> They should probably do the same experiment with cabbies preparing for their exam and take the measure before and after.
That was in the article, too:)
"Dr Maguire said: "We are now looking at the brains of taxi-drivers before they start training, and at those of retired cabbies to see whether that area of the brain gets smaller when it is not used.""
Well, the reason they looked at London cab drivers is because of the massive amount of spatial information they have to know. The hippocampus was first shown to be involved in spatial memory in rats in the '70s (if memory serves), though it is also known to be involved in episodic memory.
The original idea was that the hippocampus holds a map of spatial environments, and so if someone has a very large amount of spatial knowledge, maybe their hippocampal anatomy will reflect that. This hypothesis is supported by this evidence (that lab has been doing these studies for years, not sure why this is claimed to be so new, except perhaps the control subjects who were bus drivers in London, reducing one potential confound). It should be noted that lately it has been shown that there is a very robust spatial code outside of the hippocampus (and feeding into it) so it appears to not be quite as simple as the hippocampus just holding a map.
Now to your questions. Names, stats, and details are semantic memory, not episodic memory, and are therefore not directly related to the hippocampus (except that all semantic memory appears to start off as episodic memorys, which are slowly re-coded, if you like, into just memory of the facts and not the specific episode where you learned the facts). So if you were constantly learning large amounts of new such data, perhaps you'd see such growth in the hippocampus, but merely having it all memorized would be relying on storage out in neocortex, not the hippocampus.
As the hippocampus (specifically the dentate gyrus, one part of it) is one of the few regions known to constantly be producing new cells, it is expected that experience might cause changes in size there. In other parts of cortex it would be more surprising (to me, at least) if there was a significant change in number of neurons. There the changes are more likely to be structural: neurons making new connections with other, existing neurons.
In summary: hippocampus = spatial information and acquisition of new memories neocortex = use and storage of existing knowledge
Well, I wasn't one of the people working on the study, but, again, TFA said they used lists of highly familiar words (probably dog, soup, chair, syzygy, etc.). Then using the magic of hypnosis told the subjects to feel some words were familiar but not remember when they last saw them. Then they presented the words in a new context (with a red frame) that they had been 'primed' for versus a context (green frame) that they were differently primed for. The green frames were roughly controls, red frames the experimental set and looked for differences between the two. Am I reading a different article than everyone else? I'm not saying the result is real or not, I'm just saying the experiment was explained in TFA.
Actually deja vu isn't recall, it's familiarity (two distinct processes in the brain). But it definitely is true that Alzheimer's starts in the hippocampus, which is nestled in and intricately connected with the medial temporal lobe, which is very likely where deja vu occurs, and so the two are at least somewhat related.
Unless I misread TFA, they presented the subjects with framed words that they had not seen before, then some subjects stated that the unfamiliar word elicited a perculiar "sensation" and a smaller set of the subjects said it felt like deja vu. It's right there in the article, left to right, words and sentence.
While I haven't thoroughly read the quantum brain proposals, everything I have read makes me think it's all pretty silly stuff. Proponents of the ideas seem to think that since there's no clear way that neurons can produce consciousness, that it must be a quantum effect, without ever showing how that actually helps at all (as far as I have seen).
In my mind, the analogy is roughly: string theory:physics::quantum consciousness:neuroscience
But really, that's giving quantum consciousness theories too much credit. That may just be personal bias, given that my own research is at a neural network level so I just have a tendency to assume that a lot of things can be explained at that level, many of which are yet to come, I expect. But I suppose they ought to carry on with their quantum consciousness research, just in case it does end up being true (or at the very least it might end up making a prediction that someone can test).
It definitely is better than invasive alternatives, which is why both of these technologies have been being used for, oh, decades? This appears to just be a company that combined two common brain-related-things (EEG and TMS) and wants money for doing so (hence all the patents and this advertisement/news story).
Let's see if I can come up with a good patent... I keep food in my freezer, but it is frozen so I can't eat it. I heat frozen food in a microwave. Therefore I shall patent a machine that has a microwave on top and a freezer on the bottom.
"Food storage and preparation in the same machine was previously deemed impossible. However, a young American grad student who is pioneering the supply of food manipulation systems is inspiring a paradigm shift."
I do believe that the medial forebrain bundle is what people mean when they talk about a "pleasure center." If you stick a stimulating electrode into a rat's MFB and let it lever press to get stimulation, it will do so to its heart's desire, until it dies of dehydration from refusing to eat or drink or do anything except hit that lever.
This may be a more informative site than wikipedia (wikipedia is very bad at neuroscience--I really ought to work on that).
What a great point, which is probably why it was specifically addressed in the article. Your arguments may carry more weight if they indicate you actually familiarized yourself with the information before criticizing it.
The original research article begs to differ with your claim that there's "nothing to indicate truly common ancestry." They refer to a published paper, for instance, that used probabilistic analysis to prove that the number of generations back to the most recent common ancestor is distributed with a peak at about log2 of the size of the initial population.
Further, the concept of mobility is one of the fundamental points of the research. The above figure, log2(n), is based on pretty much random mating (i.e. complete migration, in a sense). This paper extended that research by greating reducing the amount of migration allowed and by dividing up the world into continents, countries, and towns with roughly reasonable populations for the areas. The simulation also includes the effects of more recent migration by increasing the number of ports available after the year 1500 (ports are special locations in the world through which migration is modelled). One quote from the article: "With 5% of individuals migrating out of their home town, 0.05% migrating out of their home country, and 95% of port users born in the country from which the port emanates, the simulations produce a mean MRCA date of 1,415 BC and a mean IA date of 5,353 BC."
I'll close with one other quote regarding the realism of the parameters: "Arguably, this simulation is far too conservative, especially given its prediction that, even in densely populated Eurasia, only 55.3 people will leave each country per generation in AD 1500. If the migration rate among towns is increased to 20%, the local port users are reduced to 80%, and the migration rates between countries and continents are scaled up by factors of 5 and 10, respectively, the mean MRCA date is as recent as AD 55 and the mean IA date is 2,158 BC."
note: MRCA = most recent common ancestor, IA = identical ancestor note 2: the paper in which the log2(n) figure was derived is Chang, J. T. Recent common ancestors of all present-day individuals. Adv. Appl. Probab. 31, 10021026, 10271038 (1999)
Urm, surprisingly, commercials shown on daytime TV aren't representative of the entire field of pharmacological research.
But as for the specific ailments you mention...
A cure for sleeping disorders surely wouldn't be a pill that makes you sleep forever or stay awake forever. I expect (IANAD) that sleeping disorders tend to be either environmental (stress, etc), in which case you shouldn't expect a cure in a pill, or genetic, in which a cure would have to actually change your genes.
Consider the nature of what we can and can't cure and you may realize that the things we can't yet fix are actually really complicated, so treatments are the best we can do.
Ethanol does have an effect on transmission (specifically it reduces excitability and increases the effectiveness of GABA, an inhibitory neurotransmitter), but those are effects on action potential generation. Myelination from oligodendrocytes just increases the ability of an already generated action potential to reach the end of the axon and cause synaptic activity.
So the oligodendrocytes' effect is sort of like plugging holes in a leaking pipe, whereas the effect of alcohol is more like decreasing the chance that water will actually enter the pipe in the first place. Which is to say: alcohol's work is already done before the myelination comes into play, so increasing the latter won't much affect the former.
(IAA neuroscientist, but admitedly this isn't my area of expertise so I may be slightly wrong).
'Tis a good point. But a search for 'expo science ontology' (without the single quotes) brings up a little bit. Here is a pdf of a presentation on EXPO that explains a bit more than TFA.
Slashdot Mirror
> They should probably do the same experiment with cabbies preparing for their exam and take the measure before and after.
:)
That was in the article, too
"Dr Maguire said: "We are now looking at the brains of taxi-drivers before they start training, and at those of retired cabbies to see whether that area of the brain gets smaller when it is not used.""
Well, the reason they looked at London cab drivers is because of the massive amount of spatial information they have to know. The hippocampus was first shown to be involved in spatial memory in rats in the '70s (if memory serves), though it is also known to be involved in episodic memory.
The original idea was that the hippocampus holds a map of spatial environments, and so if someone has a very large amount of spatial knowledge, maybe their hippocampal anatomy will reflect that. This hypothesis is supported by this evidence (that lab has been doing these studies for years, not sure why this is claimed to be so new, except perhaps the control subjects who were bus drivers in London, reducing one potential confound). It should be noted that lately it has been shown that there is a very robust spatial code outside of the hippocampus (and feeding into it) so it appears to not be quite as simple as the hippocampus just holding a map.
Now to your questions. Names, stats, and details are semantic memory, not episodic memory, and are therefore not directly related to the hippocampus (except that all semantic memory appears to start off as episodic memorys, which are slowly re-coded, if you like, into just memory of the facts and not the specific episode where you learned the facts). So if you were constantly learning large amounts of new such data, perhaps you'd see such growth in the hippocampus, but merely having it all memorized would be relying on storage out in neocortex, not the hippocampus.
As the hippocampus (specifically the dentate gyrus, one part of it) is one of the few regions known to constantly be producing new cells, it is expected that experience might cause changes in size there. In other parts of cortex it would be more surprising (to me, at least) if there was a significant change in number of neurons. There the changes are more likely to be structural: neurons making new connections with other, existing neurons.
In summary:
hippocampus = spatial information and acquisition of new memories
neocortex = use and storage of existing knowledge
Well, I wasn't one of the people working on the study, but, again, TFA said they used lists of highly familiar words (probably dog, soup, chair, syzygy, etc.). Then using the magic of hypnosis told the subjects to feel some words were familiar but not remember when they last saw them. Then they presented the words in a new context (with a red frame) that they had been 'primed' for versus a context (green frame) that they were differently primed for. The green frames were roughly controls, red frames the experimental set and looked for differences between the two. Am I reading a different article than everyone else? I'm not saying the result is real or not, I'm just saying the experiment was explained in TFA.
Actually deja vu isn't recall, it's familiarity (two distinct processes in the brain). But it definitely is true that Alzheimer's starts in the hippocampus, which is nestled in and intricately connected with the medial temporal lobe, which is very likely where deja vu occurs, and so the two are at least somewhat related.
Unless I misread TFA, they presented the subjects with framed words that they had not seen before, then some subjects stated that the unfamiliar word elicited a perculiar "sensation" and a smaller set of the subjects said it felt like deja vu.
It's right there in the article, left to right, words and sentence.
While I haven't thoroughly read the quantum brain proposals, everything I have read makes me think it's all pretty silly stuff. Proponents of the ideas seem to think that since there's no clear way that neurons can produce consciousness, that it must be a quantum effect, without ever showing how that actually helps at all (as far as I have seen).
In my mind, the analogy is roughly:
string theory:physics::quantum consciousness:neuroscience
But really, that's giving quantum consciousness theories too much credit. That may just be personal bias, given that my own research is at a neural network level so I just have a tendency to assume that a lot of things can be explained at that level, many of which are yet to come, I expect. But I suppose they ought to carry on with their quantum consciousness research, just in case it does end up being true (or at the very least it might end up making a prediction that someone can test).
Hells yeah, like Laser Tag!
It definitely is better than invasive alternatives, which is why both of these technologies have been being used for, oh, decades? This appears to just be a company that combined two common brain-related-things (EEG and TMS) and wants money for doing so (hence all the patents and this advertisement/news story).
Let's see if I can come up with a good patent... I keep food in my freezer, but it is frozen so I can't eat it. I heat frozen food in a microwave. Therefore I shall patent a machine that has a microwave on top and a freezer on the bottom.
"Food storage and preparation in the same machine was previously deemed impossible. However, a young American grad student who is pioneering the supply of food manipulation systems is inspiring a paradigm shift."
I do believe that the medial forebrain bundle is what people mean when they talk about a "pleasure center." If you stick a stimulating electrode into a rat's MFB and let it lever press to get stimulation, it will do so to its heart's desire, until it dies of dehydration from refusing to eat or drink or do anything except hit that lever. This may be a more informative site than wikipedia (wikipedia is very bad at neuroscience--I really ought to work on that).
And given that they have a casting cost of 0, we'll have a ton of them.
What a great point, which is probably why it was specifically addressed in the article. Your arguments may carry more weight if they indicate you actually familiarized yourself with the information before criticizing it.
The original research article begs to differ with your claim that there's "nothing to indicate truly common ancestry." They refer to a published paper, for instance, that used probabilistic analysis to prove that the number of generations back to the most recent common ancestor is distributed with a peak at about log2 of the size of the initial population.
Further, the concept of mobility is one of the fundamental points of the research. The above figure, log2(n), is based on pretty much random mating (i.e. complete migration, in a sense). This paper extended that research by greating reducing the amount of migration allowed and by dividing up the world into continents, countries, and towns with roughly reasonable populations for the areas. The simulation also includes the effects of more recent migration by increasing the number of ports available after the year 1500 (ports are special locations in the world through which migration is modelled). One quote from the article: "With 5% of individuals migrating out of their home town, 0.05% migrating out of their home country, and 95% of port users born in the country from which the port emanates, the simulations produce a mean MRCA date of 1,415 BC and a mean IA date of 5,353 BC."
I'll close with one other quote regarding the realism of the parameters:
"Arguably, this simulation is far too conservative, especially given its prediction that, even in densely populated Eurasia, only 55.3 people will leave each country per generation in AD 1500. If the migration rate among towns is increased to 20%, the local port users are reduced to 80%, and the migration rates between countries and continents are scaled up by factors of 5 and 10, respectively, the mean MRCA date is as recent as AD 55 and the mean IA date is 2,158 BC."
note: MRCA = most recent common ancestor, IA = identical ancestor
note 2: the paper in which the log2(n) figure was derived is Chang, J. T. Recent common ancestors of all present-day individuals. Adv. Appl. Probab. 31, 10021026, 10271038 (1999)
Man, I wish I could come up with jokes like that... Are you a writer for SNL?
Urm, surprisingly, commercials shown on daytime TV aren't representative of the entire field of pharmacological research.
But as for the specific ailments you mention...
A cure for sleeping disorders surely wouldn't be a pill that makes you sleep forever or stay awake forever. I expect (IANAD) that sleeping disorders tend to be either environmental (stress, etc), in which case you shouldn't expect a cure in a pill, or genetic, in which a cure would have to actually change your genes.
Consider the nature of what we can and can't cure and you may realize that the things we can't yet fix are actually really complicated, so treatments are the best we can do.
If only everything was caused by bacteria...
can't we have one discussion here that doesn't compare microsoft to a disease?
Is the girl ugly?
Ethanol does have an effect on transmission (specifically it reduces excitability and increases the effectiveness of GABA, an inhibitory neurotransmitter), but those are effects on action potential generation. Myelination from oligodendrocytes just increases the ability of an already generated action potential to reach the end of the axon and cause synaptic activity. So the oligodendrocytes' effect is sort of like plugging holes in a leaking pipe, whereas the effect of alcohol is more like decreasing the chance that water will actually enter the pipe in the first place. Which is to say: alcohol's work is already done before the myelination comes into play, so increasing the latter won't much affect the former. (IAA neuroscientist, but admitedly this isn't my area of expertise so I may be slightly wrong).
'Tis a good point. But a search for 'expo science ontology' (without the single quotes) brings up a little bit. Here is a pdf of a presentation on EXPO that explains a bit more than TFA.