Welcome to the pleasuredome: How we evolved to love music

flute Welcome to the pleasuredome: How we evolved to love music

Part of an ancient cave bear femur flute discovered in Slovenia in 1995

In 2008 at Hohle Fels, a Stone Age cave in Southern Germany, archaeologists discovered what is thought to be the oldest example of a man-made musical instrument: a vulture bone flute dating back to the period when ancestors of modern humans settled in the area (~40,000 years ago). This discovery suggests that our ancestors were probably grooving to their own beat long before this time – making music, arguably, one of the most ancient human cognitive traits.

This raises an interesting question: In a time before electric duvets and home pizza delivery, how and why did our ancestors find time to indulge in such a non-essential task as the creation of music?

This was a mystery contemplated by the father of evolution Charles Darwin. In The Descent of Man he questions why a skill which appears to provide no survival advantage should have evolved at all, stating “As neither the enjoyment nor the capacity of producing musical notes are faculties of the least direct use to man in reference to his ordinary habits of life, they must be ranked among the most mysterious with which he is endowed”. However, in his autobiography he later suggests a solution to this mystery while reflecting on his own lack of musical appreciation, lamenting “If I had to live my life again, I would have made a rule to read some poetry and listen to some music at least once every week; for perhaps the parts of my brain now atrophied would thus have kept active through use. The loss of these tastes is a loss of happiness, and more probably to the moral character, by enfeebling the emotional part of our nature”. Here Darwin seems to have stumbled upon a fact with which many of us would intuitively agree, the notion that music can enrich our life by generating and enhancing emotions. But can we find a biological basis for this assumption?

Do you hear what I hear? – How our brains process and store sounds and melodies:

Scientists believe that we are unique in the way our brains process sounds. Unlike other animals, the auditory centres of our brains are strongly interlinked with regions important for storing memories; meaning, we are very good at combining sounds experienced at different times. This ability may have been crucial for the evolution of complex verbal communication. For example, consider times when the meaning of a spoken sentence does not become apparent until the last word – we’d have a pretty hard time understanding each other if by the end of a sentence we had already forgotten how it started! This is a skill even our closest relatives appear to lack, and one which is necessary for development of both language and musical appreciation.

We are also really good at forming long term memories for sounds – think about your favourite song, are you able to hear the music in your ‘mind’s ear’? Scientists have found that most people are able to imagine music with a surprising level of accuracy.

It is believed that throughout life, as we listen to our own culturally specific music styles, our brains develop a template of what music should sound like. These templates are specific to each individual, depending on what forms of music they are exposed to. From this we develop the ability to predict how certain music styles should sound and are able to tell when something doesn’t quite fit our expectations. The musical templates we develop throughout life provide us with a standard against which we judge the desirability of new melodies.

How music tickles the brain’s pleasure centres:

Life can be a bit of a maze, and there are times when we need something or someone to give us the thumbs up and let us know that we’re doing things right. Like a parent praising a child, our brains provide us with an internal ‘reward’ signal to let us know we’re on the right track. This system, in the brain’s mesolimbic area, is responsible for the hedonistic sense of pleasure produced by evolutionarily desirable behaviours, such as eating, sex or caring for offspring. Scientists are now able to see this reward system and the behaviours which activate it using positron emission tomography (PET) imaging. Interestingly, along with activation caused by behaviours with an obvious survival advantage, researchers have found that the strong emotional response people experience when listening to music (defined as the feeling of chill you get when listening to a particularly emotionally charged piece)  also activates this reward system.

bass Welcome to the pleasuredome: How we evolved to love musicImaging studies reveal that the rewarding aspect of music is also a very personal phenomenon, since mesolimbic activation can be initiated by different melodies in different people. This is due to the way our brains are connected. Auditory and frontal cortex regions, which store our musical preferences, are linked to mesolimbic reward pathways meaning that the sensation of music-induced pleasure is defined by your own personal musical preferences.

It is therefore possible that music could have started life as a way of strengthening social groups, through shared preferences - something which still happens today. Groups linked by a shared emotional experience could form stronger bonds which may ultimately have helped group survival. These findings indicate that our ability to enjoy music may be less mysterious than Darwin originally thought.

Post by: Sarah Fox

What songs give you the chills? Have you formed long lasting friendships over shared music tastes? Let us know your stories in the comments below.

Posted in Sarah Fox | 7 Comments

The Brain in Pain

How brain imaging technology is placing emphasis on the potential for the mind to influence our physiology, and how this influence should not be underestimated.

What really determines how we feel pain? Scientists are now suggesting that the complex emotional state of the brain may in fact bias how we process and thus experience this highly protective sensation. What’s more is that this may explain how there is such variation in our pain thresholds and how some individuals can be susceptible to conditions of chronic, prolonged pain.

Our ability to detect pain acts as an alarm system, protecting and guarding our bodies against potentially damaging aspects of our environment. This imperative awareness is mediated by ‘nociceptive’ nerve fibres that innervate our skin and organs, and feed into the pain processing pathways of the central nervous system. These fibres feed via the spinal cord to the brain stem, to the pain generating centres of the brain, most commonly the somatosensory cortex.

Izzy pic 1 The Brain in PainThe complexity of the relationship between peripheral pain input, the actual painful experience, and subsequent report of the sensation makes documenting pain in clinical research particularly problematic. Over the past decade, scientists have been addressing the inherent flaws that exist in pain research, and how this limits our understanding and progress in anaesthetic therapeutics. Experimental neuroimaging is emerging as a highly efficient method in mainstream pain research to accurately identify the key areas of the brain responsible for mediating these protective and highly important sensations. By allowing access to the brain activity where these sensations originate, experimental brain imaging allows for a more accurate and objective measure of the pain experience.

The multidimensionality of pain may be explained by the variety of sensory and cognitive aspects that may ‘tune’ our individual pain thresholds. In anaesthetic research, much emphasis is now being placed on the emotional factors and thought processes that impact how we experience pain. Consider first the manner in which we can allocate our attention to different aspects of our environment. Our ability to focus on relevant events and attenuate our responses to irrelevant events is an integral component of higher cognitive functioning. So much so, that these attentional influences may have an impending impact on the intensity of our peripheral sensations. In 2003, researchers tested the power of distraction by presenting a series of unpleasant odours to subjects whilst they were subjected to thermal pain. They found, like many other psychophysical studies, that when the subject’s attention was focused on the pain, they described the sensation as more intense and unpleasant.

Izzy pic 2 The Brain in PainThen consider, how our subjective experience of pain could be impacted by our expectations and that these expectations of pain can be attributed in part to individual trait differences: fear and anxiety may play a prominent role in the activation of pain pathways. Our cognitive predictions can be impacted by false and unequivocal beliefs stemming from inaccurate memories or inappropriate anxiety that distorts our interaction with the situation in the future. In a neuroimaging investigation in 2006, researchers identified that those individuals that were more anxious about pain (as determined by the Fear of Pain Questionnaire) showed a heightened response in brain areas that encode the emotional aspects of pain, showing their anticipatory fear could actually physically heighten their sensitivity to the painful sensation.

To the ‘normal person’, pain is a mostly acute and infrequent sensation such as a headache, bruise, or the occasional back twinge. For some people however, pain can persist for months at a time, and is often completely unexplainable. Chronic pain states include migraines, neuropathic pain and arthritis. Chronic pain is one of the largest medical health problems in the developed world because it cannot often be efficiently managed or treated. This is however, not for a lack of trying. Currently, there is little research that focuses on understanding the biology of chronic pain, but the development of neuroimaging techniques may be opening the first window of insight into the neurological framework for such conditions.

The problem with chronic pain states are that ‘secondary pain’ often develop as a consequence of the negative impact of unsuccessful treatments. Prolonged worry and emotional turmoil about chronic pain diagnosis leads to the secondary development of mood disorders and depression. The majority of this area of research has identified that a positive mood has a significant pain-attenuating effect and negative mood increases sensitivity to experimentally induced pain. Furthermore, population-based longitudinal investigations have observed that depressed individuals are at an increased risk of developing chronic pain conditions, than those without mood disorders. This evidence establishes a role for emotion-based tuning of pain modulatory systems and provides a basis for novel strategies in chronic pain management by addressing the negative lifestyle impacts associated with such conditions.

It is a common fallacy that placebo effects lack credibility or significance in modern healthcare systems. In fact, since the post-World War II introduction of placebo effects into mainstream medicine, scientists have used the impact of placebos in controlled drug trials to gather information on the qualitative nature of pain. A placebo describes an ineffectual treatment (often in the form of a sugar pill) that is intended to deceive the recipient to believe they are taking a pharmacotherapy to treat their condition. Placebo research has implicated prefrontal pathways in the brain as a source of cognitive pain modulation, because studies have consistently observed that activation of this area correlates with ‘emotional detachment’ from the pain, and thus a higher ability to cope with it. With its extensive connections to the emotion and pain processing centres, this area acts as a powerful modulator in expectation and reappraisal of the placebo effect, by dampening fear by suppressing amygdala (the emotion centre) activation. Remarkably, other personality traits like dispositional optimism can seriously enhance placebo analgesia. This research reinforces the importance of positive expectations about the efficiency of a drug and may provide an explanation for why many analgesic treatments in chronic pain are unsuccessful at a population level.

Izzy pic 3 The Brain in Pain“To consider only the sensory features of pain, and ignore its motivational and affective properties, is to look at only part of the problem, not even the most important part at that” are words from the pain researchers R. Melzack and K.L. Casey who even 50 years ago, placed emphasis on the multidimensionality of pain perception. The rapid development of neuroimaging techniques means the next 20 years are predicted to be particularly prosperous for identifying new targets in surgical and pharmacological pain relief tools. In the mean time, it seems a ‘mind over matter’ attitude could be more beneficial than we would ever have expected.

Post by Isabelle Abbey-Vital

Posted in Isabelle Abbey-Vital | 3 Comments

Headed in the right direction to treating Parkinson’s?

Stem cell researchers have been exploring ways of converting human body cells into neural cells specific to dopamine, an important chemical in the brain. Now it seems they may have found one mix of factors that stimulates this conversion directly. It is hoped that one day such cells may be suitable to replace neurons lost through neurodegeneration in Parkinson’s disease (PD).

Dopamine Pathways Headed in the right direction to treating Parkinson’s?

Dopamine pathways in the brain. In Parkinson’s disease, the substantia nigra degenerates, affecting the striatum, which controls normal motor function.

PD is becoming a growing threat to today’s aging population, with 127,000 people living with this disease in the UK alone. Characterised by the progressive deterioration of dopamine neurons in an area of the brain called the substantia nigra, patients with PD suffer from debilitating movement difficulties that worsen over time. With no cure known and only a few drugs- e.g. levadopa, a dopamine source – to manage patient symptoms, stem cell research has offered a promising new platform towards finding an effective PD treatment.

Numerous studies so far have shown successful generation of dopamine neurons by reprogramming existing donor cells, using specific proteins called transcription factors. When transplanted into rodent and primate models of Parkinson’s disease, these neurons can help alleviate symptoms.

Unfortunately, the two donor cell types suggested for cell conversion until now face various issues. Embryonic stem cell (ESC) use is ethically controversial, while manipulating mature cells- for instance, fibroblasts – to dedifferentiate first to become induced pluripotent stem cells (iPSCs) is time consuming and expensive.

One potential solution? – Cut out the middle men (the iPSCs).

 Headed in the right direction to treating Parkinson’s?

A colony of embryonic stem cells. The cells in the background are mouse fibroblasts cells. (NIH image)

Xinjian Liu and his team at the Radiation Oncology department at Colorado University, have been working to generate dopamine neurons directly from human fibroblasts, without producing iPSCs first.  And it seems they may have identified a suitable combination of transcription factors that makes this happen.

Liu’s group applied transcription factors, Mash1, Ngn2, Sox2, Nurr1 and Pitx3 to human fibroblasts, and found that dopamine neuron-like cells were produced directly. These cells stained positive for dopamine neuron-specific markers and took up and released radioactively-labelled dopamine, just as the control dopamine neurons. When transplanted into rat PD models, the rats’ symptoms improved, with the animals’ rotational behaviour (a measure for their motor abilities) recovering.

Of course, the reality of generating new dopamine neurons that successfully transplant into patients with PD is still far from becoming a viable clinical treatment. Nevertheless, the discovery that Liu’s mix of transcription factors is sufficient to reprogram already mature cells directly into dopamine neuron-like cells presents an exciting step forward towards treating this devastating disorder.

Guest Post by Megan Barrett

Reference: Cell Research, DOI: 10.1038/cr.2011.181

Megan is currently working as an associate writer at a medical communication company. You can follow her on Twitter @Meg_an12.

Posted in Guest | 3 Comments

Do you want to know what secrets are concealed in your genes?

If you have been living on Earth recently, you’ll have come across the news that a certain Hollywood actress has undergone major preventative surgery due to the discovery of a faulty gene. The gene in question is called BRCA1 and, if mutated in a certain way, it is known to greatly increase a carrier’s chances of developing breast cancer. This incident has thrust genetic screening into the limelight – but how useful is it to know the secrets concealed within your genes?

DNA copy Do you want to know what secrets are concealed in your genes?We now have technology to take screening even further. Writer and journalist Carole Cadwalladr reports in the Guardian that whole-genome screening by Illumina is now available for just $5,000. That may seem a lot, but considering it would have cost $2.7 bn just 10 years ago, it’s a hell of a price cut. Several other companies, including  23andme and AncestryDNA are also offering to screen your genome and let you know what, if any, potential disease-causing mutations you have. Some of these scans cost as little as $99.

But do you really want to know what, if anything, is wrong with your genes? In some circumstances screening can be very useful – it can save lives. When Angelina Jolie tested positive for the BRCA1 mutation, she took the decision to have a preventative mastectomy. She hopes this will allow her to avoiding the pain of cancer and the pain her children would face watching their mother suffer; a pain she herself knows all too well. In cases like this, screening and early intervention is important because we know that a mastectomy can greatly reduce a carrier’s chances of developing the disease.

baby copy Do you want to know what secrets are concealed in your genes?

Photo: Ajsmen91, commons.wikimedia.org

But what if there is no prevention for the disease detected by the sequencing? One of the more famous examples of this is Huntington’s Disease. Huntington’s is a debilitating degenerative disorder characterised by shaky, jerky movements (called chorea) and progressive cognitive decline. It is caused by a single faulty gene, huntingtin. This gene is inherited in a dominant fashion, meaning that if one of your parents has the disease, you have at least a 50% chance of also suffering. As sufferers do not generally start to show symptoms until their 40s, they may not realise they carry this mutation until after having children – who will therefore also be at risk. It is now possible to screen people for the faulty huntingtin gene. However, there is no cure for Huntington’s. Knowing you have the gene will not help you to prevent the onset of disease; therefore do you want to know? This is a dilemma that many children of Huntington’s sufferers face. Some decide it’s best to know, especially if it will influence their choice to have children, but others would prefer not to have this time-bomb ticking over their heads.

Genome screening could allow people to adjust their lifestyle to counteract a faulty gene. For example, it is common knowledge that smoking can cause lung cancer. However, everyone also seems to have a great-aunt Gladys who smoked 90 a day and died at 102 after getting hit by a bus. On the flip side, there are people like the Record Breakers presenter Roy Castle, who died of lung cancer despite being a non-smoker. It may be that your genes determine whether you are more like Gladys or Roy. If you get your genome screened and it turns out you’re more like Roy, you could adjust your lifestyle accordingly and quit (or not start) smoking.

I’m also going to use a personal example here. If you are familiar with this blog, you may know that there is a history of Alzheimer’s Disease and dementia in both sides of my family. The cause of Alzheimer’s disease is so far not clear-cut; it appears to be a mixture of genetic and environmental factors but nothing is known for sure. One of the strongest genetic links so far is a gene called ApoE. If you have a version of the gene called ApoE4 you are at higher risk of developing Alzheimer’s. However, it does not necessarily mean that you will suffer from the disease.

Cumin copy Do you want to know what secrets are concealed in your genes?

Cumin Seeds
Photo: Humbads, commons.wikimedia.org

So let’s say, hypothetically, that I had my genome screened and it confirmed I had the ApoE4 gene. What can I do with this information? Well, the first thing I’d probably do is panic. I’ve seen Alzheimer’s disease happen and don’t really wish to go through that. However, I am now prepared. I am at higher risk; therefore I need to try and counteract that risk. There are several methods which have been suggested to reduce the risk of Alzheimer’s disease, including eating curcumin, a spice found in curry, and keeping the brain active by doing crosswords or learning a musical instrument. I could also avoid sugary foods, as there is increasing evidence of a link between diabetes and Alzheimer’s disease. So now I’m more informed, I can happily shovel spoonfuls of chicken tikka masala into my mouth with one hand whilst playing the piano with the other and hopefully I won’t get Alzheimer’s.

But there’s another side to this. If I have the faulty gene, I will probably have inherited it from at least one of my parents. Which one? Should they get screened too? What if it’s too late for them to take preventative measures and now all they know is that at some point they might get dementia? What happens if I have children? Should they be screened? How early on do you need to start taking preventative action? What if the screen flags up another faulty gene? Or several? What if I can’t prevent a disease caused by these other faulty genes and so will have to go through life knowing that I will at some point suffer from it?

As this is a whole-genome screen, as opposed to a screen for one particular gene, it is also likely to pick up genes that you weren’t even aware you carried. Some mutations are carried silently through families, or your DNA may have become mutated another way, e.g. through smoking or exposure to UV light. Do you want to know that you may at risk of a disease you may never even have heard of? Again, good if it’s preventable (for example you discover an allergy to a medicine that you haven’t yet had to take) but if it’s not preventable, what does that leave you with? That ticking clock over your head.

The other issue here is how this type of information will be used. Illumina loads the data onto an iPhone app for you, meaning that the data must be stored somewhere. Who else has access to that information? How secure is it? Could it be possible in the future that people start demanding to know the results of genome screens for potential prime ministers to make sure they’re not going to suddenly get cancer whilst they’re supposed to be running the county? And what if health insurance companies start demanding full-genome screens before you can get a policy?

Also, new genetic links to diseases are being discovered all the time. So a screen done now may miss a genetic mutation that is flagged up in the future as being a possible cause for disease. Would you have to get screened more than once? Maybe you’ll need to be screened every few years to keep up with discoveries being made.

I feel I should point out here that the science behind this technology is amazing. The fact that it is even possible is a huge achievement and a testament to the dedication and innovation of the scientists who developed it. And it was invented to help people – to screen for faulty genes with the idea of saving lives. I have worked in a lab which has collaborated with Illumina and in doing so the lab was able to identify a new Alzheimer’s risk gene (the catchily named PCDH11X). This is all useful and helpful information. However, my worry is that the information will be exploited by other people looking for a profit, or preying on people’s fears, as unfortunately these things so often are.

Charlemagne copy 289x300 Do you want to know what secrets are concealed in your genes?

A coin showing your ancestor, Charlemagne
Photo: Fallschirmjäger, commons.wikimedia.org

But what about if you’re having your genome screened to discover the secrets of your ancestry? This was done recently for Prince William, and the papers excitedly claimed that “he will be the first king of England to have a genetic link to India“. However, using these services to find your ancestry may be interesting but it is not always accurate. As explained by this Sense About Science leaflet, genetic screening is not an exact science. Also, when you’re told that you are related to Charlemagne, well, so is everybody else alive today (according to an episode of QI, anyway). Most genetic ancestry screens will only go via one line – either your mother’s, through mitochondrial DNA, or your father’s, through the Y chromosome line. This leaves out an awful lot of your other potential ancestors, for example your maternal grandfather or paternal grandmother. These screens do not, and probably cannot, tell you the whole story of your ancestry.

Is it a good idea to re-open Pandora’s Box, especially if you’re just curious about your genes? Will it save millions of lives or lead to a weird state where everyone has to know exactly what disease they may or may not suffer from at a given point in time? I think, like the people at risk of Huntington’s, and like Angelina, it’s a personal choice. Some people are happier not knowing, some will want or need to know. No one should ever be forced to have their genome screened. Measures also need to be taken to make sure that this information stays personal and secure. I’m nervous about the idea that what your genes hold may become public knowledge. I personally don’t think I want to know what’s in my genes. I am already aware that I am at risk of developing Alzheimer’s, and there’s no harm in taking preventative measures anyway. I do like a good curry.

Post by: Louise Walker

Posted in Louise Walker | 2 Comments

Nerve regeneration: do good things come in small packages?

The 3101400087 b3cd617096 Nerve regeneration: do good things come in small packages?holy grail of treating neuronal injuries is to persuade damaged neurones to regrow exactly as they were. Currently doctors lack the tools to do this, but hope is in sight in the world of nanotechnology.

Unfortunately, once nerves have suffered damage they don’t simply grow back to their original position. There are a number of reasons for this:

  • Inflammation gets in the way
  • Molecules found primarily in the mature nervous system inhibit growth
  • Gaps formed in nervous tissue caused by the “cleaning up” of injured cells form a barrier to growing cells
  • Cells fail to start regrowing

But how can nanotechnology help?

Nanotechnology is the science of the very small (on the scale of billionths of a millimetre) but it’s an enormous area of research – in many countries nanoscience is the priority for science budgeters.

Successful attempts have now been made to use nanotubules as a type of molecular scaffolding to support nerve growth. A nanotubule is a tiny (on the nanometer scale) tube-like structure – like a microscopic drinking straw. The first application of these tubes showed that, when coated with substances that encourage neuronal growth, carbon nanotubles were able to promote extension of rat embryonic nerve cells. These tiny tubes acted as a physical scaffold to guide the cells, while also providing chemical signals ‘telling’ them to grow and survive.

Carbon nanotube armchair povray Nerve regeneration: do good things come in small packages?

Nanotubes made of amino acids (the building blocks of proteins) have also been developed. These amino acids can interact directly with receptors on nerve cell membranes and have proved effective at encouraging growth and limiting the damaging effects of scar tissue. Because these are composed of naturally-occurring amino acids they are not toxic to cells and caused no inflammation or immune response in animals. This is a serious benefit, as inflammation can be very damaging in neuronal injury.

However, the unique features of nanomaterials could also be associated with unique problems. At high concentrations, some studies have found nanotubes of certain sizes to cause DNA damage, accumulation and inflammation in the lungs. Another concern is that nanoparticles can move around the body: one study showed that nanoparticles could be transmitted up nerves and into the brain. Nanotechnology may represent an exciting opportunity in medical science, but it also comes with the major challenge of understanding how the behaviour of these materials interacts with the human body.

Post by: Claire Scofield

Posted in Claire Scofield | 1 Comment

Synesthesia: How does your name taste?

Are you convinced that Mount Everest tastes like strawberries? Or that Friday is a deep green colour? Does hearing your friend Dave’s name make you wretch? If so, you might be entering the baffling world of synesthesia.

colour Synesthesia: How does your name taste?

Synesthesia (synaesthesia in British English) is a neurological condition whereby one’s senses literally merge. It means ‘joined perception’ and can cause names to have a particular taste, letters to have a particular colour and a whole host of other sensory fusions.

It may sound more like a psychedelic experience in a drug-induced haze but this is a sober reality for a number of people. Some of the most famous creative types of our times have been diagnosed or suspected to have synesthesia. Marilyn Monroe was described by the biographer Norman Mailer to have a “displacement of the senses which others take drugs to find… she is like a lover of rock who sees vibrations when she hears sounds”.

Stevie Wonder by CaramelBeauty77 Synesthesia: How does your name taste?

Image credit: CaramelBeauty77

Stevie Wonder reportedly has sound-colour synesthesia whereby even though he is blind, he ‘sees’ the colour of the music. This added sensation is not restricted solely to arty types, however. Richard Feynman, the excellent Nobel Prize winning physicist, claimed “When I see equations, I see the letters in colours”, before quipping, “I wonder what the hell it must look like to the students”.

Estimates put the number of synesthetes at between 1 in 200 and 1 in 100,000 (which basically means we really don’t know how many people experience synesthesia). Some even claim it could be as high as 1 in 23! If any of this sounds familiar to you, you can test whether you may have synesthesia here.

There is a lot of fascination from scientists into this condition. The organisation of the senses is seen to play a major role in formation of memories. When you form a memory of a person, you link the information from multiple senses. The sound of their voice, the colour of their hair, the letters of their name all form your memory of that person. But for most of us, these senses still exist as separate aspects of our memory of that person. You don’t intrinsically link the letters of their name to their hair colour.

Synesthetes have secondary sensory experiences that are completely involuntary. Some synesthetes say that the colour of someone’s name is actually how they remember them. They may remember the name Dave by the colour orange more than the letters of the name.

This is where the science behind it all comes in. Sensory information should be contained separately but able to be integrated at will. Different sensory information is processed in largely the same way but in distinct sensory regions. You can see below the various parts of the brain that are responsible for the different senses. As you can see they are spatially separate. The beauty of the brain is connecting this information as and when it is needed.

Senses Synesthesia: How does your name taste?

What appears to be the case in synesthetes is that these sensory regions are intrinsically connected. For example, sound-colour synesthetes seem to have more activity in colour-processing regions of their visual cortex (known as area V4) while listening to sounds. Instead of distinct pathways being linked at will, it could be the case that these two systems are bound together and stimulation of one sense also activates another.

It is interesting to be able to see these differences in the brains of synesthetes. What is not very clear, however, is why synesthesia is around at all. Does having synesthesia benefit you in any way? It appears that actually it might.

Synesthetes have been known to be better at remembering phone numbers, for example, suggesting they may have better memories. Letter-colour synesthetes have also shown they can be better at discriminating between different colours, whilst hearing-motion synesthetes are better at visual tasks. So could this be a rise of the superhumans – an evolutionary advantage to be able to process more sensory information than the rest of us?

Further research into synesthesia will not be a purely academic exercise but will contribute further to our understanding of the human brain. How the brain links information together on request is one of the major mysteries of neuroscience, a point focused on in Obama’s BRAIN initiative. As synesthetes show remarkable differences in how they integrate information, it will be fascinating to see whether they can be the valuable subjects to advance our knowledge of the brain.

Post by: Oliver Freeman @ojfreeman

 

 

Posted in Oliver Freeman | 14 Comments

The mystery of the appendix

The appendix gets a lot of bad press. We often think of it as one of the most pointless parts of our body that lacks any real purpose or function. But this may actually be far from the truth, with eye-opening research pointing towards an important role for this organ.

The appendix is a small, worm-shaped structure Appendix 1 300x203 The mystery of the appendix
located on the lower right side of the abdomen, connected to the cecum. Many of us are naïve about what it does, and often the only time that we hear about the appendix is when it becomes infected. When infection occurs we remove it without much second thought. Unlike the majority of organs in the body, little is known or understood about this mysterious organ.

Often we think of the appendix as simply an evolutionary remnant from times gone by, much like the coccyx found in humans (what remains from ancient tails or vestigial hind limbs in snakes, a reminder of past legs). Scientists as early as Darwin have theorised about its purpose, and come to the conclusion that it is an archaic organ, which became useless millions of years ago. This theory proposes that long ago the appendix was important for digesting very tough food such as leaves and tree-bark, but as human diets began to transform, so did the appendix. As humans began to eat more fruit and less vegetation that was hard to digest, the appendix began to shrink into what we recognise today. Some have even gone so far as to say that in the future the appendix will disappear entirely as it becomes redundant.

Although this explanation seems plausible, it seems naïve of us to assume that the appendix has no purpose. Why would an organ that supposedly has been redundant for so long remain in our bodies? Bill Parker from the medical centre in Durham, North Carolina has suggested a rather radical U-turn for the role of the appendix.

Appendix 2 300x169 The mystery of the appendix  Parker suggested that the appendix could be useful to the ‘good’ bacteria in our gut, ensuring the smooth running of our digestive system. We know that our bodies are made up of trillions of cells, but actually houses around 10 times that number of micro-organisms, most of which are found in our guts. We have a symbiotic relationship with these organisms; they use our energy by digesting our food, and in return these ‘good’ bacteria help to prevent the spread of harmful bacteria and this is vital to the health of our gut.

According to Parker, the appendix may be vital in protecting our intestines ‘good’ bacteria from the ‘bad’ bacteria that try to invade our gut. Essentially, you could think of the appendix as a sanctuary or a weekend spa retreat for our vital microbes. These tiny bacteria can use the appendix as an area of respite from the strain of the harsh environment in the gut. When the stores of bacteria in the gut become depleted, bacteria can be released from the appendix to fill their place.

Although this theory is interesting, there has been little in the way of supporting evidence. One study led by James Grendall at the Winthrop University Hospital in America agrees with Parker’s theory. This study involved 254 patients each of whom had a history of gut infections caused by Clostridium difficile, and had been on antibiotics as a result. Patients that remain on antibiotics for a prolonged period of time can suffer from depletion in the ‘good’ bacteria in their gut, making it harder to fight off the bad guys.

Based on Parker’s theory, those individuals with an appendix should have a better chance at fighting off the infection by producing and sending more of the ‘good’ bacteria into the gut. However, those who have had their appendix removed may be unable to release these protective bacteria to replenish the stock in the gut, and therefore the ‘bad’ bacteria can take over.

What they found was striking. Out of the 254 patients, those without an appendix and consequently the bacteria housed there, were twice as likely to have a recurrence of the infection. Recurrence was likely to occur in 45% of cases when there was no appendix, compared to 18% recurrence in individuals who did have one.

We also know that the lining of the appendix is rich in infection-fighting lymphoid cells that accumulate shortly after birth, peaking in our 20’s and 30’s but rapidly decreasing as we age. This lymphatic tissue encourages the growth of beneficial gut bacteria.

Although it is tempting to believe that our appendix is a redundant vestigial organ, there is the possibility that it plays a role in protecting the ‘good’ bacteria in our gut. There is however little in the way of research to confirm its role one way or another. I think for now the exact role of the appendix will remain a mystery, at least until more research is carried out.

Post by: Sam Lawrence

Posted in Sam Lawrence | Leave a comment