Posts tagged science
Articles and news from the latest research reports.
Smoking cannabis doesn’t make you more creative
People often think that smoking cannabis makes them more creative. However, research by Leiden psychologists Lorenza Colzato and Mikael Kowal shows that the opposite is true. They published their findings on 7 October in Psychopharmacology.
Strong cannabis doesn’t work
The findings show that cannabis with a high concentration of the psychoactive ingredient THC does not improve creativity. Smokers who ingested a low dose of THC, or none at all (they were given a placebo), performed best in the thinking tasks that the test candidates had to carry out. A high dose of THC was actually shown to have a negative effect on the ability to quickly come up with as many solutions as possible to a given problem.
Increased creativity is an illusion
The research findings contradict the claims of people who say that their thinking changes and becomes more original after smoking a joint. There’s no sign of any increased creativity in their actual performance, according to Colzato. ‘The improved creativity that they believe they experience is an illusion.’
Too much dope is counterproductive
Colzato: ‘If you want to overcome writer’s block or any other creative gap, lighting up a joint isn’t the best solution. Smoking several joints one after the other can even be counterproductive to creative thinking.’
The research method
Colzato and her PhD candidate Kowal were the first researchers to study the effects of cannabis use on creative thinking. For ethical reasons, only cannabis users were selected for this study. The test candidates were divided into three groups of 18. One group was given cannabis with a high THC content (22 mg), the second group was given a low dose (5.5 mg) and the third group was given a placebo. The high dose was equivalent to three joints and the low dose was equal to a single joint. Obviously, none of the test candidates knew what they were being given; the cannabis was administered via a vaporizer. The test candidates then had to carry out cognitive tasks that were testing for two types of creative thinking:
- Divergent thinking: generating rapid solutions for a given problem, such as: “Think of as many uses as you can for a pen?”
- Convergent thinking: Finding the only right answer to a question, such as: “What is the link between the words ‘time’, ‘hair’ and ‘stretching’. (The answer is ‘long’.)
Similar but different: new discovery for degenerative disease
Progressive Supranuclear palsy (PSP) and Parkinson’s Disease (PD) have overlapping symptoms but remain difficult to distinguish.
However, a first ever paper on the topic published in the Journal of Neuropsychology (British Psychological Society publication) now suggests that people with PSP experience more severe and extensive cognitive impairments than those with PD early on.
The study indicates that patients with PSP experience more severe and extensive impairments in higher order functions such as planning, abstract thinking, memory retrieval than those with PD.
Lead researcher Dr Young-Eun Claire Lee said the two conditions are so similar that in some cases, patients with PSP often go undiagnosed for the main part of their illness.
“PD and PSP are the two of the most common forms of neurodegenerative diseases resulting in loss of balance and deterioration in mobility,” said Dr Lee.
“Telling these differences apart can be challenging because most patients with PSP do not develop distinctive symptoms such as paralysis or weakness of the eye muscles and episodes of frequent falling until later stages,” she said.
While the study sample was small, the results indicate that cognitive profiles may aid differential diagnosis in earlier stages. PSP claimed the life of musician/actor Dudley Moore.
There are no current treatments for PSP.
![Exercise key to warding off dementia
EXERCISE is one of the best ways to protect against dementia in later life and the earlier you start, the greater the effect, research suggests.
Participating in intellectually stimulating leisure activities, paid work, volunteer work or study can also help protect against memory loss and reduce the risk of developing Alzheimer’s disease.
UWA adjunct clinical professor Nicola Lautenschlager, who led a review of strategies to delay cognitive decline, says there is a growing body of evidence that suggests exercise is beneficial for brain health.
"The knowledge we have so far basically makes it very clear that regular physical activity, even at an older age, can be very beneficial for protecting cognition," she says.
"Beyond that it’s also very effective for protecting or maintaining mental health, especially in relation to symptoms of depression or anxiety."
Prof Lautenschlager, who is based at the University of Melbourne, says older people who are well enough are advised to do 150 minutes of physical activity a week, such as going for walks.
"When it comes [to] brain health…it would be good if the walking speed isn’t very slow, so it shouldn’t be a stroll but rather what we call moderate pace," she says.
"Research has shown that the level of physical activity has to have a certain intensity so that the brain benefits."
Enjoyable hobbies key to brain health
Hobbies that keep the brain active, such as playing an instrument, going to concerts or joining a book club, can also be very helpful as long as it is an activity a person enjoys, Prof Lautenschlager says.
"The minute you prescribe an activity they hate doing…most likely the effect in terms of being beneficial for brain health is lost," she says.
"It produces so much stress in the body not wanting to do it that the stress is more harmful than the benefit of keeping the brain active."
Prof Lautenschlager says middle age is a crucial time for making lifestyle decisions that will determine a person’s health in later life.
"Usually we are talking about when you move into your 30s, definitely the 40s and also still the 50s," she says.
"Things like a high blood pressure or carrying too much weight, if you do that in these decades, it seems to harm the brain long-term in terms of how healthy a person is in their 70s or 80s."
Ideally people should aim for a healthy lifestyle from childhood but luckily research shows lifestyle changes still have an effect on brain health if a person is already old, Prof Lautenschlager says.
"Even programs…with seniors in their 70s and 80s can still make a difference," she says.
The research was published this month in the journal Maturitas.](http://31.media.tumblr.com/6aefc29f7bda88b832996d3c6bc84bc3/tumblr_ndc345d4151rog5d1o1_500.jpg)
Exercise key to warding off dementia
EXERCISE is one of the best ways to protect against dementia in later life and the earlier you start, the greater the effect, research suggests.
Participating in intellectually stimulating leisure activities, paid work, volunteer work or study can also help protect against memory loss and reduce the risk of developing Alzheimer’s disease.
UWA adjunct clinical professor Nicola Lautenschlager, who led a review of strategies to delay cognitive decline, says there is a growing body of evidence that suggests exercise is beneficial for brain health.
"The knowledge we have so far basically makes it very clear that regular physical activity, even at an older age, can be very beneficial for protecting cognition," she says.
"Beyond that it’s also very effective for protecting or maintaining mental health, especially in relation to symptoms of depression or anxiety."
Prof Lautenschlager, who is based at the University of Melbourne, says older people who are well enough are advised to do 150 minutes of physical activity a week, such as going for walks.
"When it comes [to] brain health…it would be good if the walking speed isn’t very slow, so it shouldn’t be a stroll but rather what we call moderate pace," she says.
"Research has shown that the level of physical activity has to have a certain intensity so that the brain benefits."
Enjoyable hobbies key to brain health
Hobbies that keep the brain active, such as playing an instrument, going to concerts or joining a book club, can also be very helpful as long as it is an activity a person enjoys, Prof Lautenschlager says.
"The minute you prescribe an activity they hate doing…most likely the effect in terms of being beneficial for brain health is lost," she says.
"It produces so much stress in the body not wanting to do it that the stress is more harmful than the benefit of keeping the brain active."
Prof Lautenschlager says middle age is a crucial time for making lifestyle decisions that will determine a person’s health in later life.
"Usually we are talking about when you move into your 30s, definitely the 40s and also still the 50s," she says.
"Things like a high blood pressure or carrying too much weight, if you do that in these decades, it seems to harm the brain long-term in terms of how healthy a person is in their 70s or 80s."
Ideally people should aim for a healthy lifestyle from childhood but luckily research shows lifestyle changes still have an effect on brain health if a person is already old, Prof Lautenschlager says.
"Even programs…with seniors in their 70s and 80s can still make a difference," she says.
The research was published this month in the journal Maturitas.
MagLab MRI machine provides in-depth analysis of strokes
New research conducted at the Florida State University-based National High Magnetic Field Laboratory has revealed a new, innovative way to classify the severity of a stroke, aid in diagnosis and evaluate potential treatments.
“Stroke affects millions of adults and children worldwide,” said Sam Grant, MagLab researcher and associate professor of chemical and biomedical engineering at the FAMU-FSU College of Engineering. “This research offers a new technique for the chemical analysis of metabolites during stroke and a means of evaluating dynamic changes in cell processes and size in living tissue.”
The research is detailed in two papers, “Metabolic properties in stroked rats revealed by relaxation-enhanced magnetic resonance spectroscopy at ultrahigh fields,” in Nature Communications and “Metabolic T1 dynamics and longitudinal relaxation enhancement in vivo at ultrahigh magnetic fields on ischemia” in the Journal of Cerebral Blood Flow and Metabolism.
The new technique is a way of narrowly applying energy to the metabolites of a specimen exposed to a very high magnetic field. Metabolites are the biological compounds used in the chemical process of breaking down food or other chemicals into energy and producing new materials.
By selectively “exciting” these metabolites and analyzing their distribution and confinement in brain tissue, the research team can investigate the metabolic microenvironment and tell whether cells were shrinking or expanding, a critical tool to understanding the severity of stroke, Grant said.
That information could help medical professionals better treat patients.
“Strokes cause an interruption of blood and oxygen to flow to the brain,” explained Jens Rosenberg, another MagLab researcher and one of Grant’s co-authors. “Through this research, we can see how neurons and other neural cells respond to the disruption of blood flow after stroke and use that information to better understand the full impacts of stroke.”
The MagLab’s flagship 900 MHz Ultra Widebore NMR magnet system was a critical component to the research. Utilizing this powerful magnet, the research team, which included scientists from the Champaulimod Center in Portugal and the Weizmann Institute of Science in Israel, were able to acquire localized chemical signatures of metabolites from 125-microliter volumes within the brain with high sensitivity and fidelity in six seconds.
Typical MRIs at hospitals or doctor’s offices measure around 1.5 – 3 tesla (the unit of magnetic field strength), while the 900 MHz measures a whopping 21.1 tesla, providing at least seven times the sensitivity.
“This very high field coupled with the RF pulse sequence design by our collaborators and homebuilt RF probes offer a unique non-invasive way of evaluating stroke evolution and potential treatments,” Rosenberg said.
The team also sees exciting possibilities to use this technique to further investigate debilitating diseases.
“By evaluating spectral regions previously undetectable, we hope to fingerprint certain diseases, like ischemic stroke, so that we can identify new characteristics that are specific to pathological conditions at the metabolic level in vivo,” Grant said. “There is a lot of work to be done to identify these dynamic changes and decide when and how our treatments can be most effective.”
Further research on metabolites using this technique could also be used for analysis of neurological disorders such as dementia, schizophrenia, Lou Gehrig’s, Parkinson’s, Alzheimer’s and Huntington’s diseases.
Mechanism that repairs brain after stroke discovered
A previously unknown mechanism through which the brain produces new nerve cells after a stroke has been discovered at Lund University and Karolinska Institutet in Sweden. The findings have been published in the journal Science.
A stroke is caused by a blood clot blocking a blood vessel in the brain, which leads to an interruption of blood flow and therefore a shortage of oxygen. Many nerve cells die, resulting in motor, sensory and cognitive problems.
The researchers have shown that following an induced stroke in mice, support cells, so-called astrocytes, start to form nerve cells in the injured part of the brain. Using genetic methods to map the fate of the cells, the scientists could demonstrate that astrocytes in this area formed immature nerve cells, which then developed into mature nerve cells.
”This is the first time that astrocytes have been shown to have the capacity to start a process that leads to the generation of new nerve cells after a stroke”, says Zaal Kokaia, Professor of Experimental Medical Research at Lund University.
The scientists could also identify the signalling mechanism that regulates the conversion of the astrocytes to nerve cells. In a healthy brain, this signalling mechanism is active and inhibits the conversion, and, consequently, the astrocytes do not generate nerve cells. Following a stroke, the signalling mechanism is suppressed and astrocytes can start the process of generating new cells.
”Interestingly, even when we blocked the signalling mechanism in mice not subjected to a stroke, the astrocytes formed new nerve cells”, says Zaal Kokaia.
“This indicates that it is not only a stroke that can activate the latent process in astrocytes. Therefore, the mechanism is a potentially useful target for the production of new nerve cells, when replacing dead cells following other brain diseases or damage.”
The new nerve cells were found to form specialized contacts with other cells. It remains to be shown whether the nerve cells are functional and to what extent they contribute to the spontaneous recovery that is observed in a majority of experimental animals and patients after a stroke.
A decade ago, Kokaia’s and Lindvall’s research group was the first to show that stroke leads to the formation of new nerve cells from the adult brain’s own neural stem cells. The new findings further underscore that when the adult brain suffers a major blow such as a stroke, it makes a strong effort to repair itself using a variety of mechanisms.
The major advancement with the new study is that it demonstrates for the first time that self-repair in the adult brain involves astrocytes entering a process by which they change their identity to nerve cells.
”One of the major tasks now is to explore whether astrocytes are also converted to neurons in the human brain following damage or disease. Interestingly, it is known that in the healthy human brain, new nerve cells are formed in the striatum. The new data raise the possibility that some of these nerve cells derive from local astrocytes. If the new mechanism also operates in the human brain and can be potentiated, this could become of clinical importance not only for stroke patients, but also for replacing neurons which have died, thus restoring function in patients with other disorders such as Parkinson’s disease and Huntington’s disease”, says Olle Lindvall, Senior Professor of Neurology.
A developmental study of the effect of music training on timed movements
When people clap to music, sing, play a musical instrument, or dance, they engage in temporal entrainment. We examined the effect of music training on the precision of temporal entrainment in 57 children aged 10–14 years (31 musicians, 26 non-musicians). Performance was examined for two tasks: self-paced finger tapping (discrete movements) and circle drawing (continuous movements). For each task, participants synchronized their movements with a steady pacing signal and then continued the movement at the same rate in the absence of the pacing signal. Analysis of movements during the continuation phase revealed that musicians were more accurate than non-musicians at finger tapping and, to a lesser extent, circle drawing. Performance on the finger-tapping task was positively associated with the number of years of formal music training, whereas performance on the circle-drawing task was positively associated with the age of participants. These results indicate that music training and maturation of the motor system reinforce distinct skills of timed movement.
Set of molecules found to link insulin resistance in the brain to diabetes
A key mechanism behind diabetes may start in the brain, with early signs of the disease detectable through rising levels of molecules not previously linked to insulin signaling, according to a study led by researchers at the Icahn School of Medicine at Mount Sinai published today in the journal Cell Metabolism.
(Image: Shutterstock)
Fixing a faulty molecular ‘transport hub’ could slow brain degeneration
University of Queensland researchers have gained new insights into how the body sorts and transports protein ‘cargo’ within our cells, in a finding that could eventually lead to treatments for neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
An international research team co-led by Dr Brett Collins from UQ’s Institute for Molecular Bioscience has revealed the structure of a molecular transport hub that sorts, directs and transports protein to correct destinations in the cell.
Dr Collins said protein cargoes that failed to reach the correct destinations in cells created ‘traffic jams’ that could affect neuronal activity and brain function.
“Having an understanding of how these proteins work together to sort and transport cargo could be the first step in developing drugs that reverse the effects of toxic protein accumulation in neurodegenerative disease,” he said.
Dr Collins has been studying how cargo is sorted, packaged, and trafficked within human cells for more than a decade.
He said that developing drugs that fix faulty proteins such as the transport hub was a relatively new and exciting approach to treatment.
“Traditionally, drugs are developed to try to block or inhibit the function of proteins in the body,” Dr Collins said.
“The problem with drugs that completely stop the function of a protein is that you often get harmful side-effects.”
Dr Collins said the promising finding provided new avenues to target multiple parts of the transport hub to enhance its function by stabilising the protein.
“If we can enhance or improve the function of this protein we could potentially slow down the brain degeneration that occurs in diseases such as Alzheimer’s and Parkinson’s,” he said.
(Source: uq.edu.au)
Mouse Version of an Autism Spectrum Disorder Improves When Diet Includes a Synthetic Oil
When young mice with the rodent equivalent of a rare autism spectrum disorder (ASD), called Rett syndrome, were fed a diet supplemented with the synthetic oil triheptanoin, they lived longer than mice on regular diets. Importantly, their physical and behavioral symptoms were also less severe after being on the diet, according to results of new research from The Johns Hopkins University.
(Image caption: Mitochondria (arrows) in muscle cells from mice with Rett syndrome improved in appearance after the mice were given triheptanoin oil. Top: Muscle from mice given regular food. Bottom: Muscle from mice given food supplemented with triheptanoin. Left: Healthy mice. Right: Mice with a genetic mutation that mimics Rett syndrome.)
Researchers involved in the study think that triheptanoin improved the functioning of mitochondria, energy factories common to all cells. Since mitochondrial defects are seen in other ASDs, the researchers say, the experimental results offer hope that the oil could help not just people with Rett syndrome, but also patients with other, more common ASDs.
A description of the research was published on Oct. 9 in the journal PLOS ONE.
ASDs affect an estimated one in 68 children under 8 years of age in the United States. Rett syndrome is a rare ASD caused by mutations in the MECP2 gene, which codes for methyl-CpG-binding-protein 2 (MeCP2). Rett syndrome includes autismlike signs, such as difficulty communicating, socializing and relating to others. Other hallmarks are seizures, decreased muscle tone, repetitive involuntary movements, and gastrointestinal and breathing problems. These other signs are also seen in some patients with other ASDs, suggesting underlying similarities in their causes. While the causes of most ASDs are unknown and thought to be complex, Rett syndrome is unique — and could be a source of insight for the others — because it is caused by an error in a single gene.
The research team used mice lacking the MeCP2 protein, which left them with severe Rett syndrome. In examining those mice, what stood out, according to Gabriele Ronnett, M.D., Ph.D., who led the research project at the Johns Hopkins University School of Medicine, was that they weighed the same as healthy mice but had large fat deposits accompanied by lower amounts of nonfat tissue, such as muscle. This suggested that calories were not being used to support normal tissue function but instead were being stored as fat.
This possibility led Ronnett and her research team to consider the role of mitochondria, which transform the building blocks of nutrients into a high-energy molecule, ATP. This molecule drives processes such as the building of muscle and the growth of nerve cells. Mitochondria use a series of biochemical reactions, collectively called the TCA cycle, to make this transformation possible. According to Susan Aja, Ph.D., a research associate and lead member of the research team, “If the components of the TCA cycle are low, nutrient building blocks are not processed well to create ATP. They are instead stored as fat.”
Ronnett suspected, she says, that some of Rett syndrome’s neurological symptoms could stem from metabolic deficiencies caused by faulty mitochondria and reduced energy for brain cells. “Rett syndrome becomes apparent in humans 6 to 18 months old, when the energy needs of the brain are particularly high, because a lot of new neural connections are being made,” says Ronnett. “If the mitochondria are already defective, stressed or damaged, the increased demand would be too much for them.”
Previous small clinical trials in people with a different metabolic disorder suggested that dietary intervention with triheptanoin could help. Triheptanoin is odorless, tasteless and a little thinner than olive oil. It is easily processed to produce one of the components of the TCA cycle.
When Rett syndrome mice were weaned at 4 weeks of age, they were fed a diet in which 30 percent of their calories came from triheptanoin, mixed in with their normal pelleted food. Though far from a cure, the results of the triheptanoin treatment were impressive, the researchers say. Treated mice had healthier mitochondria, improved motor function, increased social interest in other mice and lived four weeks — or 30 percent — longer than mice who did not receive the oil. The team also found that the diet normalized their body fat, glucose and fat metabolism.
“You can think of the mitochondria of the Rett syndrome model mice as damaged buckets with holes in them that allow TCA cycle components to leak out,” says Aja. “We haven’t figured out how to plug the holes, but we can keep the buckets full by providing triheptanoin to replenish the TCA cycle.”
“It is still too early to assume that this oil will work in humans with ASDs, but these results give us hope,” says Ronnett. “It’s exciting to think that we might be able to improve many ASDs without having to identify each and every contributing gene.”
According to Aja, additional mouse studies are needed to learn if female mice respond to the treatment, to perform a wider range of physiology and behavior tests, and, importantly, to assess the effects of triheptanoin treatment on the brain, which is considered the main driver of many Rett symptoms. The team would also like to provide triheptanoin at earlier ages, perhaps via the mothers’ milk, to mimic developmental ages at which most children are diagnosed with Rett syndrome.
Triheptanoin is currently made for research purposes only and is not available as a medicine or dietary supplement for humans.
(Source: hopkinsmedicine.org)
(Image caption: Neurons of love: A newly discovered type of brain cell responds to oxytocin and so regulates female mice’s interest in males, but only when the females are in heat. These star-shaped neurons (above) are shown within a brain region called the medial prefrontal cortex.)
Newly discovered brain cells explain a prosocial effect of oxytocin
Oxytocin, the body’s natural love potion, helps couples fall in love, makes mothers bond with their babies, and encourages teams to work together. Now new research at Rockefeller University reveals a mechanism by which this prosocial hormone has its effect on interactions between the sexes, at least in certain situations. The key, it turns out, is a newly discovered class of brain cells.
“By identifying a new population of neurons activated by oxytocin, we have uncovered one way this chemical signal influences interactions between male and female mice,” says Nathaniel Heintz, James and Marilyn Simons Professor and head of the Laboratory of Molecular Biology.
The findings, published today in Cell (October 9), had their beginnings in a search for a new type of interneuron, a specialized neuron that relays messages to other neurons across relatively short distances. As part of her doctoral thesis, Miho Nakajima began creating profiles of the genes expressed in interneurons using a technique known as translating ribosome affinity purification (TRAP) previously developed by the Heintz lab and Paul Greengard’s Laboratory of Molecular and Cellular Neuroscience at Rockefeller. Within some profiles from the outer layer of the brain known as the cortex, she saw an intriguing protein: a receptor that responds to oxytocin.
“This raised the question: What is this small, scattered population of interneurons doing in response to this important signal, oxytocin?” Nakajima says. “Because oxytocin is most involved in social behaviors of females, we decided to focus our experiments on females.”
To determine how these neurons, dubbed oxytocin receptor interneurons or OxtrINs, affected behavior when activated by oxytocin, she silenced only this class of interneurons and, in separate experiments, blocked the receptor’s ability to detect oxytocin in some females. She then gave them a commonly used social behavior test: Given the choice between exploring a room with a male mouse or a room with an inanimate object – in this case a plastic Lego block – what would they do? Generally, a female mouse will go for the non-stackable choice. Legos just aren’t that interesting to rodents. But Nakajima’s results were confusing: Sometimes the mice with the silenced OxtrINs showed an abnormally high interest in the Lego, and sometimes they responded normally.
This led her to suspect the influence of the female reproductive cycle. In another round of experiments, she recorded whether the female mice were in estrus, the sexually receptive phase, or diestrus, a period of sexual inactivity. Estrus, it turned out, was key. Female mice in this phase showed an unusual lack of interest in the males when their receptors were inactivated. They mostly just sniffed at the Lego. There was no effect on mice is diestrus, and there was no effect if the male love interest was replaced with a female. When Nakajima tried the same alteration in males, there was also no effect.
“In general, OxtrINs appear to sit silently when not exposed to oxytocin,” says Andreas Görlich, a postdoc in the lab who recorded the electrical activity of these neurons with and without the hormone. “The interesting part is that when exposed to oxytocin these neurons fire more frequently in female mice than they do in male mice, possibly reflecting the differences that showed up in the behavioral tests.”
“We don’t yet understand how, but we think oxytocin prompts mice in estrus to become interested in investigating their potential mates,” Nakajima says. “This suggests that the social computation going on in a female mouse’s brain differs depending on the stage of her reproductive cycle.”
Oxytocin has similar effects for humans as for mice, however, it is not yet clear if the hormone influences the human version of this mouse interaction, or if it works through a similar population of interneurons. The results do, however, help explain how humans, mice and other mammals respond to changing social situations, Heintz says.
“Oxytocin responses have been studied in many parts of the brain, and it is clear that it, or other hormones like it, can impact behavior in different ways, in different contexts and in response to different physiological cues,” he says. “In a general sense, this new research helps explain why social behavior depends on context as well as physiology.”