cells can likely be found throughout the
brain. Therefore, novel approaches to neuroregeneration will, when most
effective, make use of the activity-related effects on neuronal stem
cells in the adult brain to activate these stem cells in a targeted
manner to enhance brain function.
http://nootropics.com/neurogenesis/exercise.html
It is remarkable that neurons are able to survive and function for a
century or more in many persons that age successfully. A better
understanding of the molecular signaling mechanisms that permit such
cell survival and synaptic plasticity may therefore lead to the
development of new preventative and therapeutic strategies for
age-related neurodegenerative disorders. We all know that overeating and
lack of exercise are risk factors for many different age-related
diseases including cardiovascular disease, diabetes and cancers. Our
recent studies have shown that dietary restriction (reduced calorie
intake) can increase the resistance of neurons in the brain to
dysfunction and death in experimental models of Alzheimer's disease,
Parkinson's disease, Huntington's disease and stroke. The mechanism
underlying the beneficial effects of dietary restriction involves
stimulation of the expression of 'stress proteins' and neurotrophic
factors. The neurotrophic factors induced by dietary restriction may
protect neurons by inducing the production of proteins that suppress
oxyradical production, stabilize cellular calcium homeostasis and
inhibit apoptotic biochemical cascades. Interestingly, dietary
restriction also increases numbers of newly-generated neural cells in
the adult brain suggesting that this dietary manipulation can increase
the brain's capacity for plasticity and self-repair. Work in other
laboratories suggests that physical and intellectual activity can
similarly increase neurotrophic factor production and neurogenesis.
Collectively, the available data suggest the that dietary restriction,
and physical and mental activity, may reduce both the incidence and
severity of neurodegenerative disorders in humans. A better
understanding of the cellular and molecular mechanisms underlying these
effects of diet and behavior on the brain is also leading to novel
therapeutic agents that mimick the beneficial effects of dietary
restriction and exercise.
[Blunderov]Now this would be the ultimate Western pill! '...mimick the
beneficial effects of dietary restriction and exercise.' Run Forest,
run! (And pass the popcorn.)
http://nootropics.com/smartdrugs/brainviagra.html
Other small biotechs and big drug firms, including Merck, Johnson &
Johnson and GlaxoSmithKline, also are in pursuit. The prize is a stake
in what will be one of the next huge global drug markets.
The first users will be the four million Americans with Alzheimer's
disease, but ultimately the market may be far larger. Several million
people have so-called mild cognitive impairment, and Pfizer and J&J now
are testing whether this can be treated by their already-approved
Alzheimer's drugs, Aricept and Reminyl.
The market ratchets up quickly from there. Depending on their mechanism
of action, memory drugs might work in the treatment of millions of
people with head trauma, Down's syndrome or mental retardation. Patients
recovering from severe strokes may one day ingest memory drugs while
getting cognitive therapy to relearn basic motor skills and speech. Some
new drugs may even block bad memories
The big score: treating 76 million middle-aged folks who aren't demented
but may welcome a way to reverse the frustrating forgetfulness that
comes with age. "People in the industry are thinking about it. It would
be a huge market, but the drugs would have to be very safe," says
Novartis research chief Paul Herrling. Adds James McGaugh, a
neuroscientist at the University of California, Irvine: "Drug companies
won't tell you this, but they are really gunning for the market of
nonimpaired people--the 44-year-old salesman trying to remember the
names of his customers."
http://nootropics.com/smartmice/smartpain.html
It hurts to be smart. That's one conclusion from the latest study of
so-called Doogie mice - "smart" rodents that are genetically engineered
to have enhanced memory and learning skills.
Along with those extra IQ points, researchers have found, comes an added
sensitivity to pain.
The new work offers a sobering lesson about the difficulty of enhancing
certain brain functions without simultaneously taking a toll on others.
It might temper any momentum to engineering genetic enhancements into
people. Doogie mice, named after the main character in the television
show Doogie Howser, MD, made a big splash when they were introduced to
the world in September 1999.
Having been endowed with extra copies of a gene involved in memory
formation, the animals outperformed their normal counterparts on a
variety of tasks.
They were better at recognising objects they had seen before, remembered
painful experiences longer and recalled with greater accuracy the
location of submerged platforms in milky water.
Some scientists sniffed at the suggestion that the mice were brainy,
noting intelligence was much more than a collection of four or five
mental skills.
Nonetheless, the work was the first to show that, by adding a few extra
copies of a single gene to an embryo, researchers improved an animal's
performance on a range of memory and learning tasks.
Some suggested drugs designed to mimic the gene's effects might help
Alzheimer's patients. The new work hints it won't be that easy.
Min Zhou and his colleagues at Washington University School of Medicine
in St Louis assessed how Doogie mice responded to tissue damage and
inflammation.
They suspected that pain caused by those types of injury might be
controlled by the same "NR2B receptor" Doogie mice are overendowed with
and that gives them their superior memories.
NR2B receptors are proteins that act as "coincidence detectors" in the
brain. They recognise, for example, when a certain sound is linked to
the arrival of food and help consolidate such coincidences into learnt
associations.
The researchers subjected the mice to stimuli that caused either
short-term or long-term pain.
They heated the animals' tails, poked their foot pads with stiff fibres
and injected their paws with irritating solutions. Then they used
neurological tests to see how the animals' brains responded and tracked
their behavior.
Those tests indicated that, compared with normal mice, Doogie mice were
equally sensitive to short-term pain. But chronic inflammatory pain,
such as that caused by the injected irritants, lasted longer in Doogie
mice.
"Our results suggest that a genetic manipulation conferring enhanced
cognitive abilities may also provide unintended traits, such as
increased susceptibility to persistent pain," the team reports in
yesterday's issue of the journal Nature Neuroscience.
[Blunderov]As I darkly opined in a previous post, 'be careful of what
you wish for. You may just get it'.
I read once that Einstein's brain was abnormally heavy. The additional
weight was made up of, not as one might expect, additional neurons but
glial * cells instead. The glial cells had previously been considered to
be not much more than a matrix for the neuronal system. Now received
opinion is that the glial cells are more important in signal processing
than has been believed. I don't know whether Einstein was an Ashkenazi
Jew or not but this article from
http://atheism.about.com/b/a/176275.htm?nl=1
seems apposite in the context of the downside of intelligence: (I
believe the Japanese also have a higher average IQ than most BTW;
intermarriage the agent once again?)
<q>
Evolution of Intelligence
Human beings have evolved biologically, but to what extent have they
evolved mentally? If our mental capacities are a product of natural
selection, then it would be hard to argue that small sub-groups of
humans that have intense intermarriage couldn't evolve different mental
traits than the rest of humanity - and that includes different levels of
intelligence.
The Economist reports on the research of Gregory Cochran, who argues
that Ashkenazi Jews have evolved a higher-than-average intelligence
because of intense intermarriage during the Middle Ages:
Ashkenazim generally do well in IQ tests, scoring 12-15 points above the
mean value of 100, and have contributed disproportionately to the
intellectual and cultural life of the West... They also suffer more
often than most people from a number of nasty genetic diseases, such as
Tay-Sachs and breast cancer.
Cochran argues that the two of these go together, much like resistance
to malaria and sickle-cell anemia go together.
In the Middle Ages, European Jews [Ashkenazi are the descendants of
Jewish refugees who fled to Europe after Rome crushed the Jewish Revolt
in 70 CE] were subjected to legal discrimination, one effect of which
was to drive them into money-related professions such as banking and tax
farming which were often disdained by, or forbidden to, Christians.
This, along with the low level of intermarriage with their gentile
neighbours (which modern genetic analysis confirms was the case), is Dr
Cochran's starting point.
He argues that the professions occupied by European Jews were all ones
that put a premium on intelligence. ... European Jews at the top of
their professions in the Middle Ages raised more children to adulthood
than those at the bottom. Of course, that was true of successful
gentiles as well. But in the Middle Ages, success in Christian society
tended to be violently aristocratic (warfare and land), rather than
peacefully meritocratic (banking and trade).
Put these two things together-a correlation of intelligence and success,
and a correlation of success and fecundity-and you have circumstances
that favour the spread of genes that enhance intelligence. The questions
are, do such genes exist, and what are they if they do? Dr Cochran
thinks they do exist, and that they are exactly the genes that cause the
inherited diseases which afflict Ashkenazi society.
The sphingolipid-storage diseases, Tay-Sachs, Gaucher's and
Niemann-Pick, all involve extra growth and branching of the
protuberances that connect nerve cells together. Too much of this (as
caused in those with double copies) is clearly pathological. But it may
be that those with single copies experience a more limited, but still
enhanced, protuberance growth. That would yield better linkage between
brain cells, and might thus lead to increased intelligence.
The strength of Cochran's idea here is that he has made a testable
prediction: find out if the Jews with just one copy of these
disease-causing genes have higher IQs than others. Another test might be
to see if people with one copy of these genes end up in professions that
generally require higher levels of intelligence.
The weakness of Cochran's idea is that IQ tests aren't exactly a purely
objective and scientific test. It's not even clear what, exactly, such
tests are testing for, much less how well they differentiate between
those who "have more" and those who don't.
Thus, even if his predictions turn out to be true, it won't be easy to
say for sure that he's right because it won't be clear what he's right
about. What does it mean to say that people with one copy of these genes
are "smarter"? What do they have more of to say that they are more
"intelligent"?
If it could be shown that such people have more nerve cell connections,
that would be an objective measurement. It would be reasonable to
suppose that having more such connections would likely improve at least
the speed, if not also the quality, of some reasoning processes. Beyond
that, though, it's much harder to reach any firm conclusions. <q>
[Blunderov]PS. I originally sent (most of) this post a couple of days
ago but apparently it never arrived at Virus. At about the same time I
discovered, to my amazement, a key-stroke logger on my machine. Also I
have been getting completely blank e-mails from time to time. Whether
these things are connected or not I cannot say but it's all rather
fishy. "Once is happenstance, twice is coincidence; three times is enemy
action"? I had thought my security was pretty tight. Thoughts anyone?
* Glial cells http://en.wikipedia.org/wiki/Glia
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