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Tampilkan postingan dengan label funny. Tampilkan semua postingan

Senin, 08 Agustus 2011

Susan Greenfield Causes Autism

British neuroscientist Susan Greenfield has caused a storm with her suggestion that the recent rise in the use of the internet and social media may be related to the recent rise in autism.

I point to the increase in autism and I point to internet use. That's all. Establishing a causal relationship is very hard but there are trends out there that we must think about.


This has led to fellow Oxford neuroscientist Dorothy Bishop of BishopBlog writing an Open Letter asking her to "please, please, stop talking about autism". Twitter has been enlivened by #greenfieldism's such as "I point to the rise of Rebecca Black and the Greek sovereign debt crisis, that is all."



However, in a Neuroskeptic exclusive, I can reveal that the situation is far worse than anyone feared. Greenfield is not merely spreading unwarranted speculations about the recent rise in autism diagnoses.



She caused that rise.



The graph above shows the total number of scientific citations for Susan Greenfield's papers, over time. This is as good a measure as any of the influence Greenfield has had over our culture.



The trend is obvious, the growth is dramatic, and the correlation with the modern autism epidemic is undeniable.

Susan Greenfield Causes Autism

British neuroscientist Susan Greenfield has caused a storm with her suggestion that the recent rise in the use of the internet and social media may be related to the recent rise in autism.

I point to the increase in autism and I point to internet use. That's all. Establishing a causal relationship is very hard but there are trends out there that we must think about.


This has led to fellow Oxford neuroscientist Dorothy Bishop of BishopBlog writing an Open Letter asking her to "please, please, stop talking about autism". Twitter has been enlivened by #greenfieldism's such as "I point to the rise of Rebecca Black and the Greek sovereign debt crisis, that is all."



However, in a Neuroskeptic exclusive, I can reveal that the situation is far worse than anyone feared. Greenfield is not merely spreading unwarranted speculations about the recent rise in autism diagnoses.



She caused that rise.



The graph above shows the total number of scientific citations for Susan Greenfield's papers, over time. This is as good a measure as any of the influence Greenfield has had over our culture.



The trend is obvious, the growth is dramatic, and the correlation with the modern autism epidemic is undeniable.

Minggu, 03 Juli 2011

The NeuROFLscience of Jokes

A new paper in the Journal of Neuroscience investigates the neural basis of humour: Why Clowns Taste Funny.

The authors note that some things are funny because of ambiguous words. For example:
Q: Why don’t cannibals eat clowns?
A: Because they taste funny!
Previous studies, apparently, have shown that these kinds of jokes lead to activation in the lIFG (left inferior frontal gyrus), although it's also involved in processing ambiguity that's not funny, and indeed, language in general.

In this study they gave people fMRI and played them audio clips of sentences that were either funny or not, and that either contained ambiguity or not. Examples of non-funny ambiguity included crackers like this:
Q: What happened to the post?
A: As usual, it was given to the best-qualified applicant.

They found that, relative to straightforward ones, ambiguous sentences led to increased activation in two areas, the lIFG and also the left ITG. That fits with previous work.

By contrast, funny stimuli, whether ambiguous or not, sent the brain into overdrive, with humour causing activation all over a wide range of hilarious areas such as the amygdala, ventral striatum, hypothalamus, temporal lobes and more.

Many of these areas are known to be involved in emotion and pleasure, although some are fairly random such as visual area BA19.
There were strong associations between BOLD signal change and funniness in the midbrain, the left ventral striatum, and the left anterior and posterior IFG.
The problem is, like so many neuroimaging studies, it's not clear what this adds to our understanding of the topic. All this really shows is that linguistic ambiguity activates language areas, and enjoyable stimuli activate pleasure areas (amongst many others); it doesn't tell us why some things are funny.

So more research is needed, and future neuro-humour studies will need a new set of neuro-jokes in order to maximize the laughs. Here's a few I came up with:

Q: Why did the chicken cross the road?
A :Because of activation in the motor cortex, causing muscle contractions in his legs.

Q: What neuroimaging methodology is most useful for studying the brains of cats and dogs?
A: PET scanning.

Knock knock.
Who's there?
John.
I doubt that. The 'self' is an illusion. The concept of 'John' as an individual is incompatible with modern neuroscience.

ResearchBlogging.orgBekinschtein TA, Davis MH, Rodd JM, & Owen AM (2011). Why Clowns Taste Funny: The Relationship between Humor and Semantic Ambiguity. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31 (26), 9665-71 PMID: 21715632

The NeuROFLscience of Jokes

A new paper in the Journal of Neuroscience investigates the neural basis of humour: Why Clowns Taste Funny.

The authors note that some things are funny because of ambiguous words. For example:
Q: Why don’t cannibals eat clowns?
A: Because they taste funny!
Previous studies, apparently, have shown that these kinds of jokes lead to activation in the lIFG (left inferior frontal gyrus), although it's also involved in processing ambiguity that's not funny, and indeed, language in general.

In this study they gave people fMRI and played them audio clips of sentences that were either funny or not, and that either contained ambiguity or not. Examples of non-funny ambiguity included crackers like this:
Q: What happened to the post?
A: As usual, it was given to the best-qualified applicant.

They found that, relative to straightforward ones, ambiguous sentences led to increased activation in two areas, the lIFG and also the left ITG. That fits with previous work.

By contrast, funny stimuli, whether ambiguous or not, sent the brain into overdrive, with humour causing activation all over a wide range of hilarious areas such as the amygdala, ventral striatum, hypothalamus, temporal lobes and more.

Many of these areas are known to be involved in emotion and pleasure, although some are fairly random such as visual area BA19.
There were strong associations between BOLD signal change and funniness in the midbrain, the left ventral striatum, and the left anterior and posterior IFG.
The problem is, like so many neuroimaging studies, it's not clear what this adds to our understanding of the topic. All this really shows is that linguistic ambiguity activates language areas, and enjoyable stimuli activate pleasure areas (amongst many others); it doesn't tell us why some things are funny.

So more research is needed, and future neuro-humour studies will need a new set of neuro-jokes in order to maximize the laughs. Here's a few I came up with:

Q: Why did the chicken cross the road?
A :Because of activation in the motor cortex, causing muscle contractions in his legs.

Q: What neuroimaging methodology is most useful for studying the brains of cats and dogs?
A: PET scanning.

Knock knock.
Who's there?
John.
I doubt that. The 'self' is an illusion. The concept of 'John' as an individual is incompatible with modern neuroscience.

ResearchBlogging.orgBekinschtein TA, Davis MH, Rodd JM, & Owen AM (2011). Why Clowns Taste Funny: The Relationship between Humor and Semantic Ambiguity. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31 (26), 9665-71 PMID: 21715632

Jumat, 10 Juni 2011

Do Pigs Get Autism?

What happens to a pig if it has a gene for autism?

There has been lots of research on mice who carry the same genes associated with autism in humans. Rats and recently monkeys have been studied as well. But the possibility of autistic pigs has been strangely neglected by science.

A new paper might just change that: Characterization of porcine autism susceptibility candidate 2 as a candidate gene for the number of corpora lutea in pigs. The authors found that, in female pigs, variation in a certain gene affects the function of the ovaries.

The corpus luteum is a little yellow blob (technically speaking) in the ovary. Its job is to secrete progesterone. Women's ovaries grow a new one during every menstrual cycle, and it normally breaks down and disappears before the period. However, if you get pregnant, the corpus luteum sticks around and continues producing that hormone.

Pigs, like many animals, can have more than one of these per ovary and it turns out that one of the genes controlling the number is a homolog of the human gene AUTS2. AUTS2 mutations are linked to autism (hence the name), smoking and mental retardation. The authors of this paper found several variants in this gene in domestic pig populations, and they show that it's expressed in the pig ovary.

It's quite a long leap from porcine lady bits to autism, I would say, but this actually does make sense, if you accept the Extreme Male Brain theory of autism. Boys are at least four times more likely to have autism than girls, and some say that masculinizing hormone testosterone may be the reason. This study fits with that, given that progesterone is a female hormone. Maybe mutations in AUTS2 gene alter sex hormone production?

On the other hand, it might be a coincidence. AUTS2 is strongly expressed in the brain, as well as the ovaries. Maybe it's just required for cell function, and if it's mutated, cells stop working normally: whether they be in the brain, or the corpus luteum.

Either way, it would be interesting to see whether AUTS2 affects pig behaviour... but I'm not sure what an autistic pig would look like.

ResearchBlogging.orgSato S, Hayashi T, & Kobayashi E (2011). Characterization of porcine autism susceptibility candidate 2 as a candidate gene for the number of corpora lutea in pigs. Animal reproduction science PMID: 21641132

Do Pigs Get Autism?

What happens to a pig if it has a gene for autism?

There has been lots of research on mice who carry the same genes associated with autism in humans. Rats and recently monkeys have been studied as well. But the possibility of autistic pigs has been strangely neglected by science.

A new paper might just change that: Characterization of porcine autism susceptibility candidate 2 as a candidate gene for the number of corpora lutea in pigs. The authors found that, in female pigs, variation in a certain gene affects the function of the ovaries.

The corpus luteum is a little yellow blob (technically speaking) in the ovary. Its job is to secrete progesterone. Women's ovaries grow a new one during every menstrual cycle, and it normally breaks down and disappears before the period. However, if you get pregnant, the corpus luteum sticks around and continues producing that hormone.

Pigs, like many animals, can have more than one of these per ovary and it turns out that one of the genes controlling the number is a homolog of the human gene AUTS2. AUTS2 mutations are linked to autism (hence the name), smoking and mental retardation. The authors of this paper found several variants in this gene in domestic pig populations, and they show that it's expressed in the pig ovary.

It's quite a long leap from porcine lady bits to autism, I would say, but this actually does make sense, if you accept the Extreme Male Brain theory of autism. Boys are at least four times more likely to have autism than girls, and some say that masculinizing hormone testosterone may be the reason. This study fits with that, given that progesterone is a female hormone. Maybe mutations in AUTS2 gene alter sex hormone production?

On the other hand, it might be a coincidence. AUTS2 is strongly expressed in the brain, as well as the ovaries. Maybe it's just required for cell function, and if it's mutated, cells stop working normally: whether they be in the brain, or the corpus luteum.

Either way, it would be interesting to see whether AUTS2 affects pig behaviour... but I'm not sure what an autistic pig would look like.

ResearchBlogging.orgSato S, Hayashi T, & Kobayashi E (2011). Characterization of porcine autism susceptibility candidate 2 as a candidate gene for the number of corpora lutea in pigs. Animal reproduction science PMID: 21641132

Rabu, 18 Mei 2011

Writing Emotions

A handy guide to some of the emotional states that you may feel in the process of writing.

DELation - The relief and sense of freedom that comes from deleting a passage you've been endlessly trying to get right, as you realize that you don't need it there at all.

Obsessive Compul-Save Disorder - A state of chronic dread based on the fear that your computer will crash and all your work will be lost, leading to ritualistic clicking of the Save button at least six times after changing each sentence. Often seen in people who have suffered a catastrophic experience (when it is called Post Traumatic Save Disorder).

Keyophobia - A state in which you will do anything to avoid actually typing some words. e.g. choosing the best font, bolding and unbolding the title to see which looks better, browsing for some illustrations, or tidying up your references.

Character Count Down - The sense of crushing disappointment when you realize that the huge number you're looking at is the character count, not the word count, and you actually have 5,000 words to go.

Paste Haste - The seductive sense of accomplishment that comes from boosting your word-count by copying-and-pasting something you've previously written into your current project "just to get provide a backbone". This often ends up slowing you down in the long run, as you have to adapt and update the old stuff and this can take longer than just rewriting it. More paste, less speed.

Writer's Blaaah-k - Writer's block is when you can't think of anything to write. Writer's blaaah-k is when you're wondering why you should. This all so boring! Why am I doing this, again? This can be a sign that what you're writing really isn't interesting, but it's often just a response to the fact that you've been working on it for so long. Of course it will seem boring to you, but the readers will come to it with fresh eyes. To rekindle your enthusiasm, try re-reading your original pitch or notes.

Writing Emotions

A handy guide to some of the emotional states that you may feel in the process of writing.

DELation - The relief and sense of freedom that comes from deleting a passage you've been endlessly trying to get right, as you realize that you don't need it there at all.

Obsessive Compul-Save Disorder - A state of chronic dread based on the fear that your computer will crash and all your work will be lost, leading to ritualistic clicking of the Save button at least six times after changing each sentence. Often seen in people who have suffered a catastrophic experience (when it is called Post Traumatic Save Disorder).

Keyophobia - A state in which you will do anything to avoid actually typing some words. e.g. choosing the best font, bolding and unbolding the title to see which looks better, browsing for some illustrations, or tidying up your references.

Character Count Down - The sense of crushing disappointment when you realize that the huge number you're looking at is the character count, not the word count, and you actually have 5,000 words to go.

Paste Haste - The seductive sense of accomplishment that comes from boosting your word-count by copying-and-pasting something you've previously written into your current project "just to get provide a backbone". This often ends up slowing you down in the long run, as you have to adapt and update the old stuff and this can take longer than just rewriting it. More paste, less speed.

Writer's Blaaah-k - Writer's block is when you can't think of anything to write. Writer's blaaah-k is when you're wondering why you should. This all so boring! Why am I doing this, again? This can be a sign that what you're writing really isn't interesting, but it's often just a response to the fact that you've been working on it for so long. Of course it will seem boring to you, but the readers will come to it with fresh eyes. To rekindle your enthusiasm, try re-reading your original pitch or notes.

Sabtu, 16 April 2011

Where Papers Come From

The Scientific Paper (Publishus orperishus) is one of the most sought-after, yet elusive, creatures on earth. Though they're a common sight in journals around the world, many dedicate their lives to the art of tracking down these rare beasts and trying to convince them to reproduce.

So, here's a handy guide to the life-cycle of this creature.

1. Conception

Every Paper begins its life as a tiny seed, an idea, which worms itself deep into the brain of a host scientist, producing a pleasurable sensation. Ideas can appear anywhere, but certain places and environmental conditions are optimal. Coffee, sugar and alcohol are known to stimulate the germination of ideas.

2. Incubation

The most dangerous stage in the life of a young Paper. Once the initial buzz of the germinating idea has worn off, the infected scientist may well forget all about it, and before long it will wither away. Others become buried under the bulk of older Papers - even though, given a chance, they might have ended up as a much better specimen.

3. Birth

This can be the most painful part of the process. The scientist suddenly finds that instead of the fully-formed Paper they dreamed of, they have on their hands a messy Experiment which requires their full-time support and care. Crying and tantrums are very common. Some scientists - especially older ones - find the whole process so taxing that they routinely put their Papers up for foster care.

4. Adolescence

By this stage the Paper is growing rapidly; tables of results start to expand, faster than anyone ever imagined. This can be exciting, but as the Paper's owner starts to consider sending it out into the wild with all the other papers, doubts and anxieties arise. Is the Paper ready for this? Will other Papers make fun of it? Some keep their Papers cooped up indoors for years, but this is rarely conductive to their growth and maturity. Others resort to "doping" with performance-enhancing practices.

5. Peer review

In order to be accepted into the community, each juvenile must undergo the stressful and sometimes vicious ritual known as Peer Review. Breeders say that this ensures that only fit and healthy Papers can pass on their genes to future generations. However, some argue that it is all too often a random and arbitrary process which favours external plumage over true strength.

6. Adulthood

The paper is finally finished, though it rarely looks anything like anyone imagined all those years ago. Now it must interact with all the other Papers, and so the grand cycle begins anew. Every Paper-fancier's dream is that their Paper will go on to breed and raise many offspring of its own ("citations").

Where Papers Come From

The Scientific Paper (Publishus orperishus) is one of the most sought-after, yet elusive, creatures on earth. Though they're a common sight in journals around the world, many dedicate their lives to the art of tracking down these rare beasts and trying to convince them to reproduce.

So, here's a handy guide to the life-cycle of this creature.

1. Conception

Every Paper begins its life as a tiny seed, an idea, which worms itself deep into the brain of a host scientist, producing a pleasurable sensation. Ideas can appear anywhere, but certain places and environmental conditions are optimal. Coffee, sugar and alcohol are known to stimulate the germination of ideas.

2. Incubation

The most dangerous stage in the life of a young Paper. Once the initial buzz of the germinating idea has worn off, the infected scientist may well forget all about it, and before long it will wither away. Others become buried under the bulk of older Papers - even though, given a chance, they might have ended up as a much better specimen.

3. Birth

This can be the most painful part of the process. The scientist suddenly finds that instead of the fully-formed Paper they dreamed of, they have on their hands a messy Experiment which requires their full-time support and care. Crying and tantrums are very common. Some scientists - especially older ones - find the whole process so taxing that they routinely put their Papers up for foster care.

4. Adolescence

By this stage the Paper is growing rapidly; tables of results start to expand, faster than anyone ever imagined. This can be exciting, but as the Paper's owner starts to consider sending it out into the wild with all the other papers, doubts and anxieties arise. Is the Paper ready for this? Will other Papers make fun of it? Some keep their Papers cooped up indoors for years, but this is rarely conductive to their growth and maturity. Others resort to "doping" with performance-enhancing practices.

5. Peer review

In order to be accepted into the community, each juvenile must undergo the stressful and sometimes vicious ritual known as Peer Review. Breeders say that this ensures that only fit and healthy Papers can pass on their genes to future generations. However, some argue that it is all too often a random and arbitrary process which favours external plumage over true strength.

6. Adulthood

The paper is finally finished, though it rarely looks anything like anyone imagined all those years ago. Now it must interact with all the other Papers, and so the grand cycle begins anew. Every Paper-fancier's dream is that their Paper will go on to breed and raise many offspring of its own ("citations").

Selasa, 12 April 2011

First Fish, Now Cheese, Get Scanned

Here at Neuroskeptic we have closely followed the development of fMRI scanning on fish.


But a new study has taken it to the next level by scanning... some cheese.

OK, this is not quite true. The study used NMR spectroscopy to analyze the chemistry of some cheeses, in order to measure the effects of different kinds of probiotic bacteria on the composition of the cheese. NMR is the same technology as MRI, and indeed you can use an MRI scanner to gather NMR spectra.

In fact, NMR is Nuclear Magnetic Resonance and MRI is Magnetic Resonance Imaging; it was originally called NMRI, but they dropped the "N" because people didn't like the idea of being scanned by a "nuclear" machine. However, this study didn't actually involve putting cheese into an MRI scanner.

But the important point is that they could have done it by doing that. And if you did that, what with the salmon and now the cheese, you could get a nice MRI-based meal going. All we need is for someone to scan some vegetables, some herbs, and a slice of lemon, and we'd have a delicious dataset. Mmm.

How to cook it? Well, it's actually possible to heat stuff up with an MRI scanner. When scanning people, you set it up to make sure this doesn't happen, but the average fMRI experiment still causes mild heating. It's unavoidable.

I'm not sure what the maximum possible heating effect of an average MRI scanner would be. I doubt anyone has gone out of their way to try and maximize it, but maybe someone ought to look into it. Think of the possibilites.

You've just finished a hard day's scanning and you're really hungry, but the microwave at the MRI building is broken. Not to worry! Just pop your fillet of salmon in probiotic cheese sauce in the magnet, and scan it 'till it's done. You could inspect the images and the chemical composition of the meal before you eat it, to make sure it's just right.

Just make sure you don't use a steel saucepan...



ResearchBlogging.orgRodrigues D, Santos CH, Rocha-Santos TA, Gomes AM, Goodfellow BJ, & Freitas AC (2011). Metabolic Profiling of Potential Probiotic or Synbiotic Cheeses by Nuclear Magnetic Resonance (NMR) Spectroscopy. Journal of agricultural and food chemistry PMID: 21443163

First Fish, Now Cheese, Get Scanned

Here at Neuroskeptic we have closely followed the development of fMRI scanning on fish.


But a new study has taken it to the next level by scanning... some cheese.

OK, this is not quite true. The study used NMR spectroscopy to analyze the chemistry of some cheeses, in order to measure the effects of different kinds of probiotic bacteria on the composition of the cheese. NMR is the same technology as MRI, and indeed you can use an MRI scanner to gather NMR spectra.

In fact, NMR is Nuclear Magnetic Resonance and MRI is Magnetic Resonance Imaging; it was originally called NMRI, but they dropped the "N" because people didn't like the idea of being scanned by a "nuclear" machine. However, this study didn't actually involve putting cheese into an MRI scanner.

But the important point is that they could have done it by doing that. And if you did that, what with the salmon and now the cheese, you could get a nice MRI-based meal going. All we need is for someone to scan some vegetables, some herbs, and a slice of lemon, and we'd have a delicious dataset. Mmm.

How to cook it? Well, it's actually possible to heat stuff up with an MRI scanner. When scanning people, you set it up to make sure this doesn't happen, but the average fMRI experiment still causes mild heating. It's unavoidable.

I'm not sure what the maximum possible heating effect of an average MRI scanner would be. I doubt anyone has gone out of their way to try and maximize it, but maybe someone ought to look into it. Think of the possibilites.

You've just finished a hard day's scanning and you're really hungry, but the microwave at the MRI building is broken. Not to worry! Just pop your fillet of salmon in probiotic cheese sauce in the magnet, and scan it 'till it's done. You could inspect the images and the chemical composition of the meal before you eat it, to make sure it's just right.

Just make sure you don't use a steel saucepan...



ResearchBlogging.orgRodrigues D, Santos CH, Rocha-Santos TA, Gomes AM, Goodfellow BJ, & Freitas AC (2011). Metabolic Profiling of Potential Probiotic or Synbiotic Cheeses by Nuclear Magnetic Resonance (NMR) Spectroscopy. Journal of agricultural and food chemistry PMID: 21443163

Selasa, 15 Maret 2011

Neural Correlates of 80s Hip Hop

A ground-breaking new study reveals the neurological basis of seminal East Coast hip-hop pioneers Run-D.M.C.

The study is Diffusion tensor imaging of the hippocampus and verbal memory performance: The RUN DMC Study, and it actually has nothing to do with hip-hop, but it does have one of the best study acronyms I have ever seen.

RUN DMC stands for the "Radboud University Nijmegen Diffusion tensor and Magnetic resonance imaging Cohort study".

Or maybe it does relate to rapping. Because the paper is about verbal memory, and if there's one thing a rapper needs, it's a good memory for words, otherwise they'd forget their lyrics and... OK no, it doesn't relate to hip-hop.

It is however a very nice piece of research. They took no fewer than 503 elderly people - making this by far the single biggest neuroimaging study I have ever read. They used DTI to measure the quality of white-matter tracts in the brain and correlated this with verbal memory function. DTI is an extremely clever technique which allows you to measure the integrity of white matter pathways.

The theory behind the study is that in elderly people, white matter often shows degeneration. This is thought to be caused by vascular disease - problems with the blood flow to the brain, such as cerebral small-vessel disease which means, essentially, a series of mild strokes, which often go unnoticed at the time, but they build up to cause brain damage, specifically white matter disruption.

The symptoms of this are extremely varied and can range from cognitive and memory impairment, to depression, to motor problems (clumsiness), all depending on where in the brain it happens.

All of the people in this study had cerebral small-vessel disease as defined on the basis of symptoms and the presence of visible white matter lesions on the basic MRI scan. The authors found that the integrity of the white matter tracts in the area of the hippocampus, as measured with DTI, correlated with performance on a simple word learning task:


The healthier the hippocampal white matter, the better people did on the task. This makes sense as the hippocampus is a well known memory centre. This is only a correlation, and doesn't prove that the hippocampal damage caused the memory problems, but it seems entirely plausible. The authors controlled for things like age, gender, and the size of the hippocampus, as far as possible.

Should we all be worried about our white matter when we get older? Quite possibly - but luckily, the risk factors for vascular disease are quite well understood, and many of them are things you can change by having a healthy lifestyle.

Smoking is bad news, as are hypertension (high blood pressure), obesity, and high cholesterol. Diabetes is also a risk factor. So you should quit smoking, eat well, and ensure that you're getting tested and if necessary treated for hypertension and diabetes. All of which, of course, is a good idea from the point of view of general health as well.




ResearchBlogging.orgvan Norden AG, de Laat KF, Fick I, van Uden IW, van Oudheusden LJ, Gons RA, Norris DG, Zwiers MP, Kessels RP, & de Leeuw FE (2011). Diffusion tensor imaging of the hippocampus and verbal memory performance: The RUN DMC Study. Human brain mapping PMID: 21391278

Neural Correlates of 80s Hip Hop

A ground-breaking new study reveals the neurological basis of seminal East Coast hip-hop pioneers Run-D.M.C.

The study is Diffusion tensor imaging of the hippocampus and verbal memory performance: The RUN DMC Study, and it actually has nothing to do with hip-hop, but it does have one of the best study acronyms I have ever seen.

RUN DMC stands for the "Radboud University Nijmegen Diffusion tensor and Magnetic resonance imaging Cohort study".

Or maybe it does relate to rapping. Because the paper is about verbal memory, and if there's one thing a rapper needs, it's a good memory for words, otherwise they'd forget their lyrics and... OK no, it doesn't relate to hip-hop.

It is however a very nice piece of research. They took no fewer than 503 elderly people - making this by far the single biggest neuroimaging study I have ever read. They used DTI to measure the quality of white-matter tracts in the brain and correlated this with verbal memory function. DTI is an extremely clever technique which allows you to measure the integrity of white matter pathways.

The theory behind the study is that in elderly people, white matter often shows degeneration. This is thought to be caused by vascular disease - problems with the blood flow to the brain, such as cerebral small-vessel disease which means, essentially, a series of mild strokes, which often go unnoticed at the time, but they build up to cause brain damage, specifically white matter disruption.

The symptoms of this are extremely varied and can range from cognitive and memory impairment, to depression, to motor problems (clumsiness), all depending on where in the brain it happens.

All of the people in this study had cerebral small-vessel disease as defined on the basis of symptoms and the presence of visible white matter lesions on the basic MRI scan. The authors found that the integrity of the white matter tracts in the area of the hippocampus, as measured with DTI, correlated with performance on a simple word learning task:


The healthier the hippocampal white matter, the better people did on the task. This makes sense as the hippocampus is a well known memory centre. This is only a correlation, and doesn't prove that the hippocampal damage caused the memory problems, but it seems entirely plausible. The authors controlled for things like age, gender, and the size of the hippocampus, as far as possible.

Should we all be worried about our white matter when we get older? Quite possibly - but luckily, the risk factors for vascular disease are quite well understood, and many of them are things you can change by having a healthy lifestyle.

Smoking is bad news, as are hypertension (high blood pressure), obesity, and high cholesterol. Diabetes is also a risk factor. So you should quit smoking, eat well, and ensure that you're getting tested and if necessary treated for hypertension and diabetes. All of which, of course, is a good idea from the point of view of general health as well.




ResearchBlogging.orgvan Norden AG, de Laat KF, Fick I, van Uden IW, van Oudheusden LJ, Gons RA, Norris DG, Zwiers MP, Kessels RP, & de Leeuw FE (2011). Diffusion tensor imaging of the hippocampus and verbal memory performance: The RUN DMC Study. Human brain mapping PMID: 21391278

Sabtu, 26 Februari 2011

An Astonishingly Brilliant Epic Tour-De-Force

So I was browsing my local bookshop yesterday.

But what to buy? The back covers are not very helpful. Apparently, every novel published nowadays is, at the worse, a breathtaking masterpiece. Most are epoch-making, life-changing works of godlike genius.

OK, but which ones are actually good?

Why is this? Part of it, surely, is that literature is an incestuous world where the same authors who write the books are the first port of call when publishers want blurbs for everyone else's. Clearly you don't want to say anything bad about your peers lest you stop getting invites to dinner parties. Unless you're embroiled in a "bitter literary feud", but no-one has the energy to do that on a regular basis.

Because everyone is constantly complimenting each other in this way, praise inflation sets in and we soon reach the point where "This is a very good book" would be a serious insult.

There's also a theory, which has been around for a good few hundred years and maybe forever, that creative types are a breed apart from everyone else, possessed of divine powers and insight. Not just the really great artists, but any artist as a profession.

When Nietzsche wrote a book comparing himself favourably to Jesus, with chapters called "Why I Am So Clever" and "Why I Am A Destiny", people thought that was a bit much. (It didn't help that he went completely insane the next year.) You can't go on record and say that about yourself, but say it about your friends and get them to say it about you, and it seems to work quite nicely.

An Astonishingly Brilliant Epic Tour-De-Force

So I was browsing my local bookshop yesterday.

But what to buy? The back covers are not very helpful. Apparently, every novel published nowadays is, at the worse, a breathtaking masterpiece. Most are epoch-making, life-changing works of godlike genius.

OK, but which ones are actually good?

Why is this? Part of it, surely, is that literature is an incestuous world where the same authors who write the books are the first port of call when publishers want blurbs for everyone else's. Clearly you don't want to say anything bad about your peers lest you stop getting invites to dinner parties. Unless you're embroiled in a "bitter literary feud", but no-one has the energy to do that on a regular basis.

Because everyone is constantly complimenting each other in this way, praise inflation sets in and we soon reach the point where "This is a very good book" would be a serious insult.

There's also a theory, which has been around for a good few hundred years and maybe forever, that creative types are a breed apart from everyone else, possessed of divine powers and insight. Not just the really great artists, but any artist as a profession.

When Nietzsche wrote a book comparing himself favourably to Jesus, with chapters called "Why I Am So Clever" and "Why I Am A Destiny", people thought that was a bit much. (It didn't help that he went completely insane the next year.) You can't go on record and say that about yourself, but say it about your friends and get them to say it about you, and it seems to work quite nicely.

Rabu, 09 Februari 2011

Antidepressants Don't Work...In Fish

Here at Neuroskeptic fMRI scanning and antidepressants are both big topics.


As I discussed lask week, fish - specifically salmon - are the next big thing in fMRI and the number of salmon brains being scanned is growing at a remarkable rate. But fish haven't made much of an entrance into the world of antidepressants...until now.

Swedish scientists Holmberg et al have just published a paper asking: Does waterborne citalopram affect the aggressive and sexual behaviour of rainbow trout and guppy?

SSRI antidepressants, of which citalopram is one, are very popular. So popular, in fact, that non-trivial levels of SSRIs have been found in sewage and there's a concern that they might make their way into lakes and rivers and thereby affect the behaviour of the animals living there.

Holmberg et al set out to see what citalopram did to some fish in an attempt to find out whether this is likely to be a major problem. So they put some citalopram in the fish's water supplies and then tested their aggressiveness and also their sex drives. It turns out that one of the main ways of measure fish aggression is to put a mirror in their tank and see if they try to fight their own reflection. Fish are not very bright, really.

Anyway, the good news for fish everywhere was that seven days of citalopram exposure had no effect at all, even at doses much higher than those reported as a pollutant (the maximum dose was 0.1 mg/l). And the authors had no conflicts of interest: Big Pharma had nothing to do with this research, although Big Fish Farmer did because they bought the fish from one.

However, this may not be the end of the story, because it turned out that citalopram was very poorly absorbed into the fish's bloodstreams. But other antidepressants have been reported to accumulate in fish. Clearly, the only way to find out for sure what's going on would be to use fMRI...

ResearchBlogging.orgHolmberg A, Fogel J, Albertsson E, Fick J, Brown JN, Paxéus N, Förlin L, Johnsson JI, & Larsson DG (2011). Does waterborne citalopram affect the aggressive and sexual behaviour of rainbow trout and guppy? Journal of hazardous materials PMID: 21300431

Antidepressants Don't Work...In Fish

Here at Neuroskeptic fMRI scanning and antidepressants are both big topics.


As I discussed lask week, fish - specifically salmon - are the next big thing in fMRI and the number of salmon brains being scanned is growing at a remarkable rate. But fish haven't made much of an entrance into the world of antidepressants...until now.

Swedish scientists Holmberg et al have just published a paper asking: Does waterborne citalopram affect the aggressive and sexual behaviour of rainbow trout and guppy?

SSRI antidepressants, of which citalopram is one, are very popular. So popular, in fact, that non-trivial levels of SSRIs have been found in sewage and there's a concern that they might make their way into lakes and rivers and thereby affect the behaviour of the animals living there.

Holmberg et al set out to see what citalopram did to some fish in an attempt to find out whether this is likely to be a major problem. So they put some citalopram in the fish's water supplies and then tested their aggressiveness and also their sex drives. It turns out that one of the main ways of measure fish aggression is to put a mirror in their tank and see if they try to fight their own reflection. Fish are not very bright, really.

Anyway, the good news for fish everywhere was that seven days of citalopram exposure had no effect at all, even at doses much higher than those reported as a pollutant (the maximum dose was 0.1 mg/l). And the authors had no conflicts of interest: Big Pharma had nothing to do with this research, although Big Fish Farmer did because they bought the fish from one.

However, this may not be the end of the story, because it turned out that citalopram was very poorly absorbed into the fish's bloodstreams. But other antidepressants have been reported to accumulate in fish. Clearly, the only way to find out for sure what's going on would be to use fMRI...

ResearchBlogging.orgHolmberg A, Fogel J, Albertsson E, Fick J, Brown JN, Paxéus N, Förlin L, Johnsson JI, & Larsson DG (2011). Does waterborne citalopram affect the aggressive and sexual behaviour of rainbow trout and guppy? Journal of hazardous materials PMID: 21300431

Kamis, 27 Januari 2011

fMRI Scanning Salmon - Seriously.

Back in 2009, a crack team of neuroscientists led by Craig Bennett (blog) famously put a dead fish into an MRI scanner and showed it some pictures.



They found some blobs of activation - when they used an inappropriately lenient statistical method. Their point, of course, was to draw attention to the fact that you really shouldn't use that method for fMRI. You can read the whole paper here. The Atlantic Salmon who heroically volunteered for the study was no more than a prop. In fact, I believe he ended up getting eaten.

But now, a Japanese team have just published a serious paper which actually used fMRI to measure brain activity in some salmon: Olfactory Responses to Natal Stream Water in Sockeye Salmon by BOLD fMRI.

How do you scan a fish? Well, like this:

A total of 6 fish were scanned. The salmon were immobilized by adding an anaesthetic (eugenol) and a muscle relaxant (gallamine) to their tank of water. Then, they were carefully clamped into place to make sure they really wouldn't move, while a stream of oxygenated water was pumped through their tank.

Apart from that, it was pretty much a routine fMRI scan.

Why would you want to scan a fish? This is where the serious science comes in. Salmon are born in rivers but they swim out to live in the ocean once they reach maturity. However, they return to the river to breed. What's amazing is that salmon will return to the same river that they were born in - even if they have to travel thousands of miles to get there.

How they manage this is unclear, but the smell (or maybe taste) of the water from their birth river has long been known to be crucial at least once they've reached the right general area (see here for a good overview). Every river contains a unique mixture of chemicals, both natural and artificial (pollutants). Salmon seem to be attracted to whatever chemicals were present in the water when they were young.

In this study, the fMRI revealed that relative to pure water, home-stream water activated a part of the salmon's telencephalon - the most "advanced" part (in humans, it constitutes the vast majority of the brain; in fish, it's tiny). By contrast, a control scent (the amino acid L-serine) did not activate this area, even though the concentration of L-serine was far higher than that of anything in the home-stream water. How this happens is unclear, but further studies of the identified telencephalon area ought to shed more light on it.

So fishMRI is clearly a fast-developing area of neuroscience. In fact, as this graph shows, it's enjoying exponential growth and, if current trends continue, could become almost as popular as scanning people...

Link: Also blogged at NeuroDojo.

ResearchBlogging.orgBandoh H, Kida I, & Ueda H (2011). Olfactory Responses to Natal Stream Water in Sockeye Salmon by BOLD fMRI. PloS one, 6 (1) PMID: 21264223

fMRI Scanning Salmon - Seriously.

Back in 2009, a crack team of neuroscientists led by Craig Bennett (blog) famously put a dead fish into an MRI scanner and showed it some pictures.



They found some blobs of activation - when they used an inappropriately lenient statistical method. Their point, of course, was to draw attention to the fact that you really shouldn't use that method for fMRI. You can read the whole paper here. The Atlantic Salmon who heroically volunteered for the study was no more than a prop. In fact, I believe he ended up getting eaten.

But now, a Japanese team have just published a serious paper which actually used fMRI to measure brain activity in some salmon: Olfactory Responses to Natal Stream Water in Sockeye Salmon by BOLD fMRI.

How do you scan a fish? Well, like this:

A total of 6 fish were scanned. The salmon were immobilized by adding an anaesthetic (eugenol) and a muscle relaxant (gallamine) to their tank of water. Then, they were carefully clamped into place to make sure they really wouldn't move, while a stream of oxygenated water was pumped through their tank.

Apart from that, it was pretty much a routine fMRI scan.

Why would you want to scan a fish? This is where the serious science comes in. Salmon are born in rivers but they swim out to live in the ocean once they reach maturity. However, they return to the river to breed. What's amazing is that salmon will return to the same river that they were born in - even if they have to travel thousands of miles to get there.

How they manage this is unclear, but the smell (or maybe taste) of the water from their birth river has long been known to be crucial at least once they've reached the right general area (see here for a good overview). Every river contains a unique mixture of chemicals, both natural and artificial (pollutants). Salmon seem to be attracted to whatever chemicals were present in the water when they were young.

In this study, the fMRI revealed that relative to pure water, home-stream water activated a part of the salmon's telencephalon - the most "advanced" part (in humans, it constitutes the vast majority of the brain; in fish, it's tiny). By contrast, a control scent (the amino acid L-serine) did not activate this area, even though the concentration of L-serine was far higher than that of anything in the home-stream water. How this happens is unclear, but further studies of the identified telencephalon area ought to shed more light on it.

So fishMRI is clearly a fast-developing area of neuroscience. In fact, as this graph shows, it's enjoying exponential growth and, if current trends continue, could become almost as popular as scanning people...

Link: Also blogged at NeuroDojo.

ResearchBlogging.orgBandoh H, Kida I, & Ueda H (2011). Olfactory Responses to Natal Stream Water in Sockeye Salmon by BOLD fMRI. PloS one, 6 (1) PMID: 21264223