Sarah Fox

The term ‘haunting’ is generally applied to cases involving recurrent phenomena, of a supposedly paranormal nature, that are associated with particular places. Approaches to understanding hauntings can be divided into two categories: those that attempt to explain the manifestations ‘naturalistically’ (e.g. non-paranormal explanations), and those that employ paranormal concepts such as telepathy or the laying down of a ‘psychic trace’. – Peter A. McCue (2002)

“You know it’s all a load of b******s, just tricks of the mind….that’s why ghosts only come out at night,” I splurged as we sped along the A6. Miranda just laughed.

It was the weekend after Halloween and as a ‘bit of fun’ we had decided to drive across to Bakewell, enjoy the scenery, have a bite to eat, then, at twilight, wander down to the infamous ‘Shady Lane’. The Lane is said to be narrow and heavily wooded in parts; from all accounts a pretty creepy place to visit at any time of the day. However, according to legends the real horror comes at twilight. It is said that a procession of 12 headless men walk this lane in the failing light carrying an empty coffin. Apparently, if you are unlucky enough to catching a glimpse of these grisly coffin bearers it represents an omen of your imminent death.

I shuffled uncomfortably in my seat. Planning the trip had seemed like a bit of a laugh, something a bit different, a bit ‘hands on’ to do for Halloween and being scientists we knew it was all rubbish…didn’t we. However, I still couldn’t shake the feeling of unease.

As the bleak November countryside rushed past the window I turned to Miranda and, trying to add a sarcastic inflection to my voice, asked, “Do you think we’ll see anything?”. “I guess it depends if it’s our time or not,” she replied with a giggle, then after a pause added, “you’re not getting nervous are you?”.

“About what?” I replied, “The scary headless ghosts? Ha, there are enough real things to worry about without adding ghosts and goblins to the list. You know I have a presentation to give on Monday, now that’s scary”. She smiled and I turned back to the window.

The truth was however, that even though my logical brain knew that there was no real evidence behind the stories, just tall tales and folklore, I couldn’t shake the nagging doubt of the ‘what-if’s. That and, being a neuroscientist, I knew how amazingly deceptive the mind can be. Apparently most ghostly sightings and paranormal experiences can be explained away by tricks of the mind; states of heightened fear, tiredness, low light, even the obscure phenomena of ‘infrasound‘ can all trick us into experiencing things which just aren’t there. Yes I’d been researching it; but, despite my scepticism, after reading numerous ‘eye-witness accounts’ of experiences on Shady Lane my mind was primed for something paranormal.

It was about twelve o’clock when we eventually pulled into a small local car park. The clouds, which had been threatening a downpour since the start of our journey, finally made good on their threat and as we stepped out of the car the heavens opened. Pulling our hoods tight, we rushed for the nearest restaurant, fish and chips, no complaints there. I felt myself relax slightly as the familiar sounds and smells of the restaurant washed over me. After all, what reason did I have to be tense, this was just a normal day.

“Have you ever seen a ghost?” Miranda asked as we sat down.

“No,” I replied, “I tend to have a good relationship with the paranormal, I leave it alone and it leaves me. But actually,” I ventured, “…I do get sleep paralysis! Since I know what it is, it doesn’t scare me but I read that it’s responsible for a fair number of apparent ghost sightings”. Intrigued, Miranda leant in, “I’ve never heard of it before…..what is it?” she asked.

I decided to opt for a simple explanation, “It’s kinda the opposite of sleep walking. It’s when your mind wakes up, but your body stays paralysed. You feel like you’re awake, but you’re still mentally in a more suggestive ‘dreamy’ state. Since you can’t move or open your eyes your mind can play tricks….I often hear footsteps and sometimes feel like there’s someone or something in the room, often it feels like something is sitting on top of me”.

“Like a perverted ghost,” Miranda joked.

“Yeah, something like that,” I replied, “It’s relatively common, and can be explained scientifically, but before people knew what it was many thought they were experiencing a ghostly presence holding them down. It’s spooky stuff if you don’t know what you’re dealing with!”. Miranda looked genuinely concerned, “It sounds horrible,” she muttered.

“Yeah, but I guess it’s just an example of how complicated our minds are,” I said, “We’re all exposed to some pretty strange ideas in life, like ghosts and boogy men. I guess there are times, when you’re tired, or feeling scared, that your mind can wander; you know, create things which aren’t really there from its own imagination or fears… like your own internal horror movie ”.

I paused for a minute. The conversation had shifted and I wondered whom I was trying to convince with my rant. Perhaps, if I can recognise the reality behind these nocturnal horrors, I had no reason to be scared of Shady Lane? The logic is no different…“Are you ready to order?” chimed the waitress, snapping me back to reality with a jolt. Miranda glanced over, obviously noticing me jump at the unexpected intrusion. “You sure you’re OK?” she quizzed.

“Yeah, I’m fine, just got side-tracked” I smiled, and we ordered our meals.

As the day drew on the rain subsided and we decided to explore the town. Wandering round the shops we discussed more of our own personal ghostly experiences, debunking myths as we went, until eventually I started to wonder what I was so concerned about. Ghosts and ghouls are all in the mind; as long as you’re strong and can control your own fears you have nothing to worry about. With the acquisition of this new personal bravado I began to feel better prepared for our evening’s escapades.

It wasn’t long before the light began to wane and I soon found myself taken from the comfort of the busy shopping centre back to the car. The lane was a few miles outside Bakewell close to the village of Little Longstone. Our plan was to park up at The Packhorse Inn, a local pub in the village, then walk the rest of the journey to the lane, returning after dark for a well-deserved drink.

By the time we arrived at the pub the rain had started again, not a downpour this time, but rather a homogeneous haze, the kind of rain which manages to get you wet within minutes no matter how hard you try to avoid it. “Picked a great day for it,” I groaned.

“Well, it is November in the Peaks, what do you expect?” replied Miranda, then adding quietly, “You know if you’d rather stay here, have a drink and some food – I don’t mind”. For the first time that day I sensed a wavering in her resolve. Miranda was by far the most sensible and down-to-earth of my friends, to recognise the shudder of anxiety in her voice was particularly unusual. I’m not sure why, but something about her uncertainty spurred me on, giving me confidence… now I was the brave one!

“Ha, we can’t leave without even seeing the lane, Matt said we would chicken out, you don’t want to prove him right do you? He’ll never let us live it down,” I replied, grabbing my waterproofs from the boot of the car. “Lets do this!”

Ahead over two fields, then turn left on the Monsal Trail. Just before the railway bridge turn left up the steps then, at the top, turn right over the bridge.

We followed the directions I printed from the internet and soon found ourselves standing at the opening to the Lane. The ground was loose under our feet and a combination of the rain and waning light made it hard to see too far ahead. Miranda turned to me, “So you’re sure about this? You have been a bit off today you know”. I glanced back at her, trying to conceal the pleasure I suddenly felt over her uncertainly, “Don’t be silly,” I said with a cheeky grin, “I’m fine, lets go”.

Overcome with a sudden childish sense of accomplishment and mastery over my fears I began to run down the path. “Catch me if you can, slow coach,” I shouted as I sped around a bend.

Giggling to myself over how silly and unwarranted my earlier fears had been I slowed to catch my breath. The path was particularly narrow at this point and overhung by an unusually thick canopy considering the time of year, bloomin’ global warming. I squinted ahead through the gathering gloom, it looked as if further along another path joined the lane. Most likely the entrance to Thornbridge Hall. I glanced back to see if Miranda had caught up with me. I could just make out something moving in the distance, perhaps a flash of pink, could it be her coat? I was about to shout to her when something drew my attention, halting the words before they left my mouth. A shuffle, definitely the sound of movement coming from towards the turning. I spun around to try and glimpse the cause of the noise, but the path ahead looked deserted. Then it came again, the crunch of wet leaves underfoot, under a number of feet. My bravado all but gone, I felt my heart begin to race. If I could just get back to Miranda, get her attention, I’d be OK. But my legs wouldn’t move and my voice wouldn’t come. Cemented to the spot I stared helplessly ahead. Then they came, hazy at first and obscured by the rain, but certainly there. They were people, a group of them, moving slowly down the lane. I couldn’t see their faces, perhaps they were wearing hoods – or were they just headless? I felt faint.

Just as the last of my strength drained away and I felt the sudden pressure on my knees as I slid to the floor something else moved. Faster and smaller than the figures it appeared from between them, rushing towards me. Closing my eyes in panic I quietly prepared for the end.

Warm and wet, something landed on my chest, breathing heavily against my face and…licking… “Toby….Toby….what are you doing? Leave her alone,” a man shouted. “Are you all right luv’?”. I opened my eyes. There standing in front of me was a group of ramblers, with their hoods pulled tight against the rain and a large chocolate Labrador staring happily at me and panting. The dog’s owner looked concerned and offered me his hand. “I’m so sorry, Toby can be such a handful, he just loves people, but he doesn’t know his own strength”. My mind raced as I tried to make sense of what just happened. I reached for his hand and soon found myself lifted back to my feet. Miranda, having just caught up to me put her hand on my shoulder. “What on earth happened? Are you OK?”.

“I’m really sorry,” interrupted a young woman wearing a purple rain coat, perhaps the wife of the man who helped me up. “It’s our dog Toby, he got excited and knocked her over”. Sensing Miranda was about to jump to my defence I finally found my voice. “I’m fine really, no damage done, I have dogs too, so it’s no problem”. The woman smiled at me, “It’s getting late you know, where are you both heading?”.

“Back to the Packhorse Inn, in Little Longstone,” interrupted Miranda before I had time to speak.

“Ah so are we,” the woman replied. “How about we go together?”. Miranda caught my eye and I nodded feebly.

“It’s not like you to be floored by a dog,” she whispered as we started back towards the Inn.

“I’ll tell you all about it over a drink,” I muttered hoarsely and continued on ahead.

It had taken some time, but as we walked out of Shady Lane I began to piece the experience together in my mind. Perhaps I was more fallible than I imagined. I sighed, it seems no one is immune to fear. The group were chatting loudly amongst themselves “Did you hear the story about this lane? Apparently it’s haunted!”. “What a load of rubbish, you don’t believe in that kind of stuff do you?”. I turned to join in the conversation, but was interrupted by a sudden overpowering smell of incense, which vanished almost as quickly as it had appeared. “Did you just….” I turned to Miranda.

“Did I just what?” she replied.

I shook my head “Oh nothing, nothing, lets just get back”….

Story by: Sarah Werefox

Scientists from North Carolina have developed and implemented a neural implant designed to improve higher-order brain processing- providing hope that one day such implants may be developed to alleviate symptoms of cognitive impairments such as Alzheimer’s.

The brain: the final frontier. Neuroscientists around the world are working painstakingly to uncover the mysteries of the brain and ultimately find ways to reinstate functionality lost through damage or disease. One area of research offering such promise is the field of neural prostheses. At a basic level this work endeavors to repair faulty neural connections by interfacing the brain with computer technology. Significant advances have been made in connecting the human brain with the outside world through sensory and motor prostheses (for example the artificial retina). However, the task of restoring or improving cognitive function has yielded very different problems to those addressed in the development of sensory and motor interfaces.

To restore cognitive function, a neural implant must gather data from one area of the brain, process this information correctly and then deliver the resulting signal to another brain region, bypassing any damaged tissue. This process necessitates an understanding of how different brain regions communicate with each other and how this communication is modified as it travels through the brain in the form of electrochemical impulses. Although this is certainly not an easy task, if successful, this research will have a profound impact on the quality of life throughout society, offering promise for people suffering from a range of disorders including Alzheimer’s, stroke and various other forms of brain trauma and degeneration.

Sam Deadwyler and his team at Wake Forest University School of Medicine in Winston-Salem, North Carolina have recently taken an important step toward making cognitive enhancement via neural prostheses a reality. This group is the first to study the effect of brain implants on decision-making in behaving primates. Their work focused on an area of the brain known to be involved in decision-making; the prefrontal cortex. The structure of this region is well-known and can be separated into a number of layers, each containing different types of brain cell. These cells form connections between layers, passing information through the structure. The team developed an implant which could span a number of these layers. This implant was positioned to record activity simultaneously from both layer2/3 and layer 5 and to deliver custom-designed stimulation to layer 5 cells.

The first task faced by the team was to understand how cellular activity changed when the monkey made either a correct or incorrect decision. To achieve this, the group monitored activity across the implant as the monkeys performed a memory task (choosing a familiar image from a group of unfamiliar images). The team focused on cellular recordings taken just prior to the point when the animals made their choice: the decision period. After observing a number of trials, they found that they could predict how cells would respond to both correct and incorrect decisions. This meant that the scientists were able to ‘decode’ the language of the cells and predict what choice would be made before the animal actually made it!

Now that the group knew what a correct response looked like they were able to write a pretty complicated algorithm to mimic this activity and replay it to cells in layer 5. Amazingly they found that animals stimulated with this artificial activity pattern performed significantly better on the task than animals receiving no stimulation. Indeed, in some of the harder tasks (ones using more images) the animals improved both their speed and accuracy, in some cases improving their average performance by 10-20%. This improvement was also dependent on the stimulation provided. For example an improvement would only be seen if a monkey was provided with a ‘correct’ stimulation pattern calculated from its own data, but not when the experimenters used patterns taken from other animals or arbitrary patterns.

The next question was: if this stimulation could improve performance in normal animals, could it also recover the ability to make correct decisions in animals with specific impairments? This is an important question, since the ultimate medical goal for these implants would be to restore lost functionality. To answer this question the team used a drug that they knew reduces connectivity in the prefrontal cortex and impairs decision-making: cocaine. Monkeys given cocaine performed poorly on the task, being on average 10% worse than their sober counterparts. The team was able to monitor layer 2/3 activity in these animals and judge when an incorrect decision was about to be made, then replace the incorrect activity with their own simulated correct firing pattern. This intervention not only restored normal function but actually raised the cocaine-treated animals performance scores even higher than non-treated animals.

It can’t be denied that from both a technical and medical standpoint, these findings are amazing. However, I believe there are still a number of hurdles to be cleared before we see this technology implemented in patients suffering from cognitive deficits. Many cognitive disorders, such as Alzheimer’s, involve widespread damage incorporating a large number of higher-level processing areas. It is therefore an absolute requirement that we first understand exactly how information is processed in these systems, before we attempt to bypass or repair them. Although this implant certainly improved performance, it relies significantly upon mimicking what is known to be a correct response rather than understanding how the system works. This reminds me of my primary school recorder lessons, where I learned to play by watching where other pupils put their fingers instead of learning to read the sheet music. The end result may be similar, but you can go much further and make fewer mistakes if you fully understand the system! Therefore I think the ‘take home’ message from this study is; we have made some promising progress towards improving cognition through neural implantation, however if we ultimately want to treat widespread neural damage we still need to get a better grip on how these systems function before we move toward treatment.

Post by Sarah Fox

We are without doubt one of the worlds most complicated machines. Our bodies are made up of trillions of cells, most of which contain a full copy of our own individual genome. Despite containing identical genetic information individual cells vary hugely in structure and function, for example, just think of the differences between skin and brain cells. This variation is achieved through the specialised way each cell reads it’s own copy of the genome, allowing cells to create only the components they require to function. One of the biggest challenges faced by biologists and medics today is bringing together our understanding of genes, gene processing, cellular and systems biology to gain a better understanding of how our bodies work, and what happens when things go wrong. Such research has lead us to appreciate just how individual we really are! It has highlighted how a combination of genes, environment and even our own compliment of bacteria can profoundly affect the way our cells function and ultimately our health. This ability to delve deeper into our inner workings has also spawned a new field of medicine known as personalised medicine.

Personalised medicine refers to the idea of tailoring treatment to an individual – the right drug or medical intervention for the right patient. In practice this doesn’t mean making a new set of drugs for each individual, instead, it focuses on defining specific groups of people who are more or less likely to respond to treatment. Our current system relies on a ‘blanket’ method of treatment, i.e. everyone suffering from the same ailment will be treated with the same drugs/procedures. However, we now know that differences in genes and gene expression mean that individuals are unlikely to respond in the same way to medical treatments. This may go some way to explaining why between 30% and 70% of patients fail altogether to respond to drug treatment (1). It is ultimately hoped that a better understanding of how genes influence drug metabolism and function will improve both patient prognosis and reduce unnecessary spending on unsuccessful treatments. Indeed, progress is already being made towards a more personal approach to medicine:

One of the first major successes for personalised medicine came from the breast cancer drug Herceptin (Trastuzumab). In approximately 20% of invasive breast cancers a cell surface protein known as the HER is over produced causing cells to replicate uncontrollably. Screening tests have been produced to detect this defect and HER positive patients have been successfully treated with herceptin (an antibody which binds to the HER protein reducing cell replication). This breakthrough was soon followed by the discovery of a genetic abnormality, known as the Philadelphia translocation, associated with chronic myelogenous leukemia (CML). Since a high percentage of individuals with CML (~95%) also express this genetic abnormality, drugs targeted at blocking the protein produced by this abnormal gene were developed as a treatment. One of the most successful of these drugs (Gleevec) has now been FDA approved for the treatment of ten different cancers. These findings show how patient-specific genetic information can lead to improved health outcomes and novel therapeutics.

The scope of personalised medicine is not limited to drug development, it is also being used to assess the long term prognosis and treatment requirements of some cancer patients. A number of genetic screens have been developed to assess the likelihood of tumour recurrence following initial treatment in certain types of breast cancer. One of the more widely used tests, Oncotype DX, assesses 21 different genes found in tumour cells and, from these, predicts the likelihood of regrowth. This means that patients with low recurrence scores, therefore good prognosis, can be saved the stress of further unnecessary therapy and the healthcare system saves on the cost of providing unnecessary treatment. The success of this predictive screen has lead to further research into similar screening for other types of cancer and it is hoped that these tests will soon be widely available as predictive tools.

Beyond cancer, personalised medicine is also being investigated as a way of understanding the adverse side effects linked with certain drug treatments. Current research has highlighted a number of genes associated with drug hypersensitivity and variations in metabolism. It is hoped that this knowledge will, in the future, allow doctors to predict which individuals are more likely to experience adverse side effects to during treatment and tailor their prescriptions and doses accordingly.

However, despite these successes, personalised medicine still has a long way to go before its full potential can be realised. One of the first and arguably most important challenges facing this field will be defining which genetic and cellular abnormalities lead to disease. In a small number of cases this has already been achieved, for example we know exactly what gene leads to to cystic fibrosis. However most disorders are more complex, stemming from abnormalities an any of a number of different genes. Therefore uncovering the precise risk factors for these disorders will require a staggering amount of data from a huge number of individuals. Also, just to make things a bit more complicated, the emerging field of ‘epigenetics’ is now challenging the belief that we are simply the sum of our genes.

Epigenetics is revealing how interactions with the environment can change the way our cells read our genetic code. This means that two people with identical genes could still suffer from very different ailments depending on what environmental factors they are exposed to. Finally it is important to consider the ethical implications of these procedures, i.e. data protection, patient confidentiality and access to (perhaps costly) personalised treatments (this is discussed in more depth here).

Although certainly challenging, I don’t think these problems are insurmountable and the gains of personalised treatments will certainly be worth the scientific investment. Therefore, with continued funding and research effort I hope it is only a matter of time before we see more personalised diagnosis and treatment available to the wider public.

Post by: Sarah Fox

(1): Progress towards personalized medicine, Stewart Bates, Drug Discovery Today 2010. Subscription required for full access.

Your gut is literally teeming with microorganisms, the majority of which are bacteria. Indeed, the single celled squatters residing in our gut are estimated to outnumber our own cells 10:1 (this means that your body contains ten intestinal microorganisms for every one of its own cells!). Although these figures may make you feel uncomfortable, there is nothing sinister about our resident bacterial tenants; in fact scientists believe that the relationship we have with most these bacteria is actually beneficial. These bacteria or ‘microbiota’ help us absorb important nutrients from our food whilst also boosting the guts immune system, making them pretty much indispensable.

However, not all gut bacteria are alike. We know that, just as everyone expresses their own individual compliment of DNA , each individual also houses his or her own host of gut microorganisms. The specific compliment of bacteria resident in your gut depends heavily on environmental factors such as diet and is also liable to change throughout the course of a lifetime. Interestingly, as with DNA, different compliments of bacteria confer different properties to the host, some less favourable than others.

Work with mice suggests that certain types of gut microbiota may make an individual more prone to weight gain. This idea stems from work with three separate groups of mice: fat mice, lean mice and germ-free mice (mice with no detectable gut microorganisms). Scientists found that, unlike normal mice, germ-free animals did not gain weight when fed a high fat ‘Western’ diet. In fact, these mice needed to eat more than normal animals just to maintain a healthy weight. This is presumably because their lack of intestinal bacteria made it harder for them to absorb nutrients from their food. The researchers then moved on to investigate how these germ-free animals responded to infection from different compliments of gut microbes. They infected two separate groups of germ-free animals with gut microorganisms taken from either fat or lean mice. Both infected groups gained weight, however, only animals infected with gut microbes from the fat mice became overweight. These findings indicate that the fat mice may carry a specific array of microbes which promote excessive weight gain.

This research raises the question of how bacteria living in our guts can influence the amount of food we eat and the amount of weight we gain? Findings suggest that by-products generated by gut bacteria can influence both the amount of nutrition absorbed from food and the way the gut signals to the brain telling us to stop or start eating. Since different groups of bacteria will influence these systems in different ways, it has been suggested that the type of bacteria you house could influence both your eating habits and the nutrients gained from the food you eat.

So how do these findings fit with what we already know about weight control and the gut’s microbiome? Although the overall picture emerging from this research area is complicated, there are a few things we can be quite sure of: Firstly we know that our gut microbiota are generally more beneficial than they are harmful (note that although germ-free mice seem resistant to weight gain, they are also much more susceptible to infection and do not live as long as normal animals). We now also know that not all bacteria are equal, with some appearing more beneficial than others. Finally it is widely accepted that the role bacteria play in weight control is just one part of a much larger picture involving genetics, diet and exercise. Therefore, although I don’t think we know enough to claim that ‘good bacteria’ can offer a miracle solution to weight loss, the possibilities for further research into this area are exciting, especially since the gut’s microbiome is easily altered by changes in diet and the use of pro and prebiotics.

Post by: Sarah Fox

One of the nicest things about being part of a large University is that, if you can drag yourself away from your desk long enough, you get the opportunity to attend some pretty amazing guest lectures discussing cutting edge scientific findings. Last week I sat in on a particularly engaging talk given by a researcher from UCL on ‘superstitious’ mice. Although the title was a bit confusing, leaving me with images of mice refusing to leave their beds of Friday the 13^th and saluting whenever they saw a magpie, the actual research gave an amazing insight into how the brain balances its own internal prejudices with its actual experiences of the world. The ‘take home message’ of the talk was that mice and men don’t always believe what they see and, on occasions, will act on what they expect rather than what is actually in front of them. The research behind this finding is both elegant and eye opening and I will attempt to do it justice here:

Research in this lab was not initially intended to test the ‘superstitious’ nature of laboratory mice. The lab was instead interested in how well mice could distinguish between two images and how similar these needed to be before the animals became confused; research such as this is important for understanding how the visual system works. The experiments relied on the notion that mice can be taught to perform specific tasks in response to different commands (similar to training a dog…just on a smaller scale). Mice were kept in special cages with two separate treat dispensers and were taught to watch a screen which flashed one of two images. Each image corresponded to a different treat dispensers, I.e. when image 1 appeared the mouse could get a treat from dispenser 1 and when image two appeared the mouse could get a treat from dispenser 2. To make the task a little bit trickier the scientists sometimes manipulated the images making them harder to tell apart, with the aim of confusing the mice.

What was particularly impressive about this experiment was that the scientists worked with two groups of mice, one which performed the behavioural task and another which watched the same images whilst the researchers recorded activity from the visual areas of their brain. This meant that researchers could compare how well cells in the brain responded to the different images with how well the mice performed on the task. Now this is where the findings get interesting! The mice weren’t very consistent when it came to performing the task; meaning that some times they would perform well, even when the images were similar, whilst other times they seemed to be unable to recognise even the clearly separated images. However, when the researchers looked at the corresponding brain activity they found that the visual cells they recorded from were consistently good at differentiating between the images. This caused some serious head scratching as the scientists tried to work out how, when the mouses’ brain could distinguish the images, the mouse itself sometimes behaved as though it could not.

What the group found was that mice based the decision of which treat dispenser to visit, not only on the image they saw, but also on their past experiences – taking into account what choices had previously lead them to receive a reward or not. The mice tried to assign a pattern to the task making assumptions based on what they had already experienced, then combined this internal prediction with what they actually saw. Amazingly these internal predictions (which the researchers called superstitions) could be strong enough to win out over the animals own vision causing it to make the wrong choice. We can perhaps understand this behaviour better by thinking about the times in our lives when we assign patterns to things which are in fact entirely random. Take for example the national lottery. There was a time when you heard news reports speculating on lottery number, making the assumption that since a certain number had not been drawn for weeks it was ‘due’ whilst another number which appeared more regularly may be less likely to appear again. Of course the lottery draw is entirely random, meaning that the frequency of certain numbers being drawn on previous weeks has no influence on what the current draw will be. However, this did not stop us speculating and assigning our own patterns to the draws. It seems that the brain just loves to create patterns!

However, we would never be silly enough to ignore what our eyes were telling us in favor of a ‘superstitious’ belief, would we? Well… before you sit back, quietly mocking the poor mice for being slaves to their internal pattern maker, it is worth noting that they are not the only species to fall foul to the problems of over thinking a scenario. Yes you guessed it, it appears that we do this too! A follow-up experiment used a similar protocol with people and amazingly found the we also sometimes make the wrong decision even though our eyes are obviously capable of telling us we are wrong. So it seems that when it comes to both mice and men our superstitions can occasionally get the upper hand!

Post by:  Sarah Fox

For original work see here (subscription necessary to view full article)

Since their domestication in ancient Egypt, cats have carved their own niche within our society;  controlling pests and delighting owners worldwide. Whether our own, or our neighbours pets; the vast majority of western inhabitants interact either directly or indirectly with cats on a daily basis. Therefore, there is little wonder that at times we share more than just our living space with these animals.

Toxoplasma gondii is a single celled parasite whose life cycle is intimately connected with the cat. Indeed, this parasite is entirely dependent upon conditions within its feline hosts for sexual reproduction! Despite its dependence on cats for the sexual stage of its life cycle, T.gondii is  capable of infecting all mammals…including humans. The parasite can be transmitted from cats to other mammals through ingestion of T.gondii eggs. An infected cat will shed up to 20 million eggs in one leaving, with eggs surviving in the soil for over a year. Transmission occurs when the eggs are ingested by mammals feeding around the infected area. The most common form of transmission to humans is either through unwashed vegetables or undercooked meat.

When ingested by anything other than a cat the parasite reproduces asexually, forming small thin walled structures called cysts which lay dormant in many cells, most notably those of the brain. Although the dormant parasites can remain in this state for the entire life span of their accidental host, they cannot reproduce sexually until they return to their primary host (the cat). Therefore, ideally the parasite must find a way back to the cat!

Scientists researching the effect T.gondii has on wild and laboratory rodents have recently uncovered the unsettling means by which this parasite ensures itself a safe return back to its primary host. The parasite has been found to manipulate the rodents behaviour patterns, making them significantly more likely to be caught and eaten by cats. Infected rats were found to be more active and less intimidated by open spaces than non-infected animals, making them easy prey for a hunting cat. However, probably the most unusual finding was that infected rats, unlike their non-infected counterparts, were not scared of the smell of cat urine; actually spending more time in the area of their enclosure treated with this odour. This is particularly unusual since all uninfected rats, even those who have never encountered a cat, show a strong innate fear of this smell.

The mind control adopted by these parasites is probably linked to the presence of cysts within the hosts brain cells. Scientists are not yet certain what aspect of T.gondii infection causes these behavioural changes, however it has been suggested that the parasitic cysts may have the ability to manipulate the hosts brain chemistry. Studies have found that levels of certain neurotransmitters linked to control of movement and behavioural responses to fearful stimuli appear to be altered in infected mice. Specifically, recent findings show that the parasite contains two genes which have the ability to increase levels of the neurotransmitter dopamine in the hosts brain; this may account for observed changes in the animal’s behaviour.

Of course the idea of behavioural manipulation makes sense in the case of prey animals like rats and mice but what happens when humans, who are unlikely to fall prey to cats, become infected? Current medical understanding of T.gondii infection in humans assumes the parasite has no notable effect on the host, with the exception of infection during pregnancy and the occasional adverse reaction to first exposure. However, in light of the recent findings in rats and mice, scientists have been taking a closer look at how T.gondii may influence our behaviour. Work by Professor Jaroslav Flegr has revealed, what he believes to be, particular personality types linked to T.gondii infection. He found that; infected men have a greater tendency to disregard the rules of their society and were generally more suspecting, jealous and dogmatic than non-infected men whilst infected women appear more ‘warm-hearted’, out and easy going but also more conscientious, persistent and moralistic. Both infected men and women also appeared more prone to feelings of guilt than their uninfected counterparts. Links have also been drawn between incidences of schizophrenia and T.gondii infection, perhaps due to altered dopamine transmission.

Since the basic components of our brains are not too dissimilar to those of the rat or mouse, it seems logical to assume that something which exerts an effect on their behaviour should also influence our own. Therefore the question is now open as to how often these parasitic passengers actually jump in the drivers seat? Indeed, T.gondii is not the only parasite carried by humans, leaving open the possibility that development of our personalities has and will continue to be influenced not only by our genes and environment but also by our own personal collection of brain dwelling parasites.

Post by: Sarah Fox

The study of the self, what makes us unique and how our brains define who we are is an intriguing and often controversial area of research. Indeed, such work may eventually shape many aspects of society from education to criminal justice.

We already know that damage to the brain can permanently alter an individual’s personality and that the type of alteration depends on the region damaged. One of the most famous examples of brain damage leading to a shift in personality was the case of Phineas Gage. Gage worked as a foreman leading a team of workers preparing the ground for a new railway line. On the 13^th September 1848 an accidental explosion blew an iron rod, over 3 feet long and 1 ¼ inches in diameter at its widest point, clean through his head. Although amazingly he survived the incident, he lost sight in his left eye and suffered significant damage to his left frontal lobe. Following the accident, although his intellect remained intact, it is reported that he changed from being a conscientious well liked man to a fitful disrespectful individual with a particularly foul mouth. Indeed, the changes in his personality were so significant that his former employers were forced to let him go.

Gage’s tragic accident was one of the first pieces of evidence linking frontal cortex damage to antisocial personality traits. The knowledge that such physical brain-damage can precipitate a change in personality raises the question of whether undesirable traits seen within the general population can be linked to subtle changes in brain function and ultimately whether these ‘defects’ may be treatable.

An area where a combination of genetics and functional brain imaging is raising just such a question is the study of psychopathology. Scientists have observed genetic and physiological differences in the brains of a number of diagnosed psychopaths. Specifically, brain scans of these individuals reveal lower than average activity and reduced communication between the orbitofrontal cortex and amygdaloid brain regions. Together these regions are important for making emotionally driven decisions, learning from the emotional content of experiences and controlling impulsive behaviour.

These brain changes are often seen in combination with a rare form of the monoamine oxidase A (MAO-A) gene known as the ‘warrior gene’. This gene codes for a protein (MAO-A) which can influence the communication of cells in a number of brain regions. Alterations in this gene lead to abnormal cellular communication, and have also been linked to behavioral abnormalities.  Indeed, individuals with the ‘warrior’ version of this gene are more susceptible to developing antisocial and often violent tendencies, especially if they also experienced maltreatment during early childhood.

Although studies of many psychopathic killers reveal the presence of both the ‘warrior gene’ and reduced orbitofrontal/amygdaloid activity, this is by no means the end of the story. Amazingly James Fallon, a neuroscientist from the university of California who had been studying the brains of psychopaths, recently uncovered some disturbing family history of his own; leading to the disquieting revelation that he himself showed both the same brain type and genetic profile as the psychopathic killers he studied. Although he admits to not always being in-tune with other’s emotions, professor Fallon is a caring husband and father who has never been in trouble with the law. These findings raise the question of how important a biological predisposition towards psychopathy is and how this may be overcome. Professor Fallon notes that he was lucky to have a very warm and loving childhood, and believes that his upbringing likely played a role in preventing any biological tendencies toward psychopathy from taking effect.

Work such as this is beginning to uncover the amazing interplay between our brains and our selves. However, as knowledge in this area increases, many of us can’t help but question where this research is leading and how these findings may be used. Although I believe we are a long way from hearing ‘my brain made me do it’ as an acceptable defence in our courts, this research is already influencing our education system. One pioneering school in the south of England accepts children with behavioural difficulties associated with low amygdaloid function. Along with their regular lessons children are taught how to recognise and respond to emotions in a socially acceptable manner. These children are considered to be at risk of developing antisocial or even psychopathic tendencies and it is hoped that this training will help them integrate into society and lead normal successful lives.

Post by: Sarah Fox

Now there’s an intriguing question…

I’m sure many of us recognize that feeling just before an important interview when your palms get sweaty and your stomach becomes home to a kaleidoscope of exceedingly acrobatic butterflies. These unfortunate effects of anxiety appear largely unavoidable and are certainly not often classed as beneficial.

However, scientists from the university of Kiel (Germany) believe that the smell of anxiety may induce feelings of empathy in others. This means that the nerves you feel may actually buy you some sympathy in that feared interview.

The study collected armpit (or to use the more fancy scientific terminology: axillary) sweat samples from a group of people both during exercise (non-anxiety condition) and during a nerve wrecking oral examination (anxiety condition). A second group were then exposed to these odors whilst undergoing an fMRI brain-scan. This allowed the scientists to monitor how these odors influenced their brain activity. Interestingly, although subjects did not consciously recognize a difference between the smells of exercise and anxiety sweat, their brains told a different story!

The smell of anxiety activated a number of brain regions believed to be important for recognizing anxiety in others and converting these observations to feelings of empathy. These regions include the insula and orbitofrontal cortex, precuneus, cingulum and fusiform gyrus, shown below. These regions were not activated to the same degree by the smell of exercise sweat.

This work suggests that our brains can detect the smell of anxiety on others and respond by making us more empathetic towards that individual. However, before you decide to ditch the deodorant, it must be noted that despite these compelling fMRI findings, none of the subjects consciously reported feelings of empathy! This could mean that, although our brains can unconsciously register the smell of anxiety and prime us to fell empathy, further physical stimuli may be required before we can consciously recognize and act on these feelings.

So to answer my question ‘could stress actually help you pass a job interview’: perhaps, but more work needs to be carried out first to find whether these unconscious brain signals will actually translate to conscious feelings of empathy in such a situation.

Post by: Sarah Fox

The full paper can be accessed free of charge here: