Wednesday, November 30, 2011

Purple Haze: A Genetic Basis for Synesthesia?

Synesthesia is a neurological condition that involves hyper-connectivity, a high degree of cross-talk between senses. This extreme connection causes individuals with synesthesia to make unusual—and sometimes extremely artistically interesting—associations. For example, in colored sequence synesthesia, individuals associate graphemes—letters or numbers—with specific colors. This tendency seems to be an exaggeration of the tendency that cognitively normal humans have to use metaphor—to connect different imagery in a unique, visually-rich manner.

Multiple studies have confirmed a probable genetic basis of synesthesia using Family Linkage studies, which explore the prevalence of a disorder within a specific lineage. However, finding specific genes linked to the disorder has been extremely challenging due to the highly heterogeneous nature of the condition; over 60 different kinds of synesthesia have been identified.

In a new study, published in a 2011 issue of Behavior Brain Research, a team of researchers has discovered that color-association synesthesia, in particular, seems to be linked to a gene in the region 16q12.2-23.1. However, only two of the families used in the study showed linkage to this region; thus, CSS on its own is likely heterogenous. Thus, the study largely supports previous research, which suggested that synesthesia was likely tied to a complex interaction between many different genes. Still, though, it presents progress on the identification of specific loci.

Understanding synesthesia goes beyond simply understanding one very specific condition; this study, for example, aims “to understand how neural crosstalk arises in a healthy brain, in the hopes of ultimately understanding how this mechanism might be modified in a disease state.” Indeed, the authors suggest that we can use Synesthesia to understand disorders that involve a high degree of cross-talk, such as Autism, Alzheimer’s disease, and Schizophrenia. On the other side, understanding the genetic basis Synesthesia may also help us to more deeply understand other aspects of the human brain; perhaps, by understanding this disorder, we can start to understand a potential genetic basis for the complex processes of human creative thought.

Link to the article:

In addition, an even more recent article suggests a possible underlying evolutionary function of synesthesia; the development of the ability of humans to integrate a broad range of sensory perceptions:

For a really interesting article on sound-symbolism and a kind of synesthesia-like mechanism in language development, see:

60 "de novo" genes found in humans

An international team of researchers from Canada and China have recently discovered 60 genes in humans that were produced spontaneously from non-coding DNA (also known as "junk" DNA) since our lineage spit from that of chimpanzees several million years ago. It was only two years ago that scientists first discovered that not all "new" human genes were the product of mutation of previously existing genes. Rather, some of our genes were spontaneously created from genetic material that previously did not code for proteins, and thus were not technically genes. These genes which seem to, in a sense, appear out of nowhere, are called "de novo" genes.

Until this most recent study, it was thought that humans had only a very few de novo genes, with 3 or 4 being created every million years. But this study shows that the rate is in fact between 10 and 12 for each million years, three times higher than previously estimated. The scientists made this discovery by combing through the human genome and comparing it to the genomes of the apes most closely related to us and then ruling out all genes that resembled those (either activated or deactivated) in the apes. The 60 out of around 25,000 genes that were left over after this process was completed were considered "de novo."

This discovery is particularly interesting because the majority of the de novo genes discovered seemed to be involved in the functioning of the cerebral cortex, the part of the brain responsible for dealing with memory, emotions, language, and various other functions that most of us deem as critical to making us human. There is, however, some doubt about the specific role these genes play in the cerebral cortex, and whether they have really contributed significantly to the most obvious differences between ourselves and apes. Further research will be difficult since the necessary experimentation is obviously not possible to perform on living humans, but there are hopes that by continuing research on apes or other lab animals further results can be produced.

The original article from Scientific American describing the results of the study can be found here.

Wednesday, November 23, 2011

Yale researchers find genetic link between heart disease and brain aneurysms

Intracranial aneurysms occur with the bursting of blood vessels in the brain. Scientists had already identified five gene variants linked to aneurysms through two previous studies, and two days ago, researchers at the Yale School of Medicine announced that they have discovered three more variants associated with aneurysm risk. The study was conducted at the Yale Center for Genome Analysis and involved approximately 20,000 people. Aside from identifying the three new aneurysm-associated variants, one of the new variants was also linked to heart disease. This variant is found near the endothelin receptor type A gene, which is known to control the tone and elasticity of blood vessels. Since the endothelin receptor type A gene maintains the body's vasculature, it is no surprise that is has been associated with cardiovascular disorders. This is the first time, however, that endothelins have been linked to brain aneurysms. How exactly this gene variant increases the risk for aneurysms is unclear, but further study will continue to shed light on a deadly condition that affects more than half a million people around the world each year.

Thursday, November 17, 2011

Largest Human-Designed Protein

A group of Vanderbilt chemists has broken the record for the largest human-synthesized protein. These researchers have designed and created a variant of the protein that usually manufactures the amino acid histidine. This protein is more than twice the size of the previous record-holder, and was created using a technique that allows for the creation of functional artificial proteins on a scale never before thought possible. The algorithm used here could carry potentially powerful consequences, because we can create new antibodies and other proteins not seen in nature that could be the cure to disease like HIV. The process requires about 10 days of calculations on supercomputers and will need much more work and research before it can really be beneficial, but this new gigantic artificial protein is a huge breakthrough.

Lou Gehrig's Disease Gene

Medical News Today reported recently that a new candidate gene has been found that is associated with Lou Gehrig's Disease, or ALS. ALS is a fatal neurodegenerative disease that has already been linked to mutations in TDP-43 and FUS. A recent study shows that the disease may also be linked to other genes with similar properties. This discovery was made by examining yeast cells--both TDP-43 and FUS are known to be toxic in yeast, so the researchers looked for other proteins that were aggregate and toxic. The researchers focused on one in particular, TAF15. The yeast research was supported by samples from ALS patients, that found TAF15 variants. Ultimately, the take-away here is that aggregation of these RNA binding proteins in general contribute to Lou Gehrig's Disease, information which hopefully can speed up research on the causes and possible treatments for this disease.

Genetically Modified Mosquitoes

In an article in the New York Times, researchers reported early successes in genetically engineering mosquitoes to pass lethal genes on to their offspring. This gene would kill the young mosquitoes before adulthood, which would help curb diseases like dengue fever and malaria. Although this would have clearly have positive effects for society, some people are worried that there has not been adequate research done to justify releasing such a large population of genetically modified creatures into the environment without the possibility of recall. Work is being done to attempt to suppress the reproductive ability of these new mosquitoes in order to prevent some unforeseen consequence. Only male mosquitoes would be released, and females are the ones that bite and spread disease, so there should be little environmental impact and ideally the project would be able to just eliminate the disease. There is a possibility that the mosquitoes could develop a resistance to the lethal gene in the lab and still be released inadvertently and cause serious problems. Despite the concerns, this is still potentially a huge step in eradicating mosquito-borne disease.

"Diabetes Genes Decline out of Africa"

A November 4th article in Science magazine by Ann Gibbons described a presentation on genetics and diabetes at a recent poster session. A current Stanford graduate student, Erik Corona, explained his research on the SNPs that are connected with type II diabetes and their prevalence throughout the world. Type II diabetes results when either the body does not produce enough insulin or the cells of the body stop responding to the insulin that is produced. This causes too little glucose being removed from the bloodstream, leading to other symptoms and problems such as kidney or vision failure and heart attack or stroke. This form of diabetes is thought to be produced by a combination of environmental and lifestyle factors, preexisting conditions, and genetics.

In the United States 8.3% of the population has diabetes, with African Americans and Native Americans being the two groups with the highest rates within them. Diabetes is currently uncommon in Sub-Saharan Africa, where only 3% of the population has the disease. However, rates of diabetes have been increasing as more Africans adopt an urban and western lifestyle and diet.

Corona’s research showed that the SNPs associated with diabetes are extremely prevalent in Africa and become rarer as one moves outward from there. There is a resurgence of the SNPs in North America, possibly due to a different lifestyle and diet that migrants there may have encountered. Corona suspects that as early humans left Africa, the genes for diabetes were gradually lost. In Africa, it is likely they served a role in better blood sugar and energy use when humans had a diet that was not rich in sugar or fat and when they did not live as long. At this time, these genes would have benefitted fitness levels, unlike their role today. This could present a problem for Africans in the future as they adopt a different, more fat and sugar rich lifestyle.

The question for researchers now is how large a role these genes actually play in predisposing people to diabetes. It may turn out that environmental and lifestyle influences are exponentially more important. Corona and his associates hope to use this type of gene analysis for more diseases in the future and to have that information available to doctors.

For more information about diabetes

For the original article

Wednesday, November 16, 2011

Biologists Slow the Aging Process in Fruit Flies: Study Has Implications for Humans

ScienceDaily (Nov. 9, 2011) — UCLA life scientists have identified a gene that slows the aging process. The biologists, working with fruit flies, activated a gene called PGC-1, which increases the activity of mitochondria, the tiny power generators in cells that control cell growth and tell cells when to live and die.

"We took this gene and boosted its activity in different cells and tissues of the fly and asked whether this impacts the aging process," said David Walker, an assistant professor of integrative biology and physiology at UCLA and a senior author of the study. "We discovered that when we boost PGC-1 within the fly's digestive tract, the fly lives significantly longer. We also studied neurons, muscle and other tissue types and did not find life extension; this is telling us there is something important about the digestive tract."

The research appears in the current online edition of Cell Metabolism, the leading journal in its field, and will be published in an upcoming print edition. Co-authors are from Walker's laboratory, the Salk Institute for Biological Studies in La Jolla, Calif., and the department of biology at UC San Diego.

"By activating this one gene in this one tissue -- the intestine -- the fly lives longer; we slow aging of the intestine, and that has a positive effect on the whole animal," said Walker, a member of UCLA's Molecular Biology Institute. "Our study shows that increasing PGC-1 gene activity in the intestine can slow aging, both at the cellular level and at the level of the whole animal."

The biologists delayed the aging of the flies' intestines and extended their lives by as much as 50 percent.

Fruit flies, or Drosophila melanogaster, have a life span of about two months. They start showing signs of aging after about one month, and they slow down, become less active and die, Walker said. They are a great model for studying aging, he said, because scientists know every one of their genes and can switch individual genes on and off.

What are the study's implications for human aging?

"We all think about protecting the brain and the heart, but the intestine is a vital tissue type for healthy aging," Walker said. "If anything goes wrong with the mitochondria in cells, the consequences could be devastating, and if anything goes wrong with our intestines, that may have devastating consequences for other tissue types and organs. Not only is the intestine essential for the uptake of nutrients that are a vital source of energy, but it is also an important barrier that protects us from toxins and pathogens in the environment. The intestine has to be well-maintained.

"No one yet knows what causes aging at the cellular or tissue level," Walker said. "As we age, our mitochondria become less efficient and less active. That has far-reaching consequences, because if the mitochondria decline, then all of our cellular functions may be compromised. However, it's a dangerous road to travel to say, 'This is the cause of aging.'"

The PGC-1 gene activates the cells' mitochondria and regulates mitochondrial activity in mammals and flies. The gene is a potential target for pharmaceuticals to combat age-related diseases, Walker said.

The study raises the question of whether increasing mitochondrial activity is an effective strategy to delay aging. If so, increasing the PGC-1 gene may prove key, Walker said.

The first question Walker and his colleagues asked was whether the fruit fly version of PGC-1 has the same function as the mammalian version. They found it does.

The biologist increased levels of expression of the fly version of the PGC-1 gene and found that this made mitochondria more active. They then tested whether boosting PGC-1 activity would slow aging and, again, they found that it did, when they focused on the fly's digestive tract.

The fly's intestine is maintained by adult stem cells, previous research has shown. The biologists also asked what would happen if they used genetic and molecular tools to boost PGC-1 gene expression within only the stem cells and their immediate "daughter" cells.

"Collaborating with a stem cell group at the Salk Institute for Biological Studies, we boosted the gene expression within just the stem- and the immediate daughter-cell types and found that was sufficient to extend the life span of the flies," said Walker, who studies the basic underlying mechanisms of the aging process.

In addition, increasing the fruit fly's version of PGC-1 delays the onset of cellular changes within the intestine, thereby establishing a link between mitochondria, tissue stem cells and aging, the new study shows.

"Many scientists study the diseases of aging, and they tend to do so individually," Walker said. "One group will study Alzheimer's disease, another group will study cardiovascular disease, another will study cancer. We take a different approach. We don't single out any of these specific diseases of old age. We study the aging process itself. Aging is the No. 1 risk factor for most cancers, heart disease, Alzheimer's disease, Parkinson's disease and many others."

Co-authors on the study included Michael Rera, a UCLA postdoctoral scholar in Walker's laboratory; Sepehr Bahadorani, a former postdoctoral scholar in Walker's laboratory; and Jaehyoung Cho, a former postdoctoral scholar in Walker's laboratory.

Walker's research was funded by the National Institutes of Health and the Ellison Medical Foundation. Walker is an Ellison Medical Foundation New Scholar in Aging.

“Biochemistry: Scientists Decode the Protective Element Sickle Cell Anemia Offers Against Malaria” NYTimes November 14, 2011 Donald G. McNeil Jr.

A recent study has discovered why the sickle cell trait protects against malaria.

[To clarify, the sickle cell trait is present when an individual has inherited the sickle cell trait from only one parent. These people do not have sickle cell anemia, which is a painful disease, itself. When a person inherits the trait from both parents, they have the sickle cell anemia disease. ]

The study has shown that when malaria parasites invade sickle blood cells, they cannot inflict as much damage as they do when they attack normal red blood cells. When malaria infects a normal person’s blood cells, the parasites twist a protein “actin” from the blood cell’s membrane into a type of scaffolding that lets them cling to the cell and inject its own sticky proteins into the cell. Then, these infected blood cells cling to the walls of capillaries, the brain, and other organs keeping the infection in the body. These cells are stuck and cannot travel back to the spleen, which would clean up the infection.

However, blood cells with the sickle cell trait are resistant to “actin mining” which means the malaria infection cannot cling to the cells and the spleen can kill the malaria, protecting the infected individual from death.

Tuesday, November 15, 2011

Oldest American Primates Lived in Trees?

There is new evidence to suggest that the earliest North American human descendants lived not on land, but in the trees. Researchers at Johns Hopkins uncovered toe and ankle bone fossils which belonged to the oldest true American primate, and these bones reveal that our predecessors likely spent most of their lives in trees.

This proposition is in keeping with the fact that other primates like lemurs and hanging monkeys tend to tree-dwell. The early primates whose bones were found likely date to over 56 million years ago (the Epocene Epoch) and these bones were found by the Hopkins research team in the Bighorn Basin of Wyoming-- where hundreds of other early Eocene mammal fossils have been found.

The fossil toes found possess not claws but nails, which indicates that they are mophologically similar to living primates and the oldest existing evidence of primitive primates who possessed this modern trait. The ankle bones were also indicative of more modern prosimian morphology, specifically primates which jump frequently. Thus, the specimen at hand was clearly a small, nimble tree-dweller similar to the modern-day bush baby. These findings offer evidence of some surprising primate origins which will allow scientists to continue filling out the North American primate taxonomies and phylogeny charts as we search for the true origins of modern man.

Short Legs, Big Benefit

Just weeks ago, the American Journal of Physical Anthropology published an article which suggests that Neanderthals benefitted from significantly shorter legs than modern humans. These short legs were a necessary adaptation to the harsh, wintry climates of the Pleistocene.

Although their shorter legs slowed their movement, according to Johns Hopkins researcher and graduate student Ryan Higgins, Neanderthals were able to move quite efficiently over rocky terrain

"Studies looking at limb length have always concluded that a shorter limb, including in Neanderthals, leads to less efficiency of movement, because they had to take more steps to go a given distance. But the other studies only looked at flat land," said lead researcher Ryan Higgins, a graduate student in the Johns Hopkins Center of Functional Anatomy and Evolution. "Our study suggests that the Neanderthals' steps were not less efficient than modern humans in the sloped, mountainous environment where they lived."
Mirroring a tendency for animals from cold climates to be smaller and more compact, Neanderthals likely evolved to have these short legs so that they lost less body heat and maintained a lower center of gravity in mountainous areas of Europe and Western Asia. Their legs also helped them when moving up hills and traveling large distances. Correspondingly, humans probably adapted to warmer climates and less distance-traveling with their longer, leaner legs.

Gene Doubling Could Lead to Bigger Brains

A study by Megan Dennis of the University of Washington in Seattle suggests that a change during human evolution could have led to bigger brains. At least twice in the past 3 million years, a gene called SRGAP2 has been duplicated within the human genome. Dennis’ findings show that extra copies of this gene may account for humans’ thicker brain cortex, the area in the brain where thinking takes place. Before, the gene SRGAP2 was identified as one of the 23 genes duplicated in humans but not in other primates. However, Dennis found an ancient form of the gene, located on human chromosome 1, as having been partially duplicated on the same chromosome about 3.4 million years ago, creating a shortened version of the SRGAP2 protein. About 2.4 million years ago, a copy of the partial copy was created and added to the short arm of chromosome 1. Looking at duplicate genes in more than 150 people revealed that the copy made 3.4 million years ago is missing in some people, while the younger version of the gene has become fixed in the human population. Its rapid assimilation might indicate that the gene is key in human evolution. Researchers have found that the shortened version of the SRGAP2 protein interferes with brain cells’ ability to make projections called filopodia, which the cells use to move around. The less the number of projections, the more the cell is streamlined to mitigate futher in the brain, perhaps to the point of allowing humans to build extra cortex layers.

The OXTR Gene and Human Behavior

OXTR has a remarkable effect on the way we interact with and relate to our fellow man. This oxytocin receptor gene codes for a protein which acts as a receptor for oxytocin, a hormone and neurotransmitter. The OXTR gene may govern behavioral modulation and induce emotions almost immediately detectable by humans. On human chromosomes at the 3p25 location, the OXTR gene encodes these proteins.

So why are OXTR genes so special?

There are two types of OXTR, the A and G, which designate how the OXTR affects our social behavior. With two G-type OXTR genes, a human tends to exude more empathy and sensitive behavior. Those with one or more A-copies are less likely to exhibit these empathic or sociable tendencies. Aleksandr Kogan's study at the University of Toronto has found that the difference between these two types of OXTR genes is what constitutes the difference between two very different dispositions among people-- which strangers can sense within just minutes of meeting or watching an individual.
It's fascinating to consider that our behavior is so closely determined by our genome. Kogan's work filming individuals talking to a partner about suffering has revealed that, when volunteers watch the footage on mute for just 20 seconds, those volunteers responded almost precisely according to whether they had A or G-type OXTR genes. G-owners tended to respond more empathically, while A-owners, as expected, did not respond as emotionally. 

In addition, independent viewers of the clips with two G-copies responded to the footage with a more physical empathy: eye contact, open arms, nodding heads, etc. As a result, these viewers may be perceived as more trustworthy, social, or emotionally in-touch than others. This shows that people are incredibly sensitive to behavior as a social cue. A tiny genetic difference actually manifests in human behavior, even for mere seconds, as a huge effect on personality and sociability.

Kogan worked with a strikingly small sample size, which is why his paper has been largely criticized by other scientific scholars. However, it provides an exciting window onto the genetic underpinnings of human behavior.

Study Shows that Leopard-Print Horses Existed

A new DNA analysis prompted by paintings of polka-dotted horses on the walls of a cave in Peche-Merle, France suggests that leopard print horses didn’t exist just in art. A new study by Arne Ludwig of the Leibniz Institute for Zoo and Wildlife Research in Berlin observed DNA taken from the remains of 31 horses found in Europe and Siberia showed that prehistoric horses sported spots. Of the 31 horses studied, 18 were bay, seven were black and six carried genetic variants that produced a leopard-spotting pattern. Previous studies had suggested that horses were either bay or black before domestication, and more complex patterns emerged as humans started to impose breeding selection. When looking at paintings of spotted horses in Peche-Merle, France, art historians speculated that spotted horses may have had religious or cultural significance. However, last week’s findings suggest that the cave painters were in fact painting it like it was.

The Evolution of Primate Social Behavior

A new study of over 200 species suggests that individualistic primate groups may have evolved into complex societies in two major steps. A study by Susanne Shultz of the university of Oxford reported that about 52 million years ago, primates might have stopped foraging alone and banded together to form large, same-sex groups to search for food. Then, 16 million years ago, primates began forming more stable social groups, such as male-female pairs and groups of females led by one male. This urge to team up could’ve happened during the transition from a nocturnal life to a life in the sunshine. Primates needed a new defense strategy to deal with more predators and hunters during the day, and by joining up they could serve as lookouts for each other. Shultz’s study examined the social behavior of 217 species of primates such as baboons, gibbons and tamarins, and combined that data with information about the primates’ evolutionary tree, going on to predict about the likely transitions the creatures underwent to form these cooperative social systems. Further research would have to test transition theories in other mammals to solidify the conclusions drawn from this study.

Monday, November 14, 2011

In Defense of Darwin: The Berlusconi Government (Specifically, 2001-2005)

During Berlusconi’s political reign as Prime Minister of Italy, international media focused on airing his “dirty laundry”: rape allegations, sex parties with underage girls, mafia connections and racist slurs. After Silvio Berlusconi’s reluctant resignation on Saturday, I thought it would be fitting to write about a change his government tried to implement in the Italian educational curriculum from 2001-2005. The fact that during these years the Berlusconi government attempted a revisionist history of Darwin’s life, complete with obliteration of all evolutionist teachings, in favor of Roman Catholic ideological education, has rarely been an international “hot topic” in conversation.

{To clarify: I spent the past spring abroad in Ferrara, Italy. I enrolled directly at the local university and all my classes were in Italian, with local Italian students. For one of my courses “Man, Evolution, Environment” I read In difesa di Darwin (In Defense of Darwin), an essay turned into a small book, written by Professor Telmo Pievani who teaches at the University of Milan. If I had not taken this course, I would not have known about antievolutionist curriculums in Italy.}

In his synopsis of public education during these years Pievani criticizes the failed attempt of the Berlusconi government to remove evolution from the curriculum of middle schools and their attempt to cast doubt onto the legitimacy of Darwinian evolution. Italy remains largely Roman Catholic (think Vatican, Pope, etc.), a religion that teaches creationism. Pievani describes a covert operation of sorts, in which church leaders and the Pope conspired to eradicate evolution and to portray Darwin as a lunatic scientist, with unfounded scientific hypotheses. Pievani also insists that the government fired teachers who taught curriculums that incorporated evolution in order to replace them with religiously trained officials who were trained to teach creationism. The Berlusconi government was able to overthrow the system, but all changes made were short lived. Many school officials defended their curriculums and evolution was eventually reinstated into curriculums.

Pievani’s short essay served as a reminder to me that it is easy to forget the controversy that continues to envelop evolution; the manner in which evolution is taught remains a global topic chock-full of debate. Even in the “melting pot” of the world, the United States, contention exists. A good example is the state of Texas: In 2009 the New York Times published an article that highlights the current debate in Texas schools over how evolution should be taught and who has the right to publish, then distribute what content in regard to textbooks that contain correct information about evolution and Darwin. To conclude, some bigger questions are 1. when evolution will be accepted as a scientifically proven process? and 2. how can teachers successfully explain evolution in a sensitive way that will not undermine a child’s religious teachings?

Darwin and Emotion - The Darwin Correspondence Project

This article discusses a lesser-known experiment Darwin performed on emotions and also explains that The Darwin Correspondence Project is working to recreate this experiment to test the results of the original. In short, the experiment asked for many participants reactions to multiple pictures of a man making different facial expressions. Although the study was "somewhat unscientific by modern standards," this was a triumph for Darwin's time. The article below explains in more depth the original experiment, its merits and its purpose as well as the relocated experiment now.

Crowdsourcing Darwin's Experiment on Human Emotions

Gene associated with suicide risk

This article talks about a study identifying a gene associated with higher risks of suicide in depressed patients.

John Mann of the New York State Psychiatric Institute claims that in a sample of depressed patients, those who attempted suicide are more likely to have two copies of a particular allele at the RGS2 gene. This could suggest that the risk of suicide in depressed patients is inheritable, and it could explain why there are clusters of suicide attempts in families such as the Hemingway family (pictured).

Genes Linked to Multiple Diseases

New research at Edinburgh University has led researchers to believe that single genes can be linked to more than one disease.  For example, genes responsible for Crohn's disease are also linked to other conditions like breast cancer, high cholesterol and obesity (to name a few).  In addition, cancer and heart conditions can be linked to a common gene just as fetal haemoglobin and a risk of malaria are also linked.  A possible benefit of this study is the ability to avoid side-effects in developing medications.  In addition, the article stresses that single gene linkages to multiple diseases is more common than most people think.

Humans May Have Mated with Third Hominid Species Denisovans

This article explains how humans may have mated with Denisovans, a third hominid group that appears to have lived amongst modern humans and Neanderthals about 30,000-50,000 years ago. Denisovans, which are still a mystery to scientists, were discovered in 2008 when a group of scientists, led by Johannes Krause of Tubingen University in Germany, found fossils in Denisova Cave in the Altai Mountains in Siberia, the tip of child's finger bone and a adult's tooth, and analyzed their DNA. The DNA from the fossils did not match that of humans or Neanderthals, hence the discovery of a third hominid species. Further studies reveal that Denisovan DNA accounts for 5 percent of DNA in the inhabitants of Melanesia, a group of islands north of Australia including Papua New Guinea and Vanuatu. This past week, scientists Pontus Skoglunda and Mattias Jakobsson of Uppsala University discovered that Denisovan DNA accounts for 1 percent of DNA in Southeast Asians. This new discovery shows how widespread the mating between humans and Denisovans may have been.

Thin-slicing study of the oxytocin receptor (OXTR) gene and the evaluation and expression of the prosocial disposition

The neuropeptide oxytocin has been linked to emotional expression and trust in interpersonal relationships, especially in mother-child bonding. Now the rs53576 SNP on the oxytocin receptor gene (OXTR) has been identified as a factor in prosocial behavior (empathy or acting in a way that benefits another). This SNP is located in an intron, possibly suggesting the activity of a genetic switch able to repress or promote oxytocin sensitivity. Although this study displayed a strong correlation of those homozygous GG for rs53576 and prosocial behavior, and a correlation with reduced prosocial behavior for those with the A allele, the exact molecular effects of the allele are unknown.

The study showed a group of observers 23 video clips, each 20 seconds long (a thin slicing behavioral analysis), of a romantic couple. One member of the couple told their partner about a time of suffering in their lives. Without hearing the sound, observers rated the other partner on several metrics according to non verbal intuitive cues, including kindness and trustworthiness.

Out of the 10 rated most prosocial, 6 were GG. Out of the 10 rated least prosocial, 9 carried the A allele. Results indicate that friendship networks could form along genetic lines, ultimately leading to assortative mating. It gives another example of how we can detect genetic makeup in others even during a brief interaction.

Despite these results, in order to control the variable of culture, all targets studied were caucasian. In addition, the low number of test couples limits the decisiveness of the study. Two major questions were raised in the study. 1) What is the relationship between this SNP, other OXTR SNPs, and cultural environment. 2) How does this SNP functionally influence brain conditions to create behavioral differences?
At Neuroscience 2011, an annual meeting meeting of the Society for Neuroscience , new data was presented concerning the study of epigenetics. Epigenetics is the study of how traits acquired through environmental influences can be passed on from generation to generation; therefore it studies the passage of non-DNA information from generation to generation. The new findings exhibit that brain plasticity may be partially controlled by a protein, consumption alcohol and amphetamines by a mother can result in developmental defects in offspring (due to abnormal number of chromosomes in the brain), brain changes due to cocaine may be inheritable making the offspring more resistant to certain effects of the drug, motherhood deters some effects of stress, it is possible that certain behaviors (such as anxiety and depression) can are inheritable.

Sunday, November 13, 2011

Could cannibalism be good for evolution?

‘A Toad-Eat-Toad World,’ and Other Tales of Animal Cannibals

I just found this article and I think it brings up a really interesting concept about cannibalism. While cannibalism was previously viewed as "accidental or pathological," scientists now have reason to believe otherwise.  Cannibalism is also much more common than previously thought.

Brain Development in the Prefrontal Cortex: Humans vs. Chimpanzees

In the August 2011 edition of the journal Current Biology, the article “Differential Prefontal White Matter Development in Chimpanzees and Humans” describes a study conducted by Japanese researchers that found an increase in brain volume of human babies much more rapidly, early on than in chimpanzee babies; despite that both animals begin life with undeveloped forebrains.

Zoologist Tetsuro Matsuzawa led the study, which was conducted at the Kyoto University in Japan. The team used magnetic resonance imaging technology to scan the brains of three young chimps, starting when the chimps were 6 months old. These scans were then compared with M.R.I. scans taken of human infants and young children. Compiled data shows that the white matter in the prefrontal cortex develops much more rapidly in humans.

The prefrontal cortex is a region of the brain that plays an important role in self-awareness, creative thinking, and decision-making. Growth in the prefrontal cortex is part of what makes humans cognitively advanced. Rapid development of the prefontal cortex in humans could contribute to superior skills in social interaction and communication.

The study also indicates that brain development is shaped by life experience—a potential reason why some human babies and chimp babies share similarities, such as the impulse to smile at caregivers.

Matsuzawa and his team will continue to study brain differences between humans and chimpanzees in young adulthood by tracking the development of the same three chimpanzees observed in the study, which are now 11 years old.