Posts tagged science
Articles and news from the latest research reports.
Gestures of Human and Ape Infants Are More Similar Than You Might Expect
Thirteen years after the release of On the Origin of Species, Charles Darwin published another report on the evolution of mankind. In the 1872 book The Expression of the Emotions in Man and Animals, the naturalist argued that people from different cultures exhibit any given emotion through the same facial expression. This hypothesis didn’t quite pan out—last year, researchers poked a hole in the idea by showing that the expression of emotions such as anger, happiness and fear wasn’t universal (PDF). Nonetheless, certain basic things—such as the urge to cry out in pain, an increase in blood pressure when feeling anger, even shrugging when we don’t understand something—cross cultures.
A new study, published today in the journal Frontiers in Psychology, compares such involuntary responses, but with an added twist: Some observable behaviors aren’t only universal to the human species, but to our closest relatives too—chimpanzees and bonobos.
Using video analysis, a team of UCLA researchers found that human, chimpanzee and bonobo babies make similar gestures when interacting with caregivers. Members of all three species reach with their arms and hands for objects or people, and point with their fingers or heads. They also raise their arms up, a motion indicating that they want to be picked up, in the same manner. Such gestures, which seemed to be innate in all three species, precede and eventually lead to the development of language in humans, the researchers say.
To pick up on these behaviors, the team studied three babies of differing species through videos taken over a number of months. The child stars of these videos included a chimpanzee named Panpanzee, a bonobo called Panbanisha and a human girl, identified as GN. The apes were raised together at the Georgia State University Language Research Center in Atlanta, where researchers study language and cognitive processes in chimps, monkeys and humans. There, Panpanzee and Panbanisha were taught to communicate with their human caregivers using gestures, noises and lexigrams, abstract symbols that represent words. The human child grew up in her family’s home, where her parents facilitated her learning.
Researchers filmed the child’s development for seven months, starting when she was 11 months old, while the apes were taped from 12 months of age to 26 months. In the early stages of the study, the observed gestures were of a communicative nature: all three infants engaged in the behavior with the intention of conveying how their emotions and needs. They made eye contact with their caregivers, added non-verbal vocalizations to their movements or exerted physical effort to elicit a response.
By the second half of the experiment, the production of communicative symbols—visual ones for the apes, vocal ones for the human—increased. As she grew older, the human child began using more spoken words, while the chimpanzee and bonobo learned and used more lexigrams. Eventually, the child began speaking to convey what she felt, rather than only gesturing. The apes, on the other hand, continued to rely on gestures. The study calls this divergence in behavior “the first indication of a distinctive human pathway to language.”
The researchers speculate that the matching behaviors can be traced to the last shared ancestor of humans, chimps and bobonos, who lived between four and seven million years ago. That ancestor probably exhibited the same early gestures, which all three species then inherited. When the species diverged, humans managed to build on this communicative capacity by eventually graduating to speech.
Hints of this can be seen in how the human child paired her gestures with non-speech vocalizations, the precursors to words, far more than the apes did. It’s this successful combinationof gestures and words that may have led to the birth of human language.
What The Human Face Might Look Like 100,000 Years From Now
The human face might look very different in the future.
Artist and researcher Nickolay Lamm from U.K. discount site MyVoucherCodes.co.uk collaborated with a genomics expert to create pictures that show the evolution of the human face 20,000, 60,000, and 100,000 years from now.
In one possible future scenario, humans will have full control of human genome engineering. That is, they will be able to eliminate hereditary genetic disorders, or select desirable genetic traits like straight teeth and natural blonde hair.
Natural human evolution is still at work — the head will get bigger to make room for a larger brain — but most facial features will be molded to reflect what the majority of us perceive as attractive: big eyes, a straight nose, and facial symmetry.
Creativity Linked with Deficit in Mental Flexibility
Creative types are often seen as rather flaky — their minds leaping wildly from one bizarre idea to another, ever seeking inspiration. But a new study suggests that people who actually achieve creative success have minds that stubbornly cling to ideas, even to the point where it impairs their ability to shift focus.
In one experiment, researchers at Northwestern University in Illinois selected 34 students out of more than 300 who completed a questionnaire on creative achievement, ultimately including 19 who had outstanding achievements in music, art, science, writing or other areas and 15 of those whose scores ranked them as being among the least creative.
“We preselected people with very high and very low creative achievement,” says lead author Darya Zabelina, a graduate student at Northwestern. The research was published in Frontiers in Psychology.
During the study, participants had to shift their attention from a global level of processing to a local one, by focusing on different aspects of patterns. In some cases, they were asked to identify a large letter made up of smaller ones (for example, an “S” pattern made up of smaller “e’s”). In other instances, the correct answer was the opposite one — identifying the smaller letter.
“It’s a little counter-intuitive,” says Zabelina, “but people with high creativity actually perform badly on this test.” In fact, they made more than twice as many errors as the less creative group — and even after controlling for overall intelligence, the creative people still did less well.
A second experiment involved the same task, performed by another 39 high, moderate or low scorers in creative achievements. Again, the more creative people scored lower. And in both experiments, there was no difference in performance whether people had to shift from the “forest” focus of the larger letters to the “tree level” of the smaller ones or whether the shift was in the opposite direction. That suggests that the lower scores were not related to creative people being more focused specifically on either detail or on general patterns.
The research may help explain why autistic people, who tend to focus obsessively, can often be highly creative. Paradoxically, it may also help explain the link between attention deficit/hyperactivity disorder (ADHD) and creative success.
“The general idea is that [people with ADHD] are not able to focus on anything,” says Zabelina, “But really there are two different parts of the disorder, and one is that if they really get interested in something, they become almost like autistic people: really focused, so much so that they are not able to practice anything else.” Indeed, between 30% and 50% of autistic people also have ADHD.
The combination of an ability to range widely from one thought to another and to focus when a good idea occurs may be the sweet spot for creative success. The trick is in the timing: to mind-wander enough when seeking ideas to hit on the best ones and then to zoom in and persist once the right solution has been found.
But the study makes clear that creative achievement may come with some trade-offs in mental flexibility, when the time comes to actually shift focus. Persistence certainly matters in creative achievement — but some creative folks may not know when to stop.
(Source: TIME)
Computer Simulations Shed New Light On How The Immune System Works
Researchers at McGill University in Montreal have developed computer simulations that better explain how a person’s immune cells can detect foreign antigens and fight infections.
In an effort to determine exactly how the body’s natural defenses are able to sort through large amounts of similar-looking proteins in order to locate and eliminate harmful invaders, physics professor Paul François and graduate student Jean-Benoît Lalanne used computational tools to study how the process works.
They discovered that the antigen-fighting process is related to the phenomenon of biochemical adaptation – a mechanism that enables organisms to cope with a variety of different environmental conditions. According to the authors of the study, their work could prove essential insight into AIDS and other immune diseases.
“For immune cells, singling out foreign proteins is like looking for a needle in a haystack – where the needle may look very much like a straw, and where some straws may also look very much like a needle,” François said. “Our approach provides a simpler theoretical framework and understanding of what happens” as the immune cells sort through that “haystack” in search of foreign antigens and to trigger the body’s immune response.
The researchers’ computer simulation used an algorithm that was inspired by Darwinian evolution, the university explained. The algorithm randomly creates mathematical models of biochemical networks, and then scores them by comparing their properties to those of an actual immune system. The highest-rated networks are duplicated in the next generation and mutated, a process that is repeated until the networks achieve a perfect score.
“Our model shares many similarities with real immune networks,” explained François. “Strikingly, the simplest evolved solution we found has both similar characteristics and some of the blind spots of real immune cells we studied in a previous collaborative study with the groups of Grégoire Altan-Bonnet (Memorial Sloane Kettering, New York), Eric Siggia (Rockefeller University, New York) and Massimo Vergassola (Pasteur Institute, Paris).”
The Natural Sciences and Engineering Research Council of Canada and the Human Frontier Science Program provided funding for the research, which was published in a recent edition of the journal Physical Review Letters.
Unusual Antibodies in Cows Suggest New Ways to Make Therapies for People
Humans have been raising cows for their meat, hides and milk for millennia. Now it appears that the cow immune system also has something to offer. A new study led by scientists from The Scripps Research Institute (TSRI) focusing on an extraordinary family of cow antibodies points to new ways to make human medicines.
“These antibodies’ structure and their mechanism for creating diversity haven’t been seen before in other animals’ antibodies,” said Vaughn V. Smider, assistant professor of cell and molecular biology at TSRI and principal investigator for the study, which appears as the cover story in the June 6, 2013 issue of the journal Cell.
Big Multiple Sclerosis Breakthrough
Phase 1 trial safely resets patients’ immune systems, reduces attack on myelin protein
A phase 1 clinical trial for the first treatment to reset the immune system of multiple sclerosis (MS) patients showed the therapy was safe and dramatically reduced patients’ immune systems’ reactivity to myelin by 50 to 75 percent, according to new Northwestern Medicine research.
In MS, the immune system attacks and destroys myelin, the insulating layer that forms around nerves in the spinal cord, brain and optic nerve. When the insulation is destroyed, electrical signals can’t be effectively conducted, resulting in symptoms that range from mild limb numbness to paralysis or blindness.
“The therapy stops autoimmune responses that are already activated and prevents the activation of new autoimmune cells,” said Stephen Miller, the Judy Gugenheim Research Professor of Microbiology-Immunology at Northwestern University Feinberg School of Medicine. “Our approach leaves the function of the normal immune system intact. That’s the holy grail.”
Miller is the co-senior author of a paper on the study, which was published June 5 in the journal Science Translational Medicine. The study is a collaboration between Northwestern’s Feinberg School, University Hospital Zurich in Switzerland and University Medical Center Hamburg-Eppendorf in Germany.
The human trial is the translation of more than 30 years of preclinical research in Miller’s lab.
In the trial, the MS patients’ own specially processed white blood cells were used to stealthily deliver billions of myelin antigens into their bodies so their immune systems would recognize them as harmless and develop tolerance to them.
Current therapies for MS suppress the entire immune system, making patients more susceptible to everyday infections and higher rates of cancer.
While the trial’s nine patients — who were treated in Hamburg, Germany — were too few to statistically determine the treatment’s ability to prevent the progression of MS, the study did show patients who received the highest dose of white blood cells had the greatest reduction in myelin reactivity.
The primary aim of the study was to demonstrate the treatment’s safety and tolerability. It showed the intravenous injection of up to 3 billion white blood cells with myelin antigens caused no adverse affects in MS patients. Most importantly, it did not reactivate the patients’ disease and did not affect their healthy immunity to real pathogens.
As part of the study, researchers tested patients’ immunity to tetanus because all had received tetanus shots in their lifetime. One month after the treatment, their immune responses to tetanus remained strong, showing the treatment’s immune effect was specific only to myelin.
The human safety study sets the stage for a phase 2 trial to see if the new treatment can prevent the progression of MS in humans. Scientists are currently trying to raise $1.5 million to launch the trial, which has already been approved in Switzerland. Miller’s preclinical research demonstrated the treatment stopped the progression of relapsing-remitting MS in mice.
“In the phase 2 trial we want to treat patients as early as possible in the disease before they have paralysis due to myelin damage.” Miller said. “Once the myelin is destroyed, it’s hard to repair that.”
In the trial, patients’ white blood cells were filtered out, specially processed and coupled with myelin antigens by a complex GMP manufacturing process developed by the study co-senior authors, Roland Martin, Mireia Sospedra, and Andreas Lutterotti and their team at the University Medical Center Hamburg-Eppendorf. Then billions of these dead cells secretly carrying the myelin antigens were injected intravenously into the patients. The cells entered the spleen, which filters the blood and helps the body dispose of aging and dying blood cells. During this process, the immune cells start to recognize myelin as a harmless and immune tolerance quickly develops. This was confirmed in the patients by immune assays developed and carried out by the research team in Hamburg.
This therapy, with further testing, may be useful for treating not only MS but also a host of other autoimmune and allergic diseases simply by switching the antigens attached to the cells. Previously published preclinical research by Miller showed the therapy’s effectiveness for type 1 diabetes and airway allergy (asthma) and peanut allergy.
The MS human trial relates directly to Miller’s recently published research in mice in which he used nanoparticles — rather than a patient’s white blood cells — to deliver the myelin antigen. Using a patient’s white blood cells is a costly and labor-intensive procedure. Miller’s study showed the nanoparticles, which are potentially cheaper and more accessible to a general population, could be as effective as the white blood cells as delivery vehicles. This nanoparticle technology has been licensed to Cour Pharmaceutical Development Company and is in preclinical development.
Miller’s research represents several pillars of Northwestern’s Strategic Plan by discovering new ways to treat disease in the biomedical sciences and translating those discoveries into ideas and products that make the world a better place for everyone.
(Source: northwestern.edu)
PD-Like Sleep and Motor Problems Observed in α-Synuclein Mutant Mice
The presence of Lewy bodies in nerve cells, formed by intracellular deposits of the protein α-synuclein, is a characteristic pathologic feature of Parkinson’s Disease (PD). In the quest for an animal model of PD that mimics motor and non-motor symptoms of human PD, scientists have developed strains of mice that overexpress α-synuclein. By studying a strain of mice bred to overexpress α-synuclein via the Thy-1 promoter, scientists have found these mice develop many of the age-related progressive motor symptoms of PD and demonstrate changes in sleep and anxiety. Their results are published in the latest issue of Journal of Parkinson’s Disease.
PD is the second most common neurodegenerative disorder in the United States, affecting approximately one million Americans and five million people worldwide. Its prevalence is projected to double by 2030. The most obvious symptoms are movement-related, such as involuntary shaking and muscle stiffness; non-motor symptoms, such as increases in anxiety and sleep disturbances, can appear prior to the onset of motor symptoms. Although the drug levodopa can relieve some symptoms, there is no cure – intensifying the pressure to find an animal model that can help clarify the pathological processes underlying human PD and find new medications to treat the pathology and/or relieve symptoms.
Investigators at the National Institute on Aging compared wild type mice with specially bred mice that were transgenic for the A53T mutation of the human α-synuclein (SNCA) gene under the control of a human thymus cell antigen 1, theta (THY-1) promoter. As the mice aged, their motor performance on a rotarod test (which measures how long the mouse can remain on a rotating rod) became impaired and the length of their strides were significantly shorter than the wild type control mice.
The study also found that SNCA mice displayed fragmented nighttime activity patterns compared to wild type controls and appeared to have a reduced overall sleep time. “Despite the prevalence of abnormal sleep patterns in PD, very few studies to date have outlined sleep disturbances in animal models of PD,” says Sarah M. Rothman, PhD, a researcher with the National Institute on Aging, in Baltimore, MD.
Many PD patients typically show an increase in anxiety and depression, and in this respect the SNCA mouse model did not replicate the human condition. SNCA mice displayed an early and significant decrease in anxiety-like behavior that persisted throughout their lifespan, as shown by both open field and elevated plus maze tests (in which mice have the choice of spending time in open or closed arms of a maze). Other rodent models that utilize changes in expression of α-synuclein have also reported lower anxiety levels. The authors suggest that higher levels of serotonin found in the hypothalamus of the SNCA mice may be associated with the reduced anxiety observed.
The authors say it is important to remember that the SNCA “model utilizes the presence of a mutation that only occurs very rarely in PD. While all PD patients display α-synuclein pathology, they do not all express the mutated form of the protein,” says Dr. Rothman.
(Source: alphagalileo.org)
By trying it all, predatory sea slug learns what not to eat
Researchers have found that a type of predatory sea slug that usually isn’t picky when it comes to what it eats has more complex cognitive abilities than previously thought, allowing it to learn the warning cues of dangerous prey and thereby avoid them in the future.
The research appears in the Journal of Experimental Biology.
Pleurobranchaea californica is a deep-water species of sea slug found off the west coast of the United States. It has a relatively simple neural circuitry and set of behaviors. It is a generalist feeder, meaning, as University of Illinois professor of molecular and integrative physiology and leader of the study Rhanor Gillette put it, that members of this species “seem to try anything once.”
Another sea slug species, Flabellina iodinea, commonly known as the Spanish shawl because of the orange outgrowths called cerata that cover its purple back, also lives off the west coast. Unlike Pleurobranchaea, however, the Spanish shawl eats only one type of food, an animal called Eudendrium ramosum. According to Gillette, the Spanish shawl digests the Eudendrium’s entire body except for its embryonic, developing stinging cells. The Spanish shawl instead transports these stinging cells to its own cerata where they mature, thereby co-opting its victim’s body parts for its own defense.
The story of Gillette’s Pleurobranchaea-Flabellina research began with a happy accident that involved showing a lab visitor Pleurobranchaea’s penchant for predation.
“I had a Pleurobranchaea in a small aquarium that we were about to do a physiological experiment with, and my supplier from Monterey had just sent me these beautiful Spanish shawls,” Gillette said. “So I said to the visitor, ‘Would you like to see Pleurobranchaea eat another animal?’”
Gillette placed the Spanish shawl into the aquarium. The Pleurobranchaea approached, smelled, and bit the purple and orange newcomer. However, the Flabellina’s cerata stung the Pleurobranchaea, the Spanish shawl was rejected and left to do its typical “flamenco dance of escape,” and Pleurobranchaea also managed to escape with an avoidance turn.
Some minutes later, his curiosity piqued, Gillette placed the Spanish shawl back into the aquarium with the Pleurobranchaea. Rather than try to eat the Spanish shawl a second time, the Pleurobranchaea immediately started its avoidance turn. (Watch a video of this interaction.)
“I had never seen that before! We began testing them and found that they were learning the odor of the Spanish shawl very specifically and selectively,” Gillette said.
Gillette and his team later replicated that day’s events by placing a Pleurobranchaea in a training arena 12-15 centimeters from a Spanish shawl, then recorded the Pleurobranchaea’s behavior. They returned the Pleurobranchaea to the arena for four more trials in 20-minute intervals, then repeated the procedure 24 and 72 hours later.
In the experiments, those Pleurobranchaea whose feeding thresholds were too high (meaning they were already full) or too low (they were extremely hungry) would either not participate or completely consume the Spanish shawl, respectively. Those that were hungry, but not ravenously so, continued to exhibit the avoidance-turn behavior when placed with the Spanish shawl even 72 hours later.
This showed that Pleurobranchaea was selective in its food choices, but only on a case-by-case basis; the sea slugs already trained to avoid the Spanish shawl would readily eat a species closely related to Flabellina called Hermissenda crassicornis.
Such behaviors come in handy in Pleurobranchaea’s natural environment, Gillette said.
“If you’re a generalist like Pleurobranchaea, it’s highly strategic and advantageous to learn what’s good and what’s not good so you can decide whether or not to take the risk or of attacking certain types of prey,” he said.
These findings show that the “simple” Pleurobranchaea is much more complex than originally thought.
“We already knew the neuronal circuitry that mediates this kind of decision,” Gillette said. “Finding this highly selective type of learning enlarges our perspective of function, in terms of the animal’s ability to make cost-benefit decisions that place it on a rather higher plane of cognitive ability than previously thought for many sea slugs.”
Diabetes drug shows promise in treatment of neurodegenerative disease
Researchers in Spain have found that a drug used to control Type II diabetes can help repair the spinal cords of mice suffering from the inherited disease adrenoleukodystrophy which, untreated, leads eventually to a paralysis, a vegetative state and death. They believe that their findings may be relevant to other neurodegenerative diseases. A Phase II trial will be starting shortly. The research is published simultaneously on line in the journal Brain.
A drug used to control Type II diabetes can help repair the spinal cords of mice suffering from the inherited disease adrenoleukodystrophy which, untreated, leads eventually to a paralysis, a vegetative state and death. This is an important step along the road to the development of a therapy for the human disease for which current treatment options are scarce and only partially effective, the annual conference of the European Society of Human Genetics will hear tomorrow (Sunday).
Professor Aurora Pujol, a research professor for the Catalan Government Research Body ICREA, working as Director of the Neurometabolic Diseases Laboratory at IDIBELL, Barcelona, Spain, investigated the role of mitochondria, the power plant of the cell, in adrenoleukodystrophy, a disease caused by the inactivation of the ABCD1 transporter of fatty acids in peroxisomes. This inactivation leads to the accumulation of fatty acids in organs and blood plasma, and causes spinal cord degeneration.
“ABCD1 is a protein located in the peroxisomes, compartments of the cell that detoxify chemicals and lipids, and thus the implication of mitochondria in such a disease was not obvious. But we knew from recent research that oxidative stress – where there is increased production of chemically active oxygen-containing molecules, and also significant decrease in the effectiveness of the body’s antioxidant defences – was involved. We also knew that bioenergetic failure appeared before disease symptoms. We therefore decided to investigate the role of the mitochondria”, Professor Pujol will say.
The group of diseases known as leukodystrophies are characterised by progressive loss of the myelin sheath, the fatty covering that acts as an insulator around nerve fibres. Damage to the myelin sheath impairs the conduction of signals in the affected nerves and leads to locomotor problems.
“We knew that early oxidative damage and bioenergetic dysfunction underlay the late onset degeneration of nerve fibres observed in the mouse model of X-linked adrenoleukodystrophy (X-ALD), the most frequently inherited leukodystrophy, so we looked at mitochondria for further clues. We found that the X-ALD mice showed a loss of mitochondria at 12 months of age, prior to disease symptoms, so this could not be a consequence of the disease, but rather a contributing factor. We also knew that the pathway involved in the mitochondrial loss could be treated by the use of the diabetes drug pioglitazone, so we decided to test its effect in the mice”, Professor Pujol will say.
Pioglitazone halted the nerve fibre degeneration by preventing the loss of mitochondria, and inhibiting metabolic failure and oxidative stress in the treated mice, and hence also halted locomotor disabilities. The researchers were able to prove this both through analysis of spinal cords post mortem, and in vivo by putting the mice through a number of physical tests.
Although X-ALD is a relatively rare disease with a minimum incidence of 1 in 17 000 males, there are other neurodegenerative disorders caused by myelin sheath degeneration, for example multiple sclerosis, and many others where impaired bioenergetics combined with oxidative stress and degeneration of axons are known to be involved. The latter category of disease includes Parkinson’s, Huntington’s, and Alzheimer’s. “It is possible that our findings may be relevant to these conditions as well,” says Professor Pujol.
“Following on from these promising results, together with Professor Patrick Aubourg from the Hôpital Bicêtre, Paris, we will shortly be starting a multi-centre phase II clinical trial of pioglitazone in adult patients suffering from a late onset variant of adrenoleukodystrophy. Our research has shown that it will be feasible to monitor the biological effects of the drug by looking for biomarkers of oxidative damage in blood cells or plasma. We are happy to have made a contribution to finding a simple and effective treatment to a group of devastating diseases”, she will conclude.
(Source: alphagalileo.org)
Over-produced autism gene alters synapses, affects learning and behavior in mice
A gene linked to autism spectrum disorders that was manipulated in two lines of transgenic mice produced mature adults with irreversible deficits affecting either learning or social interaction.
The findings, published in the May 29 issue of the Journal of Neuroscience, have implications for potential gene therapies but they also suggest that there may be narrow windows of opportunity to be effective, says principal investigator Philip Washbourne, a professor of biology and member of the University of Oregon’s Institute of Neuroscience.
The research, reported by an 11-member team from three universities, targeted the impacts of alterations in the gene neuroligin 1 — one of many genes implicated in human autism spectrum disorders — to neuronal synapses in the altered mice during postnatal development and as they entered adulthood. One group over-expressed the normal gene, the other a mutated version.
Mice with higher-than-normal levels of the normal gene after a month had skewed synapses at maturity. Many were larger, appearing more mature, than normal. In these mice, Washbourne said, there were clear cognitive problems. “Behavior was just not normal. They didn’t learn very well, and they were slower to learn, but their social behavior was not impacted.”
Mice over-producing a mutated version of the gene reached adulthood with structurally immature synapses. “They were held back in development and behavior — the way they behave in terms of learning and memory, in terms of social interaction,” he said. “These were adult mice, three months old, but they behaved like normal mice at four weeks old. We saw arrested development. Learning is a little bit better, they are more flexible just like young mice, they learn faster, but their social interaction is off. To us, this looked more like Asperger’s syndrome.
"So with the same gene, doing two different manipulations — overexpressing the normal form or overexpressing a mutated form — we’ve gone to two different ends of the autism spectrum," said Washbourne, whose lab focuses on basic synapse formation and what goes wrong in relationship to autism. Work has been done in both mice and zebra fish.
"We made these mice so that we can turn the genes on and off as we want," Washbourne said. "Using an antibiotic, doxycycline, it turns off these altered genes that we inserted into their chromosomes. While on doxycycline, the mice are absolutely normal.”
However, if the inserted gene was turned off after the completion of development, mice still showed altered synapses and behavior. This result suggests that any kind of gene therapy may have to be applied to individuals with autism early on.
Effects seen in the social behavior of mice with the mutated gene, he said, are not unlike observations reported by parents of many autistic children. While normal mice prefer to engage with new mice entering their world rather than familiar others, or even a new inanimate object, these mice split their time equally. “It’s not a deficit in memory regarding which mouse is which, it’s more a weighting of their interaction. Does that mean they are autistic? I don’t know, but if you talk to parents of autistic children, one of the frustrating things they report is that their children treat complete strangers in exactly the same way that they treat them.”
While the findings provide new insights, Washbourne said, any translation into treatment could be decades away. “A problem with autism is there are many different genes potentially involved. It could be that some day, if you are diagnosed with autism, a mouth swab might allow for the identification of the exact gene that is mutated and allow for targeted therapy,” he said. “Genome sequencing already has turned up subtle mutations in lots of genes. Autism might be like cancer, with hundreds of potential combinations of faulty genes.”
(Source: uonews.uoregon.edu)