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Cristian Mihon



Investigators at Johns Hopkins have found a known genetic pathway to be active in many difficult-to-treat pediatric brain tumors called low-grade gliomas, potentially offering a new target for the treatment of these cancers.

In laboratory studies, researchers found that the pathway, called mammalian target of rapamycin (mTOR), was highly active in pediatric low-grade gliomas, and that mTOR activity could be blocked using an experimental drug, leading to decreased growth of these tumors.

“We think mTOR could function as an Achilles heel,” says study co-author Eric Raabe, M.D., Ph.D., an assistant professor of pediatrics, oncology and pathology at the Johns Hopkins Kimmel Cancer Center. “It drives cancer growth, but when mTOR is inhibited, the tumor falls apart.” The work was described Nov. 7 in the journal Neuro-Oncology.

Overall, brain tumors affect more than 4,000 children each year in the U.S., and they are the leading cause of cancer deaths in children, according to Raabe. Low-grade gliomas are the most common group of tumors of the central nervous system in children. Current treatments for these tumors include surgery and chemotherapy, which often cause significant side effects. Many of these tumors are located in areas like the optic pathway, where they can’t be easily removed by surgery without causing damage, including blindness. In addition to vision loss, some of Raabe’s patients have endured paralysis or learning problems as a result of the tumor or treatment. “Even though these tumors are considered ‘low grade’ and not particularly aggressive, many patients suffer severe, life-altering symptoms, so we desperately need better therapies,” says Raabe.

For the study, the Johns Hopkins investigators studied tissue samples from 177 pediatric low-grade gliomas, including the most common type”tumors called pilocytic astrocytomas”from patients treated at Johns Hopkins and other centers. They also tested the effect of blocking mTOR with an investigational agent known as MK8669 (ridaforolimus) in two pediatric low-grade glioma cell lines.

The mTOR pathway has been shown to be active in a variety of cancers, and drugs that block proteins in the pathway, such as rapamycin, are widely available. The pathway signals through two protein complexes, mTORC1 and mTORC2, which lead to increased cell growth and survival.

The researchers found activity of the mTORC1 pathway in 90 percent of low-grade gliomas studied, and 81 percent of tumors showed activity of both mTORC1 and mTORC2. Components of the mTOR pathway were more commonly found in tumors from optic pathways compared with those from other areas of the brain, according to Fausto Rodriguez , M.D., senior study author and assistant professor of pathology and oncology at Johns Hopkins.

The scientists also found that the mTOR-blocking drug caused up to a 73 percent reduction in cell growth over six days in one cell line, and up to a 21 percent decrease in cell growth over four days in a second cell line.

“Since the pathways are more active in some areas of the brain, compared with others, it suggests that the outcomes of drug treatments targeting those pathways may differ as well,” says Rodriguez.

Rodriguez and Raabe say they hope to build on the research in animal models and test additional inhibitors.


Researchers have managed to identify the “invisibility cloak” that allows the HIV virus to take cover inside the cells of the human body, thus evading the immune system and its defensive capabilities. The current study reveals the method through which the virus can be “uncloaked”, allowing the immune system to neutralize it. According to the research team, their findings could be the next stepping stone towards better anti-HIV therapeutic approaches.

The first line of defense against pathogens, also known as the innate immune system, is made of an alarm system that is present on all the cells of an organism. This alarm system can detect the presence of pathogens, such as bacteria, viruses, or parasites. If the alarm is set off, the infected cell has an anti-viral program that sends out a warning signal towards the rest of the surrounding cells. Until now, the ability of the HIV virus to replicate without being detected by the innate immune system has been a puzzle for scientists since the early discovery of the virus, in the late 1950s.

The research team has identified two key molecules inside the human host cells that aid the HIV replication. The effect of these two molecules is to postpone the viral replication of HIV, thus shielding the virus from the innate immune system. When these two molecules are absent from the cell, HIV triggers the activation of the innate immune system. The two molecules can be either blocked through specific medication or by cellular natural depletion – over time. Researchers suggest that instead of targeting the virus, anti-HIV therapies should target the two molecules, thus making the replication of the HIV virus more difficult.

Greg Towers, the lead author of the study, reports that the HIV virus is very capable of eluding the organism’s immune system. This ability makes the virus even more dangerous. However, their novel discovery allows for the future development of anti-HIV drugs that will target these two molecules in order to expose the hidden HIV virus. Towers added that the implication of the new study are huge, however, there’s much more research that needs to be done before new drugs can be released to the general population. Further studies will also be directed towards discovering whether the two new molecules can also be used to protect humans against the transmission of the HIV virus.

For their current study, the researchers used an experimental drug that is based on Cyclosporine. Cyclosporine is a drug that is used in order to prevent organ rejection after transplant surgery due to its ability to diminish the immune system’s response. Precedent studies have already shown that Cyclosporine can be used to block the replication of viruses, including HIV. However, due to its side effects on the immune system, it’s currently not used as a therapeutic method. The research team modified the drug, in order to make it block the effects of the two cell molecules, without the secondary effects caused on the immune system’s activity.


Scientists from the LMU (Ludwig-Maximilians-Universität), from Munich, Germany reveal a new target for cancer therapy. Their study reveals that a protein, known as c-MYC, is responsible for regulating hundreds of different genes. Some of those regulated genes are also involved in cell growth and proliferation. Any genetic changes that cause the perturbation of the protein’s activity will have a major impact of the homeostasis of the tissue, most often leading to cancer. Precedent studies have already shown that in the majority of cancer cases there is a hyperactivation of the c-MYC gene. Moreover, the c-MYC protein plays a key role in metastasis, through the stimulation of EMT (epithelial-mesenchymal transition). Thus, high levels of the c-MYC protein is responsible for inducing the metastasis of tumors.

Professor Heiko Hermeking, one of the main authors of the study, reports that through the use of a colorectal cancer model, the research team has managed to study the interactions of the ZNF281 protein with the c-MYC protein. Due to the fact that there was scarce information about the ZNF281 control mechanisms, Hermeking’s research team focused on investigating the regulatory segment of the ZNF281 gene. Their findings revealed that the ZNF281 gene is actually the hub of a very complex network that is involved in metastasis.

Researchers say that the ZNF281 is responsible for the activation of the SNAIL (also known as SNAI1 or the Drosophila embryonic protein). This creates a positive feedback loop that further increases the expression of the ZNF281 gene. However, at the same time, the ZNF281 gene also interacts with other genes that activate the epithelial-mesenchymal transition. This fact makes the interaction with SNAI1 only be a part of the metastasis process.

The study shows that the ZNF281 expression is normally limited through the action of miR-34a. In turn, the transcription of miRNA-34a is inhibited by SNAI1. Thus, the SNAI1 gene is responsible for increasing the levels of ZNF281. In Hermeking’s precedent studies, he discovered that p53 (a tumor suppressor) is responsible for the onset of the miR-34a transcription. The interaction between p53 and miR-34a is considered to be part of a protective mechanism that stops EMT, thus preventing metastasis.

SNAI1 is responsible for the promotion of metastasis through two different mechanisms. The first mechanism refers to the activation of the mRNA that encodes ZND281, subsequently provoking the second mechanism – the inhibition of the miRNA-34a expression. This type of two-pronged mechanism is also known as feed-forward regulation.

In conclusion, the research team managed to confirm that ZNF281 is directly involved in cancer metastasis by examining its effects on mouse models. Hermeking concluded that the inhibition of the ZNF281 gene is able to prevent metastasis, at least in mouse models. Therefore, it is possible that the inhibition of the ZNF281 gene could lead to the inhibition of the metastasis process in human subjects as well. Hermeking and his team hope that in their future studies they will be able to develop new anti-cancerous therapeutics that could be able to stop metastasis as well.


A research team from the University of Leicester, in the United Kingdom, has managed to map the entire structure of a key component from the human immune system – specifically, the C1 complement component. This is responsible for the neutralization of viruses and bacteria.

The C1 complement complex is actually a protein that is responsible for the detection of foreign molecules in the blood. These molecules, depending on their nature, can cause different diseases. If so, they are called pathogens. If these pathogens are bacteria, fungi, viruses or other types of pathogens, the complement system is activated. The complement system further activates the immune system by activating MAC (membrane attack complex) proteins, responsible for attacking and neutralizing the foreign molecules.

Even though the C1 complement complex was first discovered approximately 50 years ago, the process through which it aids the immune system has been incompletely elucidated until now. The current study began almost 3 years ago, and was founded by the Medical Research Council and the Wellcome Trust. The research team from Leicester worked in close collaboration with researchers from the Warwick Medical School of the University of California, from the United States, and with the Hungarian Academy of Sciences in Budapest, Hungary.

Researchers suggest that their discovery is extremely important and brings important insight towards a better understanding of the human immune system. Furthermore, such a discovery could lead to the development of specific medication that would prevent the complement system from going awry. For example, if a patient suffers from either a heart attack, or a stroke, the complement system begins to target the patient’s own tissue, thus preventing the organism from recovering faster.

The understanding of the structural build of the C1 complement complex will help researchers develop inhibitory drugs in order to stop the complement system from working against its own organism. In their study, the research team revealed the pathway through which the C1 complement complex is formed. There are 3 constituents that form the final product – the C1q (responsible for the actual recognition of the foreign molecules), and C1r & C1s (responsible for the further activation of the complement cascade).

The lead author of the study, Dr Russel Wallis, notes that they have managed, for the first time in history, to determine the whole structure of the C1 complement complex. Furthermore, the study brings new information on the pathway that activates the complement cascade. Wallis further explains that they were able to investigate the whole structure of the complex through a series of overlapping segments. According to the results, the C1 complement complex looks like a bouquet of flowers, with the C1q, C1r, and C1s proteins being linked together.

The study will aid future studies towards a better understanding of the complex pathways used bu the immune system in order to prevent various diseases. Moreover, it’s a possible stepping stone for later studies regarding the development of better drugs against the bad activation of the complement cascade in circumstances such as a heart attack, a stroke, or even an HIV/AIDS infection.


A new paper recently published in the online journal Neuron, reveals that exposure therapy is able to remodel the inhibitory junction found in the amygdala, which is the most important brain region related to fear in humans. Exposure therapy is a technique used to treat anxiety disorders such as specific phobias and PTSD (post-traumatic stress disorder). During exposure therapy, the subject is confronted with a fear or a memory of the traumatic event that led to the anxiety disorder.

The results of the study further improve the understanding of the exposure therapy technique and the processes through which it suppresses fear. The research team is from the School of Medicine, in collaboration with the Sackler School of Graduate Biomedical Sciences, both from Tufts University, in the United States. According to precedent studies, fear is responsible for the activation of a specific group of neurons from the amygdala. Exposure therapy can partially inhibit these neurons, thus subjects experience less fear when given the same situation (to find out on how fear dictates us press here) .

According  to the results of the current study, exposure therapy does not only partially inhibit these neurons, but is also responsible for inducing a remodeling effect of the perisomatic synapses. These specific synapses are known as inhibitory junctions, connecting the inhibiting neurons to other neurons in the vicinity. Through exposure therapy, the number of perisomatic synapses increases, thus causing the inhibition of more fear neurons.

Assistant professor Leon Reijmers, the senior author of the study, notes that this effect is a sign of brain remodeling. However, instead of erasing the memory of the fear situation, it suppresses it. Reijmers and his research team investigated this effect by using imaging techniques of neurons that were activated by fear in laboratory mouse models. The inhibitory connections in the mouse brains are similar to the connections in a human’s brain, thus making mice a perfect test subject for these types of studies.

The laboratory mice were put inside a box and researchers created fear-inducing situations in order to stimulate their amygdala. There were 2 groups of mice: a control group and a comparison group. The control group didn’t receive any kind of exposure therapy. The second group, the comparison group, received exposure therapy. In order to alleviate the fear response, the comparison group was placed repeatedly in the box, without exposing them to the fear-inducing situation again. This process is also known as fear extinction.

Investigators discovered that the mice who underwent exposure therapy had an increased number of inhibitory perisomatic synapses. Moreover, the majority of these synapses were located in the vicinity of the fear neurons. First author of the study, professor Stéphanie Trouche, notes that these results reveal that the remodeling of the inhibitory perisomatic synapses is closely related to the activity of the fear neurons in the amygdala. Reijmers concludes that exposure therapy is not effective for every human subject. Furthermore, the majority of patients who respond well to exposure therapy still experience fear, as the therapy has incomplete effects. Reijmers suggests that his study could possibly lead to an improvement in exposure therapy, thus making it more efficient for human patients suffering from various anxiety disorders.


The results of a new study published recently in the online edition of the American Journal of Psychiatry show that there is a genetic connection in families with one child who has autism and the other child who suffers from a specific language impairment. The study is led by a research team from the Rutgers University in collaboration with the Nationwide Children’s Hospital in Ohio, United States.

The main author of the study, professor Linda Brzustowicz, notes that the genes responsible for both the oral and the written language impairments can cause similar behavioral impairments. The regions of the chromosomes involved are 15q23-26 and 16p12. Brzustowicz reports that the similar characteristics can lead to the onset of autism for one child, while the other child will only develop a certain level of language impairment.

Specific language impairment is considered to be one of the most common learning disabilities, affecting approximately 7% of the children worldwide. However, specific language impairment isn’t considered as an autism spectrum disorder. In the United States alone, autism affects almost one in 90 children, in a 5:1 ration for boys:girls. Approximately 50% of the affected children suffer from a certain degree of language impairment.

Brzustowicz reports that in collaboration with Christopher Bartell, they tried to discover whether or not there are any genetic factors that connects the language impairment with autism. Brzustowicz says that the current study plays an important role due to the fact that in order to understand autism, the genes involved in its onset and development must be discovered.

Although researchers believe that there is a large number of genes that are responsible for increasing the risk of autism onset, both Brzustowicz and her team have been trying to identify a genetic pattern in the studies families. 79 families, the majority of whom are from Pennsylvania and New Jersey, underwent a series of extensive tests. All of the families have one child suffering from autism and at least one other child that suffers from a degree of language impairment. In addition to the blood samples that were taken for genetic tests, all of the family members were thoroughly tested in order to asses their grammar, language, and vocabulary skills.

The results of the tests show that specific behavioral characteristics can be seen within each family, in addition of the specific shared DNA patterns. Furthermore, the research team discovered very strong evidence that there is a genetic connection in the area of repetitive behavior, social interaction skills, obsessive-compulsive behaviors, and other symptoms that are frequently associated with autism.

According to professor Brzustowicz, the next step of the study will be to perform a genome sequencing test on all of the subjects of the study in order to create a comparison and investigate if there are some specific genes or genetic mutations that are common for all the subjects. Professor Brzustowicz and her team have been investigating the genetic links associated to autism for the past 10 years. Recently, her team was awarded with a $2.2 million grant. As of now, their study is opened for more families with autism, and will take place for another 4 years.


A new study that was recently published in the journal Brain shows that healthy subjects who received methylphenidate (the substance marketed as Ritalin) experienced the same increase in dopamine levels as the patients exhibiting symptoms of ADHD. According to the results of the study, both groups of subjects experienced the same improvements on their ability to concentrate and levels of attention.

The current study is led by a research team from the University of Cambridge, in collaboration with the MRC Center for Behavioral and Clinical Neuroscience Institute (BCNI). It is a double-blind study that puts all precedent suggestions about the link between ADHD and dopamine to question. Until now, one of the main causes of ADHD has been though to be an abnormality in the transmission of dopamine in the brain. However, the current study suggests that the actual cause could be found in the structural differences that are found within the grey matter of the brain. The research team believes that their results could lead to a significant improvement towards understanding and treating ADHD.

Dopamine is a crucial neurotransmitter that is involved in concentration, working memory, and attention. The way it takes part in these processes is by combining itself with specialized receptors found on the nervous cells of the brain. Methylphenidate increases the levels of dopamine in the brain, thus increasing the flow of information between the nervous cells.

Through the use of a PET (positron emission tomography) scan technique combined with fMRI (functional magnetic resonance imaging), researchers measured the effect of methylphenidate on the dopamine receptors. Both groups were given either a dose of methylphenidate, or placebo. Afterwards, the subjects were asked to perform several tasks that tested their ability to concentrate and their ability to keep their attention over a given period of time.

The group of subjects suffering from ADHD showed a significant impairment in their attention performance. Moreover, researchers discovered that methylphenidate also increased the attention performance of some of the subjects in the control group. However, the effects of methylphenidate on the levels of dopamine in the brain’s striatum, were almost the same for both groups.

According to the leader of the study, professor Barbara Sahakian, the results of the study show that the levels of concentration of anyone can be improved through the use of methylphenidate, whether or not the individuals suffer from ADHD. The novel information demonstrates that concentration can be improved by raising the levels of dopamine in the brain, specifically in the caudate nucleus of the striatum area.

The co-author of the study, professor Trevor Robbins, who is also the director of the BCNI, reports that these findings put a question mark on the precedent results of studies that suggested that the dopamine abnormalities are the main cause of ADHD. Furthermore, Robbins added that even if methylphenidate has a beneficial effect on attention performance, it is not linked to the impaired dopamine system that is found in ADHD patients.


Researchers from the Rutgers University, in the United States, have discovered possible new evidence regarding the two most common neurodegenerative diseases – Parkinson’s and Alzheimer’s disease. According to the study, the new evidence was found while researching the cause of a very rare childhood disease that eventually causes movement impairment in early adolescence.

The authors of the study are professor Karl Herrup, professor Ronald Hart, professor Jiali Li, and associate professor Alexander Kusnecov. Their study, published recently in the online edition of the journal Nature Neuroscience, also reveals new insight about the ataxia-telangiectasia (A-T) disease, which is also a neurodegenerative disease, also known as Louis“Bar syndrome. Previous research shows that almost 1 in every 40,000 births suffer from A-T. These children who are born with A-T suffer mutations in both of the ATM genes, thus suffering from a deficit of the ATM protein. Lack of a normal ATM protein leads to impairments in muscle control, equilibrium, movement, and coordination.

The researchers used both human and mouse brain tissue for their study. Their findings show that when there is not ATM protein, the levels of EZH2 (a regulatory protein), rise. Moreover, researchers have shown that the rise of the EZH2 protein is the main cause of the neuromuscular problems that affect the children suffering from A-T.

According to the research team, this study is the first to show that the EZH2 protein is involved in the alteration process of the muscles. Precedent studies have already linked the EZH2 protein to the gene on-off switching process. However, the current study, performed on mature brain cells, shows that high levels of EZH can also cause important adverse affects. Researchers investigated further and discovered that if the EZH2 protein levels were lowered, the A-T mouse models experienced better coordination, muscle control, and movement.

The laboratory mouse models with A-T, used in the study were cured of most A-T symptoms when the research team reduced the excess of EZH2. The cured mice were tested on a rotating rod, which showed similarities between the A-T mice and the normal, healthy control group. Furthermore, the research team investigated the results of the EZH2 reduction in an open space as well. A-T mice were reported to move and explore a smaller part of the open are, when compared to the normal mice.

Rutgers researchers suggest that their findings are waiting to be validated in a clinical trial. Working together with the Clinical Center at the Johns Hopkins University, in the United States, researchers begun collecting blood samples from children suffering from A-T, as well as blood samples from their parents.

Scientists believe that the new information that was discovered during this study can be used, in the near future, to create new efficient therapeutic drugs against A-T, that would reduce the neuromuscular and coordination deficits, at least. Furthermore, the research team will conduct new studies in order to determine whether or not the EZH2 protein plays a key role in other common neurodegenerative diseases, such as Parkinson’s and Alzheimer’s disease.


A team of cancer researchers from the Rice University, from the United States, discovered the genetic principles through which cancerous cells decide when and whether or not to metastasize and invade the other parts of the organism. According to their paper, which was recently published in the early edition of the journal Proceedings of the National Academy of Sciences, there is a genetic switch that can be set either on “on”, “off”, or somewhere in between. The research team says that their finding sheds new light on previous study results that were confusing, while also opening new directions towards cancer therapies.

According to the co-author of the study, professor Eshen Ben-Jacob, cancerous cells have a very complex behavior. Professor Ben-Jacob and his colleagues reveal a novel theory about the behavior of the mRNAs’ involvement in the decision-making circuits of the cancerous cells. For their study, the research team used a new framework. In order to test this new framework, they used the behavior of the genetic circuit that regulates the transition between the mesenchymal and epithelial states of cells. The two transitions are known as EMT (epithelial-mesenchymal transition) and MET (mesenchymal-epithelial transition), and are vital to embryonic development and wound healing.

Considered to be a hallmark for cancer metastasis, the EM transition is also used by the cancerous cells in order to break away from the initial tumor location, and migrate to other tissues from the organism. In order to find new ways to block metastasis, the research team conducted more than 20 studies about the genetic circuits involved in the activation of the EM transition. One of the clearest findings from precedent papers show that the key to EM and ME transitions is a two-component genetic switch. This switch contains two pairs of proteins. The first pair of proteins are known as SNAIL/miR34, while the second pair is known as ZEB/miR200.

Both protein pairs are mutually inhibitory. This means that if one of the proteins from the pair is present, it inhibits the production of its paired protein. For the mesenchymal state of the cell, both the ZEB and SNAIL proteins are present in high quantities. In the epithelial cellular state, both microRNA proteins are found in high levels. According to Ben-Jacob, their study model reveals that both SNAIL and miR34 proteins act as an integrator for the circuit. The levels of the SNAIL protein are responsible for activating ZEB and inhibiting miR200. Due to the fact that the ZEB protein has an ability to activate itself through a positive feedback loop, the cell is capable of keeping an average level of all four proteins.

Ben-Jacob suggests that this circuit supports the metastasis of cancerous cells by enabling them to migrate as a group, while also giving the cells properties that allow them to evade the person’s immune system. He concluded that the results of the study might allow further research on cancer therapies that would outsmart this three-way switch. Furthermore, the results of the current study correspond with the results of precedent studies on bacteria lead by professor Ben-Jacob and his collaborators.


According to a newly published study in the journal Pediatrics, a child’s learning capabilities and behavior can be affected by spanking. The results of the study show that children aged 9, who were spanked more than twice every week, between the ages of 3 and 5, are more violent, and rule breaking, when compared to children that weren’t spanked in their early childhood. Furthermore, the children that were spanked, are more likely to have lower grades in language comprehension and vocabulary examinations.

Associate Professor Michael MacKenzie, from the Columbia University School of Social Work, in the United States, reports that their results show that not only the behavioral development of the children is affected, but also their cognitive development. Furthermore, the effects of spanking are long-lasting, and not short-term as many believe. Moreover, children who were spanked more than twice a week experienced stronger effects.

Precedent studies, such as one published earlier this year, in March, revealed that if a child who’s genetically inclined to have an aggressive behavior is spanked, there is a major risk that the child would become even more aggressive. Another study, published in July, shows that almost 7% of adults who suffer from cognitive and mental health disorders can be linked to the different types of physical punishment received during their childhood.

Currently, there are 32 countries around the world that prohibit the acts of physical punishment on children, be it by their parents or caregivers. However, physical punishment is still unrestricted in Canada and in the United States, even though the AAP (American Academy of Pediatrics) strongly advocates against physical punishment as a form of discipline.

The current study was done on more than 2,000 families from 20 different cities from the United States. For the study, the parents were asked how many times had they spanked their children during the past month, due to misbehavior. At the time of the interrogation, all of the children were aged between 3 and 5. Later on, the research team evaluated the children’s aggressive behavior and vocabulary skills when they were aged between 3 and 9.

Spanking Detrimental for Young Children

According to the results, more than 55% of the mothers and approximately 40% of the fathers spanked their children at the age of 3. The percentages dropped to 52% and 33% for the parents of children aged 5. Children who were spanked by their mother’s were discovered to be more aggressive at the age of 9. researchers also suggest that the age of 5 is a very delicate age. Any kind of spanking coming from the mother’s side had an effect on the aggressive behavior of the children once they reached age 9. In comparison, children aged 3 when they received the physical punishment, were only discovered to be more aggressive if the physical punishment occurred more than twice a week.

Associate Professor Catherine Taylor, who has no implication in the current study, suggest that the results bring further evidence to the already existing evidence that physical punishment affects the future aggressive behavior of children. Furthermore, she notes that most parents only focus on the immediate effect of their actions, instead of the more important, distant effects. “The parent is inadvertently teaching the child that hitting, or being aggressive, is a way to solve problems.”, concluded Taylor.

However, physical punishment inflicted by the fathers appears to have no effect on the children’s later aggressive behavior. Nonetheless, it affected the children’s vocabulary skills, by the time they reached the age of 9. Children who were spanked by their fathers at the age of 5 scored poorly on the  vocabulary tests they received at the age of 9. According to Taylor, these results show that instead of having an effect on aggressive behavior, the father’s spanking actions have long-term effects on the general success and academic performance of the children.

According to the research team, there is a high probability that the families who spend time spanking their children are less likely to spend time reading or guiding their children through their language development stage. MacKenzie says that their study also shows that the cognitive development problems could be a result of the stress caused by physical punishment.

Even though the current study suggest a possible link between physical punishment and a children’s ability to behave, and learn, it doesn’t necessarily show a cause-and-effect type of connection.

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