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Researchers at the Stanford University School of Medicine have discovered that hypnosis works the way it does due to changes in a few specific areas of the brain. A person who is hypnotized can feel his eyelids getting heavy, arms limp and his body weightless.

The results of the study were published recently in the journal Cerebral Cortex. The scientists scanned and studied the brains of 57 people during guided hypnosis sessions and found that distinct sections of the brain have altered activity and connectivity when under hypnosis. Guided hypnotic sessions are clinically used to relieve people of pain, trauma and anxiety. Study’s senior author David Spiegel, MD, professor and associate chair of psychiatry and behavioral sciences opined that since it is known which brain regions are involved, this knowledge can be used to alter someone’s capacity to be hypnotized or the effectiveness of hypnosis for problems like pain control.

Hypnosis is more than just being associated with stage tricks – it is a serious science. Spiegel, who holds the Jack, Samuel and Lulu Willson Professorship in Medicine, said that hypnosis is the oldest Western form of psychotherapy, and it’s a very powerful means of changing the way we use our minds to control perception and our bodies. However, there is not much research about how it works at a physiological level. Earlier research on it studied the effects of hypnosis on pain, vision and other forms of perception, but not the state of hypnosis itself. Spiegel said that through his study he wanted to find out what goes on in the brain when one is hypnotized.

Not everyone has the same ability to be hypnotized. So, the researchers first had to find out people who could or couldn’t be hypnotized. 545 participants were screened and of them 36 people consistently scored high on tests of hypnotizability, and they found 21 control subjects who were just the opposite.

The brain of the 57 participants were observed using MRI. Scanning of each participant was done under four different conditions”while resting, while recalling a memory and during two different hypnosis sessions. Spiegel remarked that it was important to have people who aren’t able to be hypnotized as controls to be sure that the happenings in the brains of those being hypnotized is due to hypnosis or not.

The study revealed that there were three hallmarks of the brain under hypnosis. Each change was seen only in the highly hypnotizable group while they were undergoing hypnosis. First, there was a decrease in activity in an area called the dorsal anterior cingulate, part of the brain’s salience network, which signifies that the person under hypnosis is so absorbed in something that he is not aware of anything else. Secondly, an increase in connections between two other areas of the brain”the dorsolateral prefrontal cortex and the insula was seen. Lastly, the research team observed reduced connections between the dorsolateral prefrontal cortex and the default mode network, which includes the medial prefrontal and the posterior cingulate cortex. Spiegel explained that this decrease in functional connectivity likely represents a disconnect between someone’s actions and their awareness of their actions.

Spiegel explained that during hypnosis, this kind of disassociation between action and reflection allows the person to engage in activities either suggested by a clinician or self-suggested without devoting mental resources to being self-conscious about the same.

Spiegel said that the idea is that a person’s ability to be hypnotized can be altered by stimulating specific areas of the brain. Hypnosis sessions are known to be effective in lessening chronic pain, the pain of childbirth, easing anxiety, stress or phobias. The new findings about how hypnosis affects the brain might pave the way toward developing treatments for people who cannot be hypnotized so easily. More research, however, is needed before such a therapy could be implemented.








According to a new research by researchers at the University of Lyon, it is a good idea to get some sleep in between study sessions. The findings of the study that were published in Psychological Science, a journal of the Association for Psychological Science, reveal that such a strategy can make it easier to recall what you studied and relearn what you’ve forgotten, even 6 months later.

Stephanie Mazza, a psychological scientist at the University of Lyon explained that the result of their study suggest that interleaving sleep between practice sessions can reap a twofold advantage – it will help in reducing the time spent relearning and ensuring a much better long-term retention than practice alone. Some previous researches are known to suggest that sleeping after learning is definitely a good idea, but this latest study reveals that sleeping between two learning sessions greatly improves the end learning.

There have been some researches on repeated practice and sleep and it has been suggested that it can help improve memory, however there is not much research on how repetition and sleep influence memory when they are combined. The researchers working on this study assumed that sleeping in between study sessions can help in the relearning process and make it more efficient, thereby reducing the effort needed to commit information to memory.

For this study, the researchers chose 40 French adults who were randomly assigned to either a “sleep” group or a “wake” group. All participants were given 16 French-Swahili word pairs in random order at the first session. The participants were given 7 seconds to study each word pair after which the Swahili word appeared and participants were prompted to type the French translation. The correct word pair then appeared for 4 seconds. Any incorrectly translated word was presented again and again till they were correctly translated. After the initial session, the participants were given 12 hours rest and then were made to complete the recall task again, practicing the whole list of words until all 16 words were correctly translated.

The difference between the wake group and sleep group was that the wake group participants completed the first session in the morning and the second session in the evening of the same day while the sleep group completed the first session in the evening, slept, and completed the second session the following morning.

There was no difference in the results of the two groups – they didn’t show any difference in how many words they could initially recall or in the number of trials they needed to remember all 16 word pairs. However, the data after 12 hours has a different story to say. Participants who had slept between sessions recalled on an average about 10 of the 16 words, while those who hadn’t slept recalled only about 7.5 words. For relearning, the sleep group needed only about 3 trials to be able to recall all 16 words, while the wake group needed about 6 trials.

In the end both groups were able to learn the 16 word pairs, but it was seen that those who slept in between the sessions could do it in less time and with less effort. Mazza opined that memories that were not explicitly accessible at the beginning of relearning seemed to have been transformed by sleep in some way, which helped subjects to re-encode information faster and to save time during the relearning session.

The researchers added that the benefits of sleep could not be ascribed to participants’ sleep quality or sleepiness, or to their short-term or long-term memory capacity, as the two groups showed no differences on these measures.

The benefits reaped by the sleep group by sleeping in between study sessions seemed to have a lasting effect. There were follow up recall sessions a week later in which participants from the sleep group outperformed their peers. The sleep group showed very little forgetting, recalling about 15 word pairs, compared to the wake group, who were able to recall about 11 word pairs. Even when the recall test was carried out 6 months later, the benefit was still noticeable.

The study concluded that it is a good technique to sleep in between study sessions as it helps to remember information over longer periods of time with less study.

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Memories form an important part of our lives. Some memories seem etched in our mind forever. In fact, if we think about it we will realize that some memories are quite connected. For example, if we think about an important experience in our life, we might also closely remember another experience that happened around the same, like your graduation ceremony and the party you had after that, or the memory of exchanging vows at your wedding, and then how your friends danced to the music in the party later that same night. Somehow there seems to be a connection between the two memories in your mind.

In a new study led by the Hospital for Sick Children (SickKids) published recently in an online edition of Science, the connection between memories and how they become linked in the brain has been explored.

This study is supported by Canadian Institutes of Health Research, Natural Sciences and Engineering Research Council of Canada, Brain Canada, Brain and Behavior Research Foundation grants, and SickKids Foundation

The principal investigator of this study, Dr. Sheena Josselyn and her lab have been working for many years now, on how the brain forms, stores and organizes memories. Previous research from her lab had revealed about collections of neurons (engram) in the amygdala that store specific memories in mice. The amygdala is a brain region that is important in encoding important memories. The amygdala consists of thousands of neurons, but the question is how is it decided by the brain which collection of neurons encodes a particular memory?

Josselyn, who is also a Senior Scientist in Neurosciences & Mental Health at SickKids revealed that in their study they found that the activity, or excitability, of neurons in the amygdala fluctuates, and the neurons that are most excitable when an event occurs are most likely to ‘grab’ the memory. During the study, it was also noted that once a memory is encoded, the engram cells stay active for s few hours before their activity level decreases. The researchers found that if another event takes place within the activity window which is less than six hours, the memory is then encoded in the same set of neurons. Since these two memories are encoded in the same population of cells they become linked. Likewise, if a second event occurs outside the activity window of the activated neurons, they get encoded in a different population of cells. Hence, those two memories are not linked and are stored in the brain as entirely separate events.

This study have found that a key factor in determining whether two memories are linked or not is – the neuron’s excitability. The researchers also showed that by artificially manipulating the neuron’s excitability, two different memories could be encoded in the same set of amygdala neurons. Similarly, it was also possible to separate two memories that would normally be encoded in the same population of neurons.

Josselyn who is also Associate Professor in the Departments of Physiology and Psychology at the University of Toronto remarked that their study uncovers the principles of how we organize our memories”how remembering one event conjures up memories of closely related episodes.

The findings of this study can be applied to various psychiatric conditions opined Paul Frankland, co“principal investigator on the study. By understanding how memories are linked may provide hints as to how they become inappropriately connected in conditions such as schizophrenia and in the long run it might help in finding viable solutions to such problems.

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The human brain has fascinated scientists and researchers for ages and that is the reason why it has been a hot subject of research in the scientific community. Now imagine having a window to the brain.

Well, the idea of having a window to the brain may sound far-fetched, but, researchers at the University of California, Riverside who have been working on this idea for a while have some good news to share. They have revealed that the idea of having a ‘Window to the Brain’ transparent skull implant is closer to reality through the findings of two studies that have been published in the journals- Lasers in Surgery and Medicine and Nanomedicine: Nanotechnology, Biology and Medicine.

The implant which is under development phase will literally provide a window to the brain. It can help patients with life-threatening neurological disorders, such as brain cancers, traumatic brain injuries, neurodegenerative diseases and stroke, by allowing doctors to deliver minimally invasive laser-based treatments. The recent studies have highlighted that the implant material is biocompatible and has the ability to endure bacterial infections.

The Window to the Brain project led by Gisuillermo Aguilar, professor of mechanical engineering in UCR’s Bourns College of Engineering, and Santiago Camacho-López, from the Centro de Investigación Científica y de Educación Superior de Ensenada (CICESE) in Mexico is a mammoth project that is multi-institutional and interdisciplinary. Aguilar and his team had developed a transparent version of the material yttria-stabilized zirconia (YSZ) ” it is the same ceramic product used in hip implants and dental crowns. With its development, this projected started off. The team hopes to use it as a window-like implant, which will enable doctors to aim laser-based treatments into patients’ brains when needed. This will rule out the need to perform repeated craniotomies – which are highly invasive procedures used to access the brain.

YSZ boasts of internal toughness which is more impact resistant than glass-based materials developed by other researchers. It makes it the only transparent skull implant that could conceivably be used in humans. The two recent studies also support the claim that YSZ can be a promising alternative for currently available cranial implants.

The most recent study published recently in the journal Lasers in Surgery and Medicine, it is demonstrated by using transparent YSZ may allow doctors to combat bacterial infections, which are the number one cause of cranial implant failure. In lab studies, E-Coli infections were treated by researchers by aiming laser light through the implant without having to remove it and without damaging the surrounding tissues.

Devin Binder, M.D., a neurosurgeon and neuroscientist in UCR’s School of Medicine and a collaborator on the project opined that it is an important finding as it showed that the combination of our transparent implant and laser-based therapies had the ability to help treat not only brain disorders, but also to tackle bacterial infections that are common after cranial implants. These infections are particularly challenging to treat because many antibiotics do not penetrate the blood brain barrier.

The other study which supports YSZ explored its biocompatibility in an animal model. The findings were published in the journal Nanomedicine: Nanotechnology, Biology and Medicine. As a part of this study, YSZ was integrated into the host tissue without causing an immune response or other adverse effects.

Aguilar shared that YSZ was actually found to be more biocompatible than currently available materials, such as titanium or thermo-plastic polymers. It is definitely very encouraging news in the development of transparent YSZ as the material of choice for cranial implants.







An international team of researchers, led by scientists at the Imperial College London have identified two genes that are switched on only when a child is suffering from a bacterial infection. This finding can let doctors easily distinguish between a viral or bacterial illness, which can help in identifying early cases of potentially deadly infections. The findings of the study were published recently in Journal of the American Medical Association (JAMA).

The researchers are now keen on developing a rapid test for use in hospitals and doctors’ surgeries. Conditions such as meningitis, septicemia or pneumonia caused by bacterial infections can be caught more rapidly with the help of such a rest. It will also prevent children with viral infections being unnecessarily prescribed antibiotics and hence aid in combating the threat of antibiotic resistance.

Presently, there is no quick method of distinguishing a viral and bacterial infection. In hospitals diagnosis is made by taking a sample of blood or spinal fluid, and seeing if bacteria grow in the sample. This process can take more than 48 hours and this time can be very crucial for a patient. Viral infections are more commons compared to bacterial infections, but the later can be deadlier in many cases.

Fever is one of the most common reasons why children are brought to medical care. But, sometimes a bacterial infection is thought to be a viral infection and this wrong diagnosis can be life threatening for them. Similarly, many children are admitted to hospital and receive antibiotics because there is no way to differentiate bacterial infection from a viral one,- but later it is confirmed that they are suffering from a virus.

Professor Michael Levin, from Department of Medicine at Imperial College London, who led the study opined that even though this research is at an early stage, the results show bacterial infection can be distinguished from other causes of fever, such as a viral infection, using the pattern of genes that are switched on or off in response to the infection. The next step is to transform our findings into a diagnostic test that can be used in hospital emergency departments or GP surgeries, to identify those children who need antibiotics.

For the study, 240 children with an average age of 19 months were studied by the researchers. These kids arrived at hospitals with fever across the UK, Spain, the Netherlands and the USA. Once it was determined Using traditional methods whether they were suffering from a viral or bacterial infection, the team studied the genes that had been switched on in the children’s white blood cells. A method known as RNA micro array which needs only a drop of blood to measure changes in 48,000 genes simultaneously was used. The team found two genes are switched on in bacterial infections. Further tests were carried out and it was found that these genes, called IFI44L and FAM89A, predicted a bacterial infection with 95-100 per cent accuracy.

Dr Jethro Herberg, senior lecturer in pediatric infectious diseases at Imperial, and co-author of the research remarked that since the threat of antibiotic resistant bacteria is larger than ever today, the need of today is to quickly distinguish a bacterial infection from a viral one. A rapid test based on the two genes identified in the study could transform pediatric practice, and allow doctors to use antibiotics only on those children who actually have a bacterial infection.

Vinny Smith, Chief Executive of Meningitis Research Foundation added that the latest development in the study is very exciting. Bacterial meningitis and septicaemia can kill in hours, and can leave survivors with life-changing after effects. Once we have a tool to rapidly determine whether an infection is bacterial or viral, it will enable faster detection and treatment of meningitis and septicemia.







Since ages pomegranates have been touted as a superfood that can counteract the aging process. However, there were practically no scientific researches to back such claims until now. A team of researchers from EPFL and the company Amazentis decided to find out the facts about this plump pink by delving deeper into it. Their research revealed that a molecule in pomegranates, transformed by microbes in the gut, enables muscle cells to protect themselves against one of the major causes of aging. While human trials are in the process, the effect noted in nematodes and rodents, is quite encouraging.

The initial findings have been published in the journal Nature Medicine.

Aging happens because over the years our cells losses their capabilities to recycle their powerhouse – mitochondria. Since, it cannot carry out its vital functions, waste accumulation starts in the cells which affect the health of many tissues resulting in their weakening over the years. It is also believed that buildup of dysfunctional mitochondria play a role in other again related diseases, like Parkinson’s disease.

The researchers discovered a molecule – urolithin A, which was capable of re-establishing the cell’s capacity to recycle the components of the defective mitochondria – a process called mitophagy. Patrick Aebischer, co-author on the study added that is a completely natural substance and its effect are powerful and measurable. The team carried out their hypothesis on the nematode C. elegans – a favorite test subject among aging experts as at the age of just 8-10 days it is considered elderly. When the worms were exposed to urolithin A, their lifespan increased by more than 45% compared with the control group.

The results encouraged the team to test the molecule on rodents. A significant reduction in the number of redundant mitochondria was observed in the rodents, indicating that a robust cellular recycling process was taking place. Older mice showed 42% better endurance while running than equally old mice in the control group.

While it might be tempting for you to head out and stock up on pomegranates, it must be remembered that the fruit doesn’t contain the miracle molecule, but rather its precursor. It gets converted into Urolithin A by the microbes in the intestine. So, the amount of urolithin A produced will depend on the species of animal and the flora present in the gut microbiome. So, not every individual will have the same result.

If you are one who doesn’t have the right microbes in the gut, don’t worry, scientists are already working on a solution.  The study’s co-authors founded a start-up company, Amazentis, which has developed a method to deliver finely calibrated doses of urolithin A. The first clinical trials testing of the molecule in humans are underway in European hospitals.

Johan Auwerx, study’s co-author opined that it seems likely that Urolithin A will be effective in humans as well. To back his notion, he adds that species that are evolutionarily quite distant, like C elegans and the rat, react to the substance in the same way and that is a good indication. The function of Urolithin A is the result of tens of millions of years of parallel evolution between plants, bacteria and animals. Chris Rinsch, co-author and CEO of Amazentis, adds that this evolutionary process explains the molecule’s effectiveness. Nuts and berries also contain the precursors to Urolithin A in tiny amount. However, in order for it to be produced in our intestines, the bacteria should be able to break down what we are eating. Through digestion when a substance is produced that is of benefit to us, natural selection favors both the bacteria involved and their host.

The researchers reiterated that their objective is to follow strict clinical validations, so that everyone can benefit from this discovery. This could help fight and counteract effects of aging. Since, it works by helping the body renew itself, urolithin A could well succeed where so many pharmaceutical products, most of which have tried to increase muscle mass, have failed.

Auwerx opined that these studies could change the way aging is seen in medical world. Since, it is a nutritional approach, it opens up territory that traditional pharma has never explored. It’s a true shift in the scientific paradigm.

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Our brains are at work even when we sleep. It is busy sorting and consolidating our day’s happening and storing information in our memory so that we can use it when need be. Memory impairment is debilitating for people suffering from neurological conditions – it affects their everyday life in several ways. The researchers at the UNC School of Medicine have for the first time used transcranial alternating current stimulation, or tACS, to target a specific kind of brain activity during sleep and strengthen memory. The findings of the study were published recently in the journal Current Biology.

This research offer a non-invasive way that has the potential to help millions of people suffering from conditions such as autism, Alzheimer’s disease, schizophrenia, and major depressive disorder. The electrical brain activity during sleep oscillates; they present as waves on an electroencephalogram (EEG) and are called sleep spindles. Researchers have suspected the involvement of sleep spindles in cataloging and storing memories while we sleep.

Flavio Frohlich, PhD, assistant professor of psychiatry and member of the UNC Neuroscience Center remarked that it was not known for sure if sleep spindles enable or even cause memories to be stored and consolidated. It was also possible that they were merely byproducts of other brain processes that helped in storing what we learn as a memory. But, this study has shown evidence that the spindles are key to the process of creating memories we need for every-day life. Hence, they can be targeted to enhance memory.

It is for the first time selective targeting of sleep spindles without increasing other natural electrical brain activity during sleep have been done by a research group. The same couldn’t be accomplished with tDCS – transcranial direct current stimulation – in which a constant stream of weak electrical current is applied to the scalp.

Frohlich’s team previously used tACS to target the brain’s natural alpha oscillations to boost creativity. This was a proof of concept. It showed it was possible to target these particular brain waves, which are prominent as we create ideas, daydream, or meditate. These waves are impaired in people with neurological and psychiatric illnesses, including depression

The 16 male participants who volunteered for the study underwent a screening night of sleep before completing two nights of sleep for the study. The participants were made to perform two common memory exercises before going to sleep each night – these exercises were – associative word-pairing tests and motor sequence tapping tasks, which involved repeatedly finger-tapping a specific sequence.

On the night of study, each participant had electrodes placed at specific spots on their scalps. During sleep on one night each person received tACS – an alternating current of weak electricity synchronized with the brain’s natural sleep spindles and the other night, each person received sham stimulation as placebo. On both the mornings the participants were made to perform the same memory tests. No improvement in test scores for associative word-pairing was noted by the research team but a significant improvement in the motor tasks when comparing the results between the stimulation and placebo night.

Frohlich opined that this demonstrates a direct causal link between the electric activity pattern of sleep spindles and the process of motor memory consolidation.

Caroline Lustenberger, PhD, first author and postdoctoral fellow in the Frohlich lab remarked that they were excited about this discovery. It is known that sleep spindles, along with memory formation, are impaired in a number of disorders, such as schizophrenia and Alzheimer’s. So, the researchers are hopeful that by targeting these sleep spindles a new type of treatment for memory impairment and cognitive deficits could be devised.

The researchers now to aim try the same intervention, the same type of non-invasive brain stimulation, in patients that have known deficits in these spindle activity patterns.

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Huntington’s disease is an inherited and fatal neurodegenerative disorder. A research by the scientists at Johns Hopkins Medicine, the findings of which have been published in a recent issue of  ˜Proceedings of the National Academy of Sciences', have revealed that a biochemical pathway linking oxidative stress and the amino acid cysteine in Huntington’s disease have been identified. The findings of the study provide a mechanism through which oxidative stress specifically damages nerve cells in Huntington’s disease.

Cysteine deficiency and oxidative stress are known to be playing a role in diseases like Alzheimer’s disease, arthritis, cardiovascular disease, AIDS and cancer. So, the researchers are of the opinion that the findings of this study may aid in finding therapeutic strategies for many serious conditions. There are many ways human cells regulate oxidative stress but, those involving cysteine play a central role remarked researchers Juan Sbodio, Ph.D.; Solomon Snyder, M.D., Ph.D., D.Sc.; and Bindu Paul, Ph.D., all of the Johns Hopkins University School of Medicine’s Solomon H. Snyder Department of Neuroscience. Paul added that if you deplete cysteine, a majority of these antioxidant defenses will be affected.

In a previous research work, the researchers had found that the protein responsible for making cysteine, cystathionine gamma-lyase (CSE), is decreased in HD. When the levels of amino acids are low, CSE is activated by the normal cells using a protein called activating transcription factor 4 (ATF4). ATF4 tell the cell to start up the cysteine production line for protein synthesis and generation of other protective molecules derived from cysteine. Cells low in cysteine can use alternate pathways for a short time; however as time passes such cells are overwhelmed by oxidation and die. This study revealed that in Huntington disease, ATF4 is disrupted in cells which affect cysteine production.

As a part of this study, the researchers grew both healthy control brain cells and brain cells that were derived from mice with Huntington’s disease under low cysteine conditions. It was found that the healthy cells increased the activity of ATF4 under low cysteine conditions. However, in the cells from mice with Huntington’s disease they could not detect ATF4. The researchers then grew cells in conditions depleted of other amino acids and found that ATF4 levels were normal in both control and Huntington’s cells. The researchers concluded that effect was unique to cysteine which led them to wonder if elevated oxidative stress would affect the response of ATF4 because of cysteine’s role in cellular defense.

In order to find that, the researchers induced oxidative stress in healthy cells and then cut off their cysteine supply. They found that the cells’ expression of ATF4 was greatly diminished. Conversely, when Huntington’s cells were grown in cysteine-depleted conditions but given an antioxidant, vitamin C, the cells regained their ability to create ATF4 and create their own cysteine.

Sbodio remarked that it is a vicious cycle – low levels of cysteine cause oxidative stress, which in turn decrease cysteine levels, thereby creating more oxidative stress which further slows cysteine production. In their previous study, the researchers’ had found that supplementing cysteine in the diets of mice exhibiting Huntington’s disease delays the progression of the disease’s symptoms. This study reveals how cysteine is regulated and how oxidative stress affects this system.

Antioxidants are known to be beneficial for health but the researchers cautioned that more information is needed on cysteine’s role in the body before researchers can confirm its therapeutic value. Too much of anything is bad – same is the case with cysteine. So, patient should abstain from self-medicating. It is always advisable to  consult a doctor before beginning any supplement.





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Researchers at the North Western Medicine University have shown that by manipulating a novel target in the brain using gene therapy, new treatments for depression can be found.  Clinical depression is becoming a common phenomenon. It can cause severe symptoms and can affect how one feels, thinks, and handles daily activities, such as sleeping, eating, or working. If left untreated, it can also have life threatening results.

The researchers working on the study in context found that when a set of proteins called HCN channels were decreased, it reduced depression like behavior in mice. If the same could be replicated in humans, the findings could result in new therapies which could help millions of patients who do not respond to the existing therapies and treatment for depression.

The findings of the study were published recently in an issue of the journal ‘Molecular Psychiatry’.

Dr. Dane Chetkovich, study’s senior author and professor of neurology and of physiology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine neurologist remarked that drugs that are presently available for treating depression help most patients, but they stop working for some patients and don’t work from the get-go for others. Hence, there is a huge need for novel therapies to help patients desperate for alternatives to the available therapeutic options. The antidepressants available today work on the emotions and mood of a patient by enhancing the levels of neurotransmitters called monoamines, namely serotonin, dopamine and norepinephrine. But, since these drugs are not effective for many patients indicate that there are additional mechanisms underlying depression that need to be discovered. Newer therapies could be used to help such patients.

In an earlier research at Chetkovich’s lab, it was found that those mechanisms might involve the hippocampus. It is the region of the brain important for learning, memory and emotional regulation. The researchers discovered that changes to HCN channels, typically involved in controlling the electrical activity of cells in the heart and brain, had a critical role to play in behaviors linked to depression. To take these findings forward, a group of Northwestern scientists led by Chetkovich, who is also director of Feinberg’s Medical Scientist Training Program, took steps in this new study to translate that insight into a potential gene therapy using mouse models.

In order to turn off HCN channel function in hippocampus neurons, the scientists surgically injected mice with a nontoxic virus engineered that expresses a gene to turn off HCN channel function. Chetkovich explained that when the HCN channels stopped working, the mice behaved like they’d been given antidepressant medications. When the opposite was tried, i.e., when the function of HCN channels were increased, the antidepressant effect disappeared.

The depression like behavior was calculated by measuring how long mice would seek to escape an environment before giving up. It is common test that is a conducted by the pharmaceutical industry to screen compounds for effectiveness as antidepressants, including medications currently on the market.

Chetkovich opined that this work is novel as it not only identifies a totally new treatment target for depression but it provides a detailed molecular description of the structures that need to be manipulated for it to act as an antidepressant and develops viral tools to do so.

Next, the researchers are focusing on adapting the viral gene therapy approach to human patients. They also have a grant from the National Institute of Mental Health to research on small molecules that are good candidates to be developed into oral medications to turn off HCN channels in the brain.

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Do you like to enjoy a glass of wine with dinner? Well, if you are counting on its heart benefits while you enjoy your sips, then this piece of research may worry you. A recent research study by UC San Francisco investigators have found that the structure of the heart is changed by even moderate consumption of alcohol in ways that enhances the risk of atrial fibrillation.

Atrial fibrillation is the most common heart rhythm disturbance in the world. It is characterized by rapid and irregular beating. Typically, it starts with brief periods of abnormal beating and over time it becomes longer and constant. Some people also experience heart palpitations, fainting, shortness of breath, or chest pain along with it.

Gregory Marcus, MD, endowed professor of atrial fibrillation research at UCSF and senior author of the study published in the Journal of the American Heart Association opined that there is growing evidence that points that alcohol even in moderate amounts may be a risk for atrial fibrillation. However, the exact mechanism by which alcohol eventually leads to atrial fibrillation is still unknown.

It is known that atrial fibrillation is a risk factor for stroke. It causes irregular pumping of blood and that sets the stage for blood clots – which can travel to the brain and cause stroke.

As a part of the study, the data from more than 5000 adults were collected over several years in the Framingham Heart Study was analyzed. This data includes echocardiograms, medical history and self reported alcohol intake. The participants in the study all in the age group of 40 to 60 and are mostly white. They reported of having just over a drink per day. It was noted that atrial fibrillation in the group was 8.4 cases per 1000 people per year which translates to 8 cases of atrial fibrillation per 100 people in a year. If we increase another drink per day, the risk increases by 5% every year. Another finding of the study states with every additional drink per day, the left atrium enlarges by .16 millimeter.  This fact highlights a possible site of damage in the heart caused by alcohol consumption.

The relationship between alcohol and heart is complex and the findings of the new study shed some light on it to help us understand it better remarked Marcus. Previous researches have revealed that moderate drinking can reduce the risk of heart attack while increasing the risk of atrial fibrillation. Marcus and his team of researchers had published a study earlier this year analyzing the hospital admissions in dry and wet counties of Texas. In their study they found that patients in counties permitting alcohol sales were more likely to have atrial fibrillation but less likely to have heart attacks and congestive heart failure. Atrial fibrillation is gradually growing in importance as the success in preventing heart attack in increasing

Another pattern that has been noticed by UCSF’s Health eHeart Study is that people who believe alcohol is good for the heart tend to drink more. Marcus, who is also a practicing cardiologist, said that he constantly tells his patients that there are various forms of heart diseases and not all are related to heart attacks. He also added that alcohol has properties to protect as well as to harm the heart and it is likely that they likely operate through different mechanisms and vary from person to person. Through their research the group of investigators seeks to decipher these mechanisms, which will help designing therapies for heart conditions and enable physicians to give personalized advice to patients.

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