Neuroscience
Month
Are you a morning lark or a night owl? Scientists use that simplified categorization to explain that different people have different internal body clocks, commonly called circadian clocks. Sleep-wake cycles, digestive activities, and many other physiological processes are controlled by these clocks. In recent years, researchers have found that internal body clocks can also affect how patients react to drugs. For example, timing a course of chemotherapy to the internal body time of cancer patients can improve treatment efficacy and reduce side effects.
Round the clock. Tracking the levels of 50 hormones and amino acids in blood samples (shown by ribbons) reveals a body’s internal time. Credit: PNAS
But physicians have not been able to exploit these findings because determining internal body time is, well, time consuming. It’s also cumbersome. The most established and reliable method requires taking blood samples from a patient hourly and tracking levels of the hormone melatonin, which previous research has tied closely to internal body time.
Now a Japanese group has come up with an alternative method of determining internal body time by constructing what it calls a molecular timetable based on levels in blood samples of more than 50 metabolites—hormones and amino acids—that result from biological activity. The researchers established a molecular timetable based on samples from three subjects and validated it using the conventional melatonin measurement. They then used that timetable to determine the internal body times of other subjects by checking the levels of the metabolites in just two blood samples from each subject per day.
Having such a timetable could allow doctors to synchronize drug delivery to internal body time, the team reports online today in the Proceedings of the National Academy of Sciences. “Usually personalized medicine is focusing on genetic differences, but there are also temporal differences [among patients]. That will be the next step in personalized medicine,” says systems biologist Hiroki Ueda of the RIKEN Center for Developmental Biology in Kobe, Japan, who heads the research group.
"In principle, the method holds great promise as a way of replacing the cumbersome melatonin assay," says Steven Brown, a molecular biologist at the University of Zurich in Switzerland. "The authors show in a small-scale, well-controlled experiment that they are able to predict internal body time within a precision frame of 3 hours," says Urs Albrecht of the University of Fribourg in Switzerland. Both researchers say further work will be necessary to make the technique more practical and more widely applicable, and Ueda agrees. The experimental subjects were all young men, and different molecular timetables are likely needed for women and for people of different ages. He would also like to improve the precision and make it reliable with just one blood sample per day.
Source: ScienceNOW
ScienceDaily (Aug. 27, 2012) — Muscular dystrophy is a complicated set of genetic diseases in which genetic mutations affect the various proteins that contribute to a complex that is required for a structural bridge between muscle cells and the extracellular matrix (ECM) that provides the physical and chemical environment required for their development and function.
The affects of these genetic mutations in patients vary widely, even when the same gene is affected. In order to develop treatments for this disease, it is important to have an animal model that accurately reflects the course of the disease in humans. In this issue of the Journal of Clinical Investigation, researchers at the University of Iowa report the development of a mouse model of Fukuyama’s muscular dystrophy that copies the pathology seen in the human form of the disease.
By removing the gene fukutin from mouse embryos at various points during development, researchers led by Kevin Campbell were able to determine that fukutin disrupts important modifications of dystrophin that prevent the muscle cells from attaching to the ECM. Disruption of the gene earlier in development led to a more severe form of the disease, suggesting that fukutin is important for muscle maturation. Disruptions in later stages of development caused a less severe form of the disease. In a companion piece, Elizabeth McNally of the University of Chicago discusses the implications of this disease model for the development of new therapies to treat muscular dystrophy.
Source: Science Daily
August 26, 2012
Vitamin B12 is essential to human health. However, some people have inherited conditions that leave them unable to process vitamin B12. As a result they are prone to serious health problems, including developmental delay, psychosis, stroke and dementia. An international research team recently discovered a new genetic disease related to vitamin B12 deficiency by identifying a gene that is vital to the transport of vitamin into the cells of the body. This discovery will help doctors better diagnose this rare genetic disorder and open the door to new treatments. The findings are published in the journal Nature Genetics.
"We found that a second transport protein was involved in the uptake of the vitamin into the cells, thus providing evidence of another cause of hereditary vitamin B12 deficiency", said Dr. David Rosenblatt, one of the study’s co-authors, scientist in medical genetics and genomics at the Research Institute of the McGill University Health Centre (RI MUHC) and Dodd Q. Chu and Family Chair in Medical Genetics and the Chair of the Department of Human Genetics at McGill University. "It is also the first description of a new genetic disease associated with how vitamin B12 is handled by the body".
These results build on previous research by the same team from the RI MUHC and McGill University, with their colleagues in Switzerland, Germany and the United States. In previous work, the researchers discovered that vitamin B12 enters our cells with help from of a specific transport protein. In this study, they were working independently with two patients showing symptoms of the cblF gene defect of vitamin B12 metabolism but without an actual defect in this gene. Their work led to the discovery of a new gene, ABCD4, associated with the transport of B12 and responsible for a new disease called cblJ combined homocystinuria and methylmalonic aciduria (cblJ-Hcy-MMA).
Using next generation sequencing of the patients’ genetic information, the scientists identified two mutations in the same ABCD4 gene, in both patients. “We were also able to compensate for the genetic mutation by adding an intact ABCD4 protein to the patients’ cells, thus allowing the vitamin to be properly integrated into the cells,” explained Dr. Matthias Baumgartner, senior author of the study and a Professor of metabolic diseases at Zurich’s University Children’s Hospital.
Vitamin B12, or cobalamin, is essential for healthy functioning of the human nervous system and red blood cell synthesis. Unable to produce the vitamin itself, the human body has to obtain it from animal-based foods such as milk products, eggs, red meat, chicken, fish, and shellfish – or vitamin supplements. Vitamin B12 is not found in vegetables.
"This discovery will lead to the early diagnosis of this serious genetic disorder and has given us new paths to explore treatment options. It also helps explain how vitamin B12 functions in the body, even for those without the disorder," said Dr. Rosenblatt who is the director of one of only two referral laboratories in the world for patients suspected of having this genetic inability to absorb vitamin B12. Dr. Rosenblatt points out that the study of patients with rare diseases is essential to the advancement of our knowledge of human biology.
Source: medicalxpress.com
26 August 2012 by Mo Costandi
Subjects trained to sniff pleasant smells while asleep retain the conditioning when they wake up.
It sounds like every student’s dream: research published today in Nature Neuroscience shows that we can learn entirely new information while we snooze.
TIPS/Photoshot
Anat Arzi of the Weizmann Institute of Science in Rehovot, Israel, and her colleagues used a simple form of learning called classical conditioning to teach 55 healthy participants to associate odours with sounds as they slept.
They repeatedly exposed the sleeping participants to pleasant odours, such as deodorant and shampoo, and unpleasant odours such as rotting fish and meat, and played a specific sound to accompany each scent.
It is well known that sleep has an important role in strengthening existing memories, and this conditioning was already known to alter sniffing behaviour in people who are awake. The subjects sniff strongly when they hear a tone associated with a pleasant smell, but only weakly in response to a tone associated with an unpleasant one.
But the latest research shows that the sleep conditioning persists even after they wake up, causing them to sniff strongly or weakly on hearing the relevant tone — even if there was no odour. The participants were completely unaware that they had learned the relationship between smells and sounds. The effect was seen regardless of when the conditioning was done during the sleep cycle. However, the sniffing responses were slightly more pronounced in those participants who learned the association during the rapid eye movement (REM) stage, which typically occurs during the second half of a night’s sleep.
Pillow power
Arzi thinks that we could probably learn more complex information while we sleep. “This does not imply that you can place your homework under the pillow and know it in the morning,” she says. “There will be clear limits on what we can learn in sleep, but I speculate that they will be beyond what we have demonstrated.”
In 2009, Tristan Bekinschtein, a neuroscientist at the UK Medical Research Council’s Cognition and Brain Sciences Unit in Cambridge, and his colleagues reported that some patients who are minimally conscious or in a vegetative state can be classically conditioned to blink in response to air puffed into their eyes. Conditioned responses such as these could eventually help clinicians to diagnose these neurological conditions, and to predict which patients might subsequently recover. “It remains to be seen if the neural networks involved in sleep learning are similar to the ones recruited during wakefulness,” says Bekinschtein.
The findings by Arzi and her colleagues might also be useful for these purposes, and could lead to ‘sleep therapies’ that help to alter behaviour in conditions such as phobia.
“We are now trying to implement helpful behavioural modification through sleep-learning,” says Arzi. “We also want to investigate the brain mechanisms involved, and the type of learning we use in other states of altered consciousness, such as vegetative state and coma.”
Source: Nature
The nervous system is a complex collection of nerves and specialized cells known as neurons that transmit signals between different parts of the body. Vertebrates — animals with backbones and spinal columns — have central and peripheral nervous systems.
The central nervous system is made up of the brain, spinal cord and retina. The peripheral nervous system consists of sensory neurons, ganglia (clusters of neurons) and nerves that connect to one another and to the central nervous system.
Credit: iDesign, Shutterstock
Description of the nervous system
The nervous system is essentially the body’s electrical wiring. It is composed of nerves, which are cylindrical bundles of fibers that start at the brain and central cord and branch out to every other part of the body.
Neurons send signals to other cells through thin fibers called axons, which cause chemicals known as neurotransmitters to be released at junctions called synapses. A synapse gives a command to the cell and the entire communication process typically takes only a fraction of a millisecond.
Sensory neurons react to physical stimuli such as light, sound and touch and send feedback to the central nervous system about the body’s surrounding environment. Motor neurons, located in the central nervous system or in peripheral ganglia, transmit signals to activate the muscles or glands.
Glial cells, derived from the Greek word for “glue,” support the neurons and hold them in place. Glial cells also feed nutrients to neurons, destroy pathogens, remove dead neurons and act as traffic cops by directing the axons of neurons to their targets. Specific types of glial cells (oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system) generate layers of a fatty substance called myelin that wraps around axons and provides electrical insulation to enable them to rapidly and efficiently transmit signals.
24 August 2012 by Michael Marshall
THE latest twist in the origin-of-life tale is double helical. Chemists are close to demonstrating that the building blocks of DNA can form spontaneously from chemicals thought to be present on the primordial Earth. If they succeed, their work would suggest that DNA could have predated the birth of life.
Lurking at the dawn of time (Image: Snorri Gunnarsson/Flickr/Getty)
DNA is essential to almost all life on Earth, yet most biologists think that life began with RNA. Just like DNA, it stores genetic information. What’s more, RNA can fold into complex shapes that can clamp onto other molecules and speed up chemical reactions, just like a protein, and it is structurally simpler than DNA, so might be easier to make.
After decades of trying, in 2009 researchers finally managed to generate RNA using chemicals that probably existed on the early Earth. Matthew Powner, now at University College London, and his colleagues synthesised two of the four nucleotides that make up RNA. Their achievement suggested that RNA may have formed spontaneously - powerful support for the idea that life began in an “RNA world”.
August 24th, 2012
Researchers from the Laboratory of astrocyte biology and CNS regeneration headed by Prof. Milos Pekny just published a research article in a prestigious journal Stem Cells on the molecular mechanism that controls generation of new neurons in the brain.
Astrocytes are cells that have many functions in the central nervous system, such as the control of neuronal synapses, blood flow, or the brain’s response to neurotrauma or stroke.
Reduces brain tissue damage
Prof. Pekny’s laboratory together with collaborators have earlier demonstrated that astrocytes reduce the brain tissue damage after stroke and that the integration of transplanted neural stem cells can be largely improved by modulating the activity of astrocytes.
Generation of new neurons
In their current study, the Sahlgrenska Academy researchers show how astrocytes control the generation of new neurons in the brain. An important contribution to this project came from Åbo Academy, one of Sahlgrenska’s traditional collaborative partners.
“In the brain, astrocytes control how many new neurons are formed from neural stem cells and survive to integrate into the existing neuronal networks. Astrocytes do this by secreting specific molecules but also by much less understood direct cell-cell interactions with stem cells”, says Prof. Milos Pekny.
Image shows GFAP stained cortex from a TgAPP mouse showing activated astrocytes from a different study.
Important regulator
“Astrocytes are in physical contact with neural stem cells and we have shown that they signal through the Notch pathway to stem cells to keep the birth rate of new neurons low. We have also shown that the intermediate filament system of astrocytes is an important regulator of this process. It seems that astrocyte intermediate filaments can be used as a target to increase the birthrate of new neurons.”
Target for future therapies
“We are starting to understand some of the cellular and molecular mechanisms behind the control of neurogenesis. Neurogenesis is one of the components of brain plasticity, which plays a role in the learning process as well as in the recovery after brain injury or stroke. This work helps us to understand how plasticity and regenerative response can be therapeutically promoted in the future”, says Prof. Milos Pekny.
Source: Neuroscience News
The researchers from Lancaster University have found that those with the degenerative brain disease have difficulty with one particular test. They also found that the inability to carry out the tests in those who had already been diagnosed with Alzheimer’s was linked to lower memory function.
Photo: ALAMY
Dr Trevor Crawford said the latest results were potentially exciting. They showed, for the first time, a physical connection with the memory impairment that so often is the first noticeable symptom in Alzheimer’s.
Dr Crawford, of the department of Psychology and the Centre for Ageing Research, Lancaster University, said: “The diagnosis of Alzheimer’s disease is currently heavily dependent on the results of a series of lengthy neuropsychological tests.
"However, patients with a dementia often find that these tests are difficult to complete due to a lack of clear understanding and lapse in their attention or motivation.
"Over the last 10 years, researchers in laboratories around the world have been working on an alternative approach based on the brain’s control of the movements of the eye as a tool for investigating cognitive abilities, such as attention, cognitive inhibition and memory."
During the study, 18 patients with Alzheimer’s disease, 25 patients with Parkinson’s disease, 17 healthy young people and 18 healthy older people were asked to follow the movements of light on a computer monitor. In some instances they were asked to look away from the light. Detailed eye–tracking measurements showed stark contrasts in results.
Patients with Alzheimer’s made errors on the task when they were asked to look away from the light. They were unable correct those errors, despite being able to respond normally when they were asked to look towards the light.
These uncorrected errors were 10 times more frequent in the Alzheimers’ patients than the control groups. Researchers also measured memory function among those Alzheimer’s patients who found the test difficult and were able to show a clear correlation with lower memory function. Dr Crawford added: “The light tracking test could play a vital role in the diagnosis of Alzheimer’s.”
August 24, 2012 By Barbara Bronson Gray
(HealthDay)—Whether it’s an email from an unknown gentleman on another continent pleading for money or a financial scammer selling a promising penny stock, the young and old tend to be more easily duped than middle-aged people.
Changes in this region could explain why seniors, children are less doubting.
Now, researchers have pinpointed the area of the brain responsible for this gullibility and have theorized why it makes children, teens and seniors less likely to doubt.
The ventromedial area of the prefrontal cortex of the brain—a softball-sized lobe in the front of your head, just above your eyes—appears to be responsible for allowing you to pause after hearing or reading something and consider whether it’s true, according to a study published recently in the journal Frontiers in Neuroscience.
ScienceDaily (Aug. 23, 2012) — We use language every day to express our emotions, but can this language actually affect what and how we feel? Two new studies from Psychological Science, a journal of the Association for Psychological Science, explore the ways in which the interaction between language and emotion influences our well-being.
Putting Feelings into Words Can Help Us Cope with Scary Situations
Katharina Kircanski and colleagues at the University of California, Los Angeles investigated whether verbalizing a current emotional experience, even when that experience is negative, might be an effective method for treating for people with spider phobias. In an exposure therapy study, participants were split into different experimental groups and they were instructed to approach a spider over several consecutive days.
One group was told to put their feelings into words by describing their negative emotions about approaching the spider. Another group was asked to ‘reappraise’ the situation by describing the spider using emotionally neutral words. A third group was told to talk about an unrelated topic (things in their home) and a fourth group received no intervention. Participants who put their negative feelings into words were most effective at lowering their levels of physiological arousal. They were also slightly more willing to approach the spider. The findings suggest that talking about your feelings — even if they’re negative — may help you to cope with a scary situation.
Unlocking Past Emotion: The Verbs We Use Can Affect Mood and Happiness
Our memory for events is influenced by the language we use. When we talk about a past occurrence, we can describe it as ongoing (I was running) or already completed (I ran). To investigate whether using these different wordings might affect our mood and overall happiness, Will Hart of the University of Alabama conducted four experiments in which participants either recalled or experienced a positive, negative, or neutral event. They found that people who described a positive event with words that suggested it was ongoing felt more positive. And when they described a negative event in the same way, they felt more negative.
The authors conclude that one potential way to improve mood could be to talk about negative past events as something that already happened as opposed to something that was happening.
Source: Science Daily
ScienceDaily (Aug. 23, 2012) — Scientists at the University of Houston (UH) have discovered what may possibly be a key ingredient in the fight against Parkinson’s disease.
Affecting more than 500,000 people in the U.S., Parkinson’s disease is a degenerative disorder of the central nervous system marked by a loss of certain nerve cells in the brain, causing a lack of dopamine. These dopamine-producing neurons are in a section of the midbrain that regulates body control and movement. In a study recently published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the UH Center for Nuclear Receptors and Cell Signaling (CNRCS) demonstrated that the nuclear receptor liver X receptor beta (LXRbeta) may play a role in the prevention and treatment of this progressive neurodegenerative disease.
"LXRbeta performs an important function in the development of the central nervous system, and our work indicates that the presence of LXRbeta promotes the survival of dopaminergic neurons, which are the main source of dopamine in the central nervous system," said CNRCS director and professor Jan-Åke Gustafsson, whose lab discovered LXRbeta in 1995. "The receptor continues to show promise as a potential therapeutic target for this disease, as well as other neurological disorders."
To better understand the relationship between LXRbeta and Parkinson’s disease, the team worked with a potent neurotoxin, called MPTP, a contaminant found in street drugs that caused Parkinson’s in people who consumed these drugs. In lab settings, MPTP is used in murine models to simulate the disease and to study its pathology and possible treatments.
The researchers found that the absence of LXRbeta increased the harmful effects of MPTP on dopamine-producing neurons. Additionally, they found that using a drug that activates LXRbeta receptors prevented the destructive effects of MPTP and, therefore, may offer protection against the neurodegeneration of the midbrain.
"LXRbeta is not expressed in the dopamine-producing neurons, but instead in the microglia surrounding the neurons," Gustafsson said. "Microglia are the police of the brain, keeping things in order. In Parkinson’s disease the microglia are overactive and begin to destroy the healthy neurons in the neighborhood of those neurons damaged by MPTP. LXRbeta calms down the microglia and prevents collateral damage. Thus, we have discovered a novel therapeutic target for treatment of Parkinson’s disease."
Source: Science Daily
Better diagnosis and treatment of a crippling inherited nerve disorder may be just around the corner thanks to an international team that spanned Asia, Europe and the United States. The team had been hunting DNA strands for the cause of the inherited nerve disorder known as spinocerebellar ataxia, or SCA. The disease causes progressive loss of balance, muscle control and ability to walk. Thanks to their diligence and detective work they have discovered the disease gene in a region of chromosome 1 where another group from the Netherlands had previously shown linkage with a form of SCA called SCA19, and the Taiwanese group on the new paper had shown similar linkage in a family for a form of the disease that was then called SCA22. The international team, from France, Japan, Taiwan and the USA have published their discovery in the Annals of Neurology. The Dutch group has also published results in the same issue of the journal.
Their paper reveals that mutations in the gene KCND3 were found in six families in Asia, Europe and the United States that have been haunted by SCA. Their results will allow for a better understanding of why nerves in the brain’s movement-controlling centre die, and how new DNA mapping techniques can find the causes of other diseases that run in families.
Margit Burmeister, Ph.D., a geneticist at University of Michigan Health System (U-M), helped lead the work and stressed that the gene could not have been found without a great deal of DNA detective work and the cooperation of the families who volunteered to let researchers map all the DNA of multiple members of their family tree. ‘We combined traditional genetic linkage analysis in families with inherited diseases with whole exome sequencing of an individual’s DNA, allowing us to narrow down and ultimately identify the mutation,’ she says. ‘This new type of approach has already resulted in many new gene identifications, and will bring in many more.’
The gene is very important as it manages the production of a protein that allows nerve cells to ‘talk’ to one another through the flow of potassium. Pinpointing its role as a cause of ataxia will now allow more people with ataxia to learn the exact cause of their disease, give a very specific target for new treatments, and perhaps allow the families to stop the disease from affecting future generations.
U-M neurologist Vikram Shakkottai, M.D., Ph.D., an ataxia specialist and co-author on the paper, also notes that the new genetic information will help patients find out the specific cause of their disease. He and his colleagues are already working to find drugs that might alter potassium flow, and provide a treatment for a group of diseases that currently are only treated with supportive care such as physical activity and balance training as patients deteriorate. ‘Many of the families who come to our clinic for treatment don’t have a recognised genetic mutation, so it’s important to find new genetic mutations to explain their symptoms,’ says Shakkottai. ‘But at the same time, this research is helping us understand a common mechanism of nerve cell dysfunction in progressive and non-progressive disease.’
Their findings however are not restricted to just ataxia. The researchers were also able to show that when KCND3 is mutated, it causes poor communication between nerve cells in the cerebellum as well as the death of those cells. This discovery could aid research on other neurological disorders involving balance and movement.
The Dutch team, that also published its findings about KCND3 at the same time, studied families in the Netherlands and found that mutations on the gene are responsible for SCA19, the cause of which had up until now been a mystery. ‘In other words, mutations in this gene are not uncommon and present all over the world,’ says Burmeister. ‘This means that in the future, this gene should be tested for mutations as part of a clinical genetic test panel for patients with ataxia symptoms. Because a generation can be skipped, it may even be relevant in some sporadic cases - those where the patient isn’t aware of any other family members with a similar disease.’
Source: Cordis News
Helium reveals gibbon’s soprano skill
Apes are unlikely to become virtuosos at the opera house, but gibbons have naturally mastered some of the vocal techniques that human sopranos rely on, scientists in Japan report.
The research shows that, like humans, gibbons use a ‘source–filter’ mode of sound generation. The sound originates from the creatures’ vocal folds as a mixture of different harmonics, which are multiples of the frequency at which the vocal folds vibrate. The resonant frequencies of the vocal tract then determine which of these harmonics are projected. By altering the position of the mouth, lips and teeth, humans vary these resonant frequencies to make the different sounds required for speech.
The gibbon’s melodious calling bears many similarities to the techniques of human singers. Like professional sopranos, gibbons tune the resonant frequency of their vocal tract to the pitch frequency generated by the vocal folds to amplify the sound. Acoustic physicist Joe Wolfe of the University of New South Wales in Sydney, Australia, says that this type of “resonance tuning” is something that comes fairly easily to human singers and is key to their ability to project their voice over a loud orchestra.
22 August 2012
Scientists have found a switch in the brain which may explain why smoking cannabis causes psychosis and addiction in more than one-in-ten users.
The team, at Aberdeen University found a genetic difference in the switch, probably inherited from early humans who smoked the drug in prehistoric times. The difference may also explain why some people could be more susceptible to conditions such as obesity.
The researchers, at the university’s Kosterlitz Centre for Therapeutics, studied genetic differences around a gene called ‘CNR1’, which produces what are known as cannabinoid receptors in the brain which control parts of the brain involved in memory, mood, appetite and pain.
Cannabinoid receptors activate these areas of the brain when they are triggered by naturally-occurring chemicals in the body known as endocannabinoids. Chemicals found in the cannabis and ‘skunk’ mimic the action of endocannabinoids. It is known that cannabis has pain-relieving and anti-inflammatory properties which can help treat diseases such as multiple sclerosis and arthritis.
However, developing drugs from cannabis to treat these conditions is hampered by the fact that such drugs will have psychoactive side effects - and smoked cannabis can cause addiction and psychosis in up to 12 per cent of users.
Dr Alasdair MacKenzie, who led the research, said:
We looked at one specific genetic difference in CNR1 because we know it is linked to obesity and addiction. What we found was a mutation that caused a change in the genetic switch for the gene itself - a switch that is very ancient and has remained relatively unchanged in over three hundred million years of evolution, since before the time of the dinosaurs.
These genetic ‘switches’ regulate the gene itself, ensuring that it is turned on or off in the right place at the right time and in the right amount. It is normally thought that mutations cause disease by reducing the function of the gene, or the switch that controls it. In this case however, the mutation actually increased the activity of the switch in parts of the brain that control appetite and pain, and also, and most especially, in the part of the brain called the hippocampus, which is affected in psychosis.
He added: We know that this overactive switch is relatively rare in Europeans, but is quite common in African populations. But we were all once African, so something must have decreased it in our early ancestors who left Africa and migrated through Central Asia towards Europe and the north. One possibility we are keen to explore is that once in Central Asia these early migrants came into contact with the cannabis plant, which we know was endemic across that area at that time.
It is possible that the side effects of taking cannabis were such that people with the mutation were not so effective in producing and raising children. Therefore, over the generations the numbers of people with the mutation decreased.
This work is at a very early stage however, and there are likely to be more exciting discoveries - not only on how these differences came about, but also about the role of this genetic switch in health and disease.
Co-researcher Dr Scott Davidson said: Further analysis of this mutation will help us to understand many of the side effects which are associated with cannabis use such as addiction and psychosis.
Professor Ruth Ross, head of the Kosterlitz Centre, an internationally recognised expert in cannabis pharmacology, said: Previously in drug research, attempts to detect the causes of adverse drug reactions have focused on the genes themselves.
Our study is one of the first to explore the possibility that changes in gene switches are involved in causing side effects to drugs. We believe this approach will be crucially important in the future development of more effective personalised medicine, with fewer side effects.
One question that is intriguing the research team is why this overactive genetic switch evolved in the first place.