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Cristian Mihon



According to several precedent studies, in the United States, there is a higher need for treatment against marijuana abuse, rather than treatment for heroin or cocaine abuse. However, until now, no viable drugs against marijuana abuse were discovered. Professor Robert Schwarcz, from the School of Medicine, at the University of Maryland, along with his research team, has discovered a new synthetic drug that decreases the effects of the main active ingredient in marijuana. The results of the paper were published earlier this week in the journal Nature Neuroscience.

The main psychoactive ingredient of marijuana is known as THC (tetrahydrocannabinol). It is responsible for producing the feeling of high and pleasure due to the fact that it increases the levels of dopamine inside the VTA (ventral tegmental area) and inside the nucleus accumbens. The VTA is an area located in the mesencephalon. The origins of all the dopaminergic neurons found in the mesocorticolimbic dopamine system are found within the VTA. The nucleus accumbens is found in the basal forebrain of each brain hemisphere. Precedent studies have linked the nucleus accumbens to emotional intelligence of pleasure, and the placebo effect.

The research team suggests that if individuals abusing marijuana would take a drug that is able to reduce dopamine activity in these regions of the brain, the euphoria effect of marijuana would be diminished, or even abolished. The synthetic drug tested by researchers is named Ro 61-8048. Its effect increases the levels of KYNA (kynurenic acid). The increased level of KYNA in both the VTA and nucleus accumbens is responsible for reducing the THC stimulation. The research team suggests that their results show that KYNA is able to block the dopamine receptors, thus reducing the euphoric effects of marijuana.

Laboratory tests were done on rats. Instead of THC, the researchers used a synthetic compound known as WIN 55,212-2, which has effects close to those of THC. The laboratory rats were taught how to press a lever and receive the synthetic compound. As a sign of addiction, the rats pressed the lever for WIN 55,212-2 rather often. However, after the new Ro 61-8048 drug was administered to a group of rats, the rats stopped pushing the lever as often as before. Researchers also tested if the new drug is able to prevent a relapse. Further results were also obtained by using the same drug on squirrel monkeys that were taking THC.

Professor Schwarcz and his research team, consisting of his colleagues and a group of researchers from the National Institute on Drug Abuse, concluded that further research is necessary before the FDA will approve the new drug for human use. Other studies have shown that higher levels of KYNA can cause cognitive damage, thus the new drug could prove to have more side effects than beneficial effects.

However, the individuals who support the legalization of marijuana use will advocate for the fact that marijuana addiction doesn’t necessarily need treatment.


According to a new study conducted by a research team led by professor Susan Hughes, from the Albright College, in the United States, both men and women experience alterations in their voices when speaking to their lovers, in comparison to speaking to their friends and family. Hughes suggests that these voice variations might be used in the future to detect infidelity in couples.

Hughes, who is an associate professor and an expert in evolutionary psychology, reports that the changes of our voice can be easily perceived by others as well, if they pay close attention. Her findings were published in an article from the Journal of Nonverbal Behavior, at the start of the month. The research team, comprised of Hughes, Jack LaFayette and Sally Farley, shows how and individual’s voice alters when speaking over the phone with either their close, same-sex friends, or their romantic partners. In order to conduct their study, researchers invited a total number of 24 participants. Each participant was considered to be “newly in love”, as they were all recruited during their honeymoon period. All 24 participants were asked to call their romantic partner, and their closest same-sex friend. The conversations were short and very specific, including lines such as “What are you doing?” and “How are you?”.

For the second part of the study, the research team played the recording of the 24 participants to 80 independent individuals who were asked to judge the phone conversations based on 3 criteria. The criteria were romantic interest, sexiness, and pleasantness. Despite the fact that some of the judges were only exposed to the conversations for less than 2 seconds, while other judges only heard one end of the conversation, the majority were able to accurately identify if the person to whom the caller was speaking to was their romantic partner or their friend.

The results of the study suggest that the vocal samples that were directed towards each participants’ romantic partner sounded sexier and more pleasant, while also reflecting a higher romantic interest. Furthermore, the research team used a spectrogram analysis on the voice samples. The results of the spectrogram analysis show that both men and women are more likely to mimic, or even match, their romantic partner’s voice pitch. Men are more likely to use a higher pitch while speaking to their romantic partners, while women are more likely to use a lower pitch in the same situation. The research team suggests that these results show that both romantic partners are trying to communicate both affection and relational connection in a more intimate way.

However, researchers were startled by the fact that the paralanguage analysis test showed that the voices of the participants showed stress, lack of confidence and nervousness, when speaking on the phone with their romantic partners. The paralanguage analysis is done by taking out-of-context bits of the voice samples while also maintaining intonation and inflection.

Hughes concludes that the subjects, who were newly in love, were perhaps experiencing the fear of rejection.


Whitehead Institute researchers have redefined the function of a gene whose mutation causes Rett syndrome, a neuro developmental autism spectrum disorder. This new research offers an improved understanding of the defects found in the neurons of Rett syndrome patients and could lead to novel therapies for the disease.

“The action of the MECP2  is just the opposite of how it was held for the past 15 years,” says Whitehead Founding Member Rudolf Jaenisch, who is also a professor of biology at MIT. “It was thought that this protein globally repressed the expression of methylated DNA. What this work shows is when you do the analysis in a way that takes cell size into account”cell size is very different in Rett  compared to wild type”then suddenly we can see that the protein acts like a global activator. We’ve defined the function of MECP2 in a totally different way.”

Rett syndrome is an X-linked genetic disease affecting one in 10,000 newborn girls. Infants with the disease appear to develop normally for their first six to 18 months, at which point their movement and language skills begin to deteriorate. Loss of speech, reduced head size, breathing and heart rhythm irregularities, and autistic-like symptoms are common by age four. Some symptoms may be treated with prescription drugs, but no cure or disease-modifying therapy exists. Previous work by the Jaenisch lab has provided some hope for the families of Rett patients. In a mouse model lacking the MECP2 gene, which is mutated in approximately 95% of girls with Rett syndrome, mice injected with the protein IGF-1 had more regular breathing and heart rhythms than did untreated mice. In addition, the brains of treated mice had greater mass and more of the vital neuronal projections that are missing in Rett syndrome mice and human patients.

In the current research, Yun Li, a postdoctoral researcher in the Jaenisch lab, analyzed the global gene expression of MECP2-deficient neurons derived from human embryonic stem cells. Unlike earlier research, Li took into account the Rett neurons’ smaller size when comparing their  to neurons with intact MECP2. The Rett neurons had decreased mRNA transcription, reduced , and severe defects in the AKT/mTOR signaling pathway, which is activated by IGF-1. Li’s work is published in the October 2nd issue of Cell Stem Cell.

“We have always found it strange that MECP2 mutant mice, which share many of the severe neurological problems as really sick kids with Rett syndrome, have very few transcriptional changes detectable on a microarray. That doesn’t seem to support a global repressor role for the MECP2 protein. There had to be something wrong,” says Li. “Now we have a much better understanding of the function of MECP2, and the severity of the disease on a cellular level. Knowing that human Rett neurons are impaired in both global transcription and translation is important for us to design therapeutic strategies for Rett. Growth factors such as BDNF and IGF-1 are known to activate the AKT/mTOR pathway and increase protein synthesis. Down the road, we are interested in further exploring the Akt/mTOR pathway, and investigate how activation of this pathway could reverse the disease.”


A new brain imaging study may help explain why people with insomnia often complain that they struggle to concentrate during the day even when objective evidence of a cognitive problem is lacking.

“We found that insomnia subjects did not properly turn on brain regions critical to a working memory task and did not turn off ‘mind-wandering’ brain regions irrelevant to the task,” said lead author Sean P.A. Drummond, PhD, associate professor in the department of psychiatry at the University of California, San Diego, and the VA San Diego Healthcare System, and Secretary/Treasurer of the Sleep Research Society. “Based on these results, it is not surprising that someone with insomnia would feel like they are working harder to do the same job as a healthy sleeper.”

The research team led by Drummond and co-principal investigator Matthew Walker, PhD, studied 25 people with primary insomnia and 25 good sleepers. Participants had an average age of 32 years. The study subjects underwent a functional  scan while performing a working memory task.

Results published in the September issue of the journal Sleep show that participants with insomnia did not differ from good sleepers in objective cognitive performance on the working memory task. However, the MRI scans revealed that people with insomnia could not modulate activity in brain regions typically used to perform the task.

As the task got harder, good sleepers used more resources within the working memory network of the brain, especially the . Insomnia subjects, however, were unable to recruit more resources in these brain regions. Furthermore, as the task got harder, participants with insomnia did not dial down the “default mode” regions of the brain that are normally only active when our minds are wandering.

“The data help us understand that people with insomnia not only have trouble sleeping at night, but their brains are not functioning as efficiently during the day,” said Drummond. “Some aspects of insomnia are as much of a daytime problem as a nighttime problem. These daytime problems are associated with organic, measurable abnormalities of brain activity, giving us a biological marker for treatment success.”

According to the authors, the study is the largest to examine cerebral activation with functional MRI during cognitive performance in people with primary insomnia, relative to well-matched good sleepers. It also is the first to characterize functional MRI differences in  in people with primary insomnia.

The American Academy of Sleep Medicine reports that about 10 to 15 percent of adults have an insomnia disorder with distress or daytime impairment. Most often insomnia is a comorbid disorder occurring with another problem such as depression or chronic pain, or caused by a medication or substance. Fewer people suffering from insomnia are considered to have primary insomnia, which is defined as a difficulty falling asleep or maintaining sleep in the absence of a coexisting condition.


A recent study conducted in the United States reveals that the number of young adults smoking mentholated cigarettes has increased in the past few years. These results indicate that the efforts to reduce the smoking habits of young adults are countered by the marketing and selling of mentholated cigarettes, including several newly established youth cigarette brands. The results of the study were published earlier in the international journal Tobacco Control.

Smoking is considered to be on the main causes of preventable death worldwide. In the United States alone, almost 500,000 deaths per year are related to smoking or smoking-related disorders. According to various studies, male patients lose an average of 13 years of their lives due to smoking, while female patients lose an average of 14 years of their lives.

According to professor Gary Giovino, from the Buffalo Department of Community Health and Health Behaviors, in the state of New York, the findings of the study show that most young adults are heavy consumers of cigarettes, especially mentholated cigarettes. Even though the numbers of non-menthol smokers have decreased, the number of mentholated cigarettes smokers has either increased or has remained constant.

Professor Giovino is one of the leading surveillance researchers for tobacco usage. His study included data taken from approximately 400,000 individuals, over the course of 6 years, between 2004 and 2010. Of the approximately 400,000 subjects, more than 85,000 were smokers. All subjects were over the age of 12, and all of them took part in the National Surveys on Drug Use and Health. Some of the results of the study show that mentholated cigarettes are more frequently smoked by teenagers (between the ages of 12 and 17), and young adults (between the ages of 18 and 25). Approximately 56% of teenagers admittedly smoke mentholated cigarettes, while only 45% of young adults reported smoking mentholated cigarettes. The results also show that only 30% of subjects older than 25 smoke menthol cigarettes.

The results of the study also show that the majority of mentholated cigarettes smokers were young, non-white, and female. Furthermore, among all adolescents and young adults, the percentage of non-menthol smokers has decreased from 2004, however menthol smoker numbers have either remained constant or have increased. Professor Giovino says that the results of his study should show the FDA that banning the mentholated cigarettes could have a beneficial impact on the general public health.

Giovino says that the FDA is already considering a ban on the mentholated cigarettes. He believes that his study provides important information on the smoking habits and menthol use. One major alarm signal that Giovino considers, is that most menthol smokers are young females of non-white ethnicity. He concludes that the results of the study show that mentholated cigarettes are a ‘starter pack’ for children, mostly due to the fact that menthol makes it easier for beginners to inhale. In other words, according to Giovino, menthol sweetens the poison, making it easier to inhale and smoke.


An odd and little-known feature of nerve cells may be linked to several forms of inherited intellectual disability, researchers at Washington University School of Medicine in St. Louis have learned.

The scientists report that a genetic mutation that causes intellectual disability also blocks formation of the neuronal primary , a hair-like structure that protrudes from the bodies of nerve cells.

“The primary cilium acts as a kind of antenna for nerve cells,” said first author Yoshiho Ikeuchi, PhD, a staff scientist. “It’s covered in receptors that monitor environmental conditions outside the cell and may influence the cell’s functions.”

Learning more about how the mutation sabotages production of the nerve cell cilium eventually will help scientists develop drugs to treat intellectual disability, according to senior author Azad Bonni, MD, PhD, the Edison Professor and chairman of the Department of Anatomy and Neurobiology.

“Intellectual disability”sometimes known as mental retardation”affects 1 to 2 percent of the general population, and researchers have identified more than 100 genes on the X chromosome that can cause these conditions,” Bonni said. “But we don’t know what most of these genes do, and that information is essential for new treatments.”

The research appears online Aug. 29 in Cell Reports.

Nearly every cell in the mammalian body has a primary cilium”a structure that acts as an environmental sensor. Some cells have many cilia that move together in waves. Problems with cilia are associated with disorders throughout the body, including illnesses of the kidneys, eyes and reproductive organs.

“Some of the X-linked intellectual disorders are syndromes that not only hamper  but also cause problems elsewhere in the body,” Bonni said. “That makes sense in the context of this new connection we’ve identified between intellectual disability and the primary cilium.”

Scientists only recently have recognized the potential of a primary cilium malfunction to impair nerve cell development and function. Studies have suggested that the primary cilium may be where nerve cells receive the growth signals that allow them to extend branches to each other and form circuits. Other research has shown that blocking of signal receptors on the primary cilium leads to memory problems in mice.

Bonni’s path to the primary cilium led through the nucleus, the command center that contains a cell’s DNA. Proteins found inside a cell’s nucleus often regulate the turning on or off of other genes, making them influential in orchestrating the responses and functions of cells.

Bonni and his colleagues scanned the literature on X chromosome genes linked to intellectual disability to learn which genes produce proteins found in the nucleus. When they disabled 15 such genes in individual nerve cells, they found that the loss of the gene for polyglutamine-binding protein 1 (PQBP1) produced the most dramatic effect, leaving nerve cells with shortened primary cilia or no cilia at all.

In other cell types outside the brain, PQBP1 is typically found only in the nucleus. But the new results show that in neurons the protein is present both in the nucleus and, surprisingly, at the base of the primary cilium.

The scientists learned PQBP1 binds to another protein outside the nucleus that suppresses growth of the primary cilium. By binding to the suppressor, PQBP1 gets that suppressor out of the way, allowing cilium formation to proceed normally.

Scientists may one day try to imitate this effect with drugs, potentially allowing the brain to develop more normally when PQBP1 is mutated. For now, the researchers want to learn more about the suppressor protein and also are investigating the possibility that PQBP1 may continue to influence the functions of the primary cilium after it is formed.


A team of researchers from UC Davis, UC San Diego and other institutions has identified a key mechanism behind aggressive prostate cancer. Published on August 14, 2013 in Nature, the study shows that two long non-coding RNAs (PRNCR1 and PCGEM1) activate androgen receptors, circumventing androgen-deprivation therapy. In their active state, these receptors turn on genes that spur growth and metastasis, making these cancers highly treatment-resistant. The study illustrates how prostate cancer can thrive, even when deprived of hormones, and provides tempting targets for new therapies.

“Androgen-deprivation therapy will often put cancer in remission, but tumors come back, even without testosterone,” said contributor Christopher Evans, professor and chair of the Department of Urology at the UC Davis School of Medicine. “We found that these long non-coding RNAs were activating the androgen receptor. When we knocked them out, cancer growth decreased in both cell lines and tumors in animals.”

Evans’ UC Davis group was part of a larger team, led by Michael Geoff Rosenfeld, professor at the Howard Hughes Medical Institute in the School of Medicine at UC San Diego, which has been eager to determine how androgen-dependent cancers become androgen-independent (also called castration-resistant). These prostate cancers are very aggressive and usually fatal, but their continued growth, despite being deprived of hormones, is just now being better understood. It’s not unlike removing the key from a car ignition, only to have the vehicle re-start on its own.

In this case, the aberrant starting mechanisms are long non-coding RNAs, a class of genetic material that regulates  but does not code for proteins. Using patient samples from UC Davis, the group determined that both PRNCR1 and PCGEM1 are highly expressed in . These RNAs bind to androgen receptors and activate them in the absence of testosterone, turning on as many as 617 genes.

Further investigation determined that one of these long non-coding RNAs is turning on androgen receptors by an alternate switching mechanism, like a car with a second ignition. This is critically important because many prostate cancer treatments work by blocking a part of the androgen receptor called the C-terminus. However, PCGEM1 activates another part of the receptor, called the N-terminus, which also turns on genes”with bad results.

“The androgen receptor is unique, if you knock out the C-terminus, that remaining part still has the ability to transcribe genes,” said Evans.

In addition, about 25 percent of these cancers have a mutated version of the androgen receptor that has no C-terminus. These receptors are locked in the “on” position, activating genes associated with tumor aggression.

Regardless of the receptor’s status, PRNCR1 and PCGEM1 are crucial to prostate cancer growth. In turn, knocking out these RNAs has a profound impact on gene expression, both in cell lines and animal models. The team used complementary , called antisense, to knock out the RNAs and observe how the tumors and cells responded. In each case, there was a direct relationship between RNA activity, gene expression and cancer growth.

“These long non-coding RNAs are a required component for these castration-resistant cancers to keep growing,” said Evans. “Now we have preclinical proof of principle that if we knock them out, we decrease .”

The research team’s next step is developing treatments that specifically target these long non-coding RNAs. That process has already begun.

“Most treatments for castration-resistant prostate cancer will get us around two to three years of survival,” said Evans. “We rarely cure these patients. The tumor will continue to evolve resistance mechanisms. But now that we have additional insight into what’s activating these receptors, we can begin developing new types of therapies to prevent it.”


Researchers from Case Western Reserve University School of Dental Medicine have discovered how a common oral bacterium can contribute to colorectal cancer, a finding that opens promising new research avenues for the development of approaches to prevent and treat the disease.

“We found this  is linked to an infection from [the ],” said Yiping Han, professor of periodontics at the dental school and the study’s lead investigator. “This discovery creates the potential for new  and therapies to treat and prevent the cancer.”

The results of the research appear in the current issue of Cell Host & Microbe, in conjunction with a second study from a different research group that highlights how the bacteria can speed the accumulation of cancerous cells.

The researchers also learned how to prevent the microorganism, called Fusobacterium nucleatum (Fn), from attaching to colon cells and potentially triggering a cascade of changes that can lead to cancer.

The latest findings advance research from 2011, in which Han and her team identified an adhesive molecule on Fn’s surface, called FadA, which can attach to VE-cadherin, a cell receptor from the cadherin group on blood vessels.

As Han completed the work on FadA and VE-cadherin, researchers from Harvard University and the University of British Columbia discovered the presence of Fn was higher in malignant tumors compared to the surrounding tissue.

Han said she immediately suspected Fn interacted with cells in the colon similarly to those in blood vessels and shifted her lab’s work to focus on colorectal cancer.

“This was one of those serendipitous scientific moments in making this discovery,” Han said.

Because her lab was able to track Fn’s ability to attach to the VE-cadherin receptor on blood vessels, Han said it didn’t take long before her team found how FadA attached to the E-cadherin receptor on cells in the colon.

Subsequently, FadA’s attachment to E-cadherin set in motion a protein called ß-catenin, which, among its many functions, produces two important actions in the cancer process: an inflammatory response that alters the immune system, and another that spurs cancer cell growth.

Han’s lab designed a novel synthetic peptide that prevents FadA from attaching to E-cadherin and inciting actions that lead to cancer development.

They also found that the FadA gene levels are 10 to 100 times higher than normal in precancerous and malignant colon polyps.

Thus, Han said, “FadA can be used as a diagnostic marker for early detection of colon cancer. It can also be used to determine if treatment works effectively at reducing Fn load in the colon and the mouth.”

A patent application has been filed on work associated with this research.

At the same time, Han emphasized that the results highlight the importance of oral health. Fn is an opportunistic bacterium that increases dramatically in gum disease.


According to the results of a new study conducted by a research team from the University of Colorado Boulder, in the United States, subjects who spent one week camping in the Rocky Mountains, exposed exclusively to natural light, managed to reset and sync their circadian clocks to the sunrise and sunset. The study was recently published in the journal Current Biology. The research team investigated a number of 8 subjects, who were picked regardless of their sleeping habits during their day-to-day life.

According to the research team, electric light affects our internal circadian clocks. Our circadian clock is the process through which our brain tells our bodies when to prepare for sleep and when to wake up. In order to quantify the effects that electric light has on people, the research team, led by professor Wright, monitored the 8 subjects over a week of their normal day-to-day lives. Each subject received a wrist monitor that measured the intensity of the light to which subjects were exposed, while also recording the amount of time subjects were exposed to light, and at what hours.

At the end of the first week of study, all of the data was recorded and introduced into a database. Researchers further investigated the hormone known as melatonin. Melatonin is a hormone released by the pineal gland that acts as a signal for the circadian clock. The levels of melatonin rise when the biological night begins and decrease when our biological day begins.

The same parameters were once again monitored during a second week of investigations. However, instead of their normal day-to-day lives, the subjects went camping in the Rocky Mountains. During the camping week, all of the 8 subjects were exposed exclusively to natural sunlight and the glow of fire from a campfire. No flashlights or other electronic devices were allowed during the one week period. The results of the study revealed that the average biological night started 2 hours earlier when the subjects were exposed only to natural light. Furthermore, the subjects also woke up earlier than their natural start of the biological day.

Researchers affirm that in the days following the camping trip, the study subjects experienced a more natural circadian rhythm, with the biological nighttime starting at sunset and ending close to sunrise. According to professor Wright, people who live in the modern urban world are very different from each other. Some like to stay up late, others like to wake up early. He reports that the results of the study show that these differences can be decreased dramatically if the circadian clocks are reset.

The study, demonstrating the, also shows possible solutions for individuals with strong effect of natural light for each individual’s circadian clock bad sleeping habits. As an example, the results show that individuals with sleeping habits that involve staying up late at night might also experience difficulties in feeling alert early in the morning. This could be linked to the fact that the melatonin levels indicate that they woke up during their biological night-times, instead of being in their biological day-times.

Wright also suggests that in order to correct their own circadian clock, people should consider more light exposure during mornings and during midday. Furthermore, diminishing the amount of exposure to electric lights at night, such as TV, laptop screens, and other personal devices, can improve the circadian clocks and get them attuned to the solar day.


A research team from the University of Washington, in the United States, has managed to use a technique known as reverse engineering to gather vital information about the disrupted gene network found in patients suffering from schizophrenia. Researchers traced the spontaneous mutations responsible for the brain damage caused by schizophrenia. Their results revealed that patients suffering from schizophrenia may have an improper neurogenesis process from birth, causing the neurons found in the frontal part of he brain to suffer impairments. The study was published at the start of this month in the journal Cell.

Professor Mary-Claire King, a grantee of the NIMH (National Institute of Mental Health), explains that these critical processes can be investigated through the mutations that cause their disruption. Genetic mutations are responsible for the loss of integrity for the whole neurological pathway. She says that the results of their study reveal the mutation of the genes forming a network responsible for the onset of neurogenesis in the prefrontal cortex of the brain, for patients suffering from schizophrenia.

The director of NIMH, Dr Thomas Insel, says that the research team managed to link the genetic mutations to their functional counterparts. This has allowed them to better understand the early development of the brain of patients who will eventually develop signs and symptoms of schizophrenia.

Previous studies have shown that spontaneous mutations are linked to a form of non-familial schizophrenia. These mutations were of genes responsible for the early development process of the brain. However, there was little knowledge about the convergent effects that the genetic mutations had on these pathways. King and her colleagues managed to integrate the genomic data with transcriptome resources available online. For their study, researchers used 105 subjects. They compared the spontaneous mutations that occurred in the genome of the ill subjects with their unaffected siblings.

The results of their investigation revealed that the expression levels of most of the 50 mutated genes had their highest values during fetal development. The expression levels of these genes dropped during childhood. However, in early adulthood, researchers discovered that the expression levels rose again. Their discovery could be linked to the onset of schizophrenia, due to the fact that  most patients experience their early symptoms around the same period of young adulthood.

Subjects with an elderly father had an increased chance of suffering from the aforementioned genetic mutations. However, only the affected siblings had a higher chance to suffer from mutations that were responsible for damaging the functions of proteins. These types of mutations were estimated to cause approximately 20% of all schizophrenia cases.

The research team found out that the networks that are formed by these genes vary in connectivity, based on protein interaction and co-expression. The gene networks found in the study subjects were found to have more connection points, when compared to the gene networks of the subjects’ siblings. Researchers found that the mutated genes of patients suffering from schizophrenia formed a much denser network, with more connection points, unlike the gene networks of their siblings, who weren’t affected by schizophrenia.

The results of the current study are also consistent with previous study results that link the prefrontal cortex to the onset of schizophrenia. The prefrontal cortex is the region of the brain responsible for organizing the information collected from the other regions of the brain. It is responsible for the coordination of functions such as planning, self-regulation, memory, attention span, and thinking. The research team suggests that changes in these functions in early adulthood could mean there is a possibility that schizophrenia might set.

The chief of the Genomics Research Branch from the NIMH, professor Thomas Lehner, concludes that the results of the study are very important, revealing that schizophrenia can’t be completely understood unless there is an investigation on the genetic mutations that cause the neurodevelopment impairment responsible for the onset of the disease.