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Scientists Discover Cause Of and Potential Treatment for Muscle Weakness and Loss Due To Aging

Oct 23, 2015

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Aging

Aging is one of the inevitable facts of life. As we age, we lose our vitality, strength and muscle mass. However, why our muscles become weak with increasing age is still a mystery. Scientists at the University of Iowa have unraveled the mystery through their recent study. They have discovered the first example of a protein that causes muscle weakness and loss during aging.

The findings of the study were published online recently in the Journal of Biological Chemistry.

The protein known as ATF4 is a transcription factor which changes gene expression in skeletal muscle which in turn causes reduction of muscle protein synthesis, strength, and mass. This finding is significant as it can be instrumental in leading to new therapies for age-related muscle weakness and atrophy. Scientists working on this study have also discovered two natural compounds, one found in apples and one found in green tomatoes, which can lower ATF4 activity in aged skeletal muscle.

Christopher Adams, MD, PhD, UI professor of internal medicine and senior study author said that it is known that muscle weakness and atrophy are big problems as we get older and these problems can have a big impact on the quality of our lives and overall health.

In a previous study, Adam and his team had identified ursolic acid � a compound found in apple peel, and tomatidine, which is available in green tomatoes, as small molecules which can be helpful in preventing acute muscle wasting caused by starvation and inactivity. Those studies came in really handy to set the stage further and it lead to the testing if ursolic acid and tomatidine are effective in blocking the largest cause of muscle weakness and atrophy: aging.

Adam's team carried out their experiments on mice and found very encouraging results. It was found that ursolic acid and tomatidine dramatically reduce age-related muscle weakness and atrophy in mice. Elderly mice with age-related muscle weakness and atrophy were given diets that contained or lacked either 0.27 percent ursolic acid, or 0.05 percent tomatidine for two months. After 2 months, it was seem that the mice showed a 10 % increased muscle mass; also the muscle quality and strength improved by 30%. These highly noticeable changes suggest that the compounds actually restored muscle mass and strength to young adult levels.

Adam, who also is a member of the Fraternal Order of Eagles Diabetes Research Center at the UI and a staff physician with the Iowa City Veterans Affairs Medical Center, opined that these results are very positive about the potential of ursolic acid and tomatidine for dealing with muscle weakness and atrophy during aging. The researchers also toyed with the idea of using ursolic acid and tomatidine as tools to find a root cause of muscle weakness and atrophy during aging.

When Adam's team studied the molecular effects of ursolic acid and tomatidine in aged skeletal muscle, they found that both compounds turn off a group of genes that are turned on by the transcription factor ATF4. This finding made the scientist to engineer and study a new strain of mice � the ones that lacked ATF4 in skeletal muscle. It was found that like old muscles that were treated with ursolic acid and tomatidine, old muscles that lacked ATF4 were resistant to the effects of aging.

Adam said that it can be concluded that by reducing ATF4 activity, ursolic acid and tomatidine allow skeletal muscle to recover from effects of aging.

The UI study was done in collaboration with Emmyon, Inc., a UI-based biotechnology company founded by Adams. It is now working to translate ursolic acid and tomatidine into foods, supplements, and pharmaceuticals that can help to fight muscle aging and atrophy.

Looking for a natural way to fight aging? Try this guide.

References

https://medicalxpress.com/news/2015-09-scientists-potential-treatment-muscle-weakness.html

https://now.uiowa.edu/2015/09/keeping-older-muscles-strong

Could marijuana chemical help ease epilepsy?

Oct 22, 2015

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Marijuana

A new study published in the Sept. 10 issue of the New England Journal of Medicine, has revealed that a chemical found in marijuana can help in preventing epilepsy seizures. However, since law forbids the use of marijuana, research efforts in the direction have been hampered.

One of the main active ingredients found in marijuana is Cannabidiol, but this is not the ingredient that makes people high. Lead author Dr. Daniel Friedman, a neurologist and epilepsy specialist at NYU Langone Medical Center in New York City said that it has already been found to prevent seizures in animal studies and in an ongoing human trial. But, since marijuana is a schedule I controlled substance, the U.S. Drug Enforcement Agency classifies it as a drug with “no currently accepted medical use and a high potential for abuse.” So, large scale trials that could prove the effectiveness and safety of Cannabidiol in epilepsy is difficult.

Phil Gattone, Epilepsy Foundation President and CEO said that the current federal laws have limited our understanding of marijuana’s potential effectiveness as an anti-seizure medication.

Friedman and co-author Dr. Orrin Devinsky opined that even though the long-term and short-term side effects of using cannabis and Cannabidiol, we do know the impact of uncontrolled epilepsy, and that reason must be considered when looking at the use of cannabis. There are about 20 different anti-seizure drugs in the market. Despite that about 30% of people suffering from this condition have uncontrolled seizures.

A major brain receptor that responds to marijuana�cannabinoid receptor 1, or CB1�seems to have anti-seizure effects when activated. The CB1 receptor is most strongly activated by THC, the chemical in Cannabidiol that causes intoxication. But, a review of animal studies found that non-intoxicating cannabidiol shows the most promise in preventing seizures, the researchers said.

In an ongoing human trial that involves Epidiolex which is a British-made cannabis extract that’s 99 percent cannabidiol, it is seen that the chemical can be effective in humans. For the trial, several institutions in the United States received compassionate use waivers from the U.S. Food and Drug Administration. Friedman said that almost 2 in every 5 patients suffering from severe treatment-resistant epilepsy experienced a 50 percent reduction in the frequency of their major seizures. Not just that, some of the patients with epilepsy who have never had prolonged periods of seizure freedom became seizure-free, at least in the short-term of this study.

Excited with these results, three companies have begun developing cannabidiol-based drugs. However, it is also presumed that since it was an open-label trial, the results might be a bit biased. Since, both the patients and the researchers knew what drug was being administered; so people may have experienced some improvement because they expected the drug to produce positive results.

Also there are some concerns regarding marijuana’s effect on the developing brain. There are studies that show that it can alter the structure of the brain in young people. To counteract that Friedman said that it is known severe epilepsy also affect brain development, and it is widely believed that some of the approved anti-seizure medications may also affect the brain. So, a risk- benefit calculation is all that can be resorted to until there are more long-term safety data.

A good news for the researchers here is that the director of the U.S. National Institute on Drug Abuse said that her agency will support future cannabidiol (CBD) research.

Dr. Nathan Fountain, chair of the Epilepsy Foundation Professional Advisory Board, said he hopes the upcoming clinical trials will solve the unresolved queries that are there regarding cannabidiol use.

If you’re not in favor of using marijuana and wish to quit then you should try this awesome guide.

References

https://medicalxpress.com/news/2015-09-marijuana-chemical-ease-epilepsy.html

https://www.webmd.com/epilepsy/news/20150909/could-marijuana-chemical-help-ease-epilepsy

Common Antidepressant Sertraline May Change Brain Structures

Oct 21, 2015

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A new research at Wake Forest Baptist Medical Center has revealed a worrying fact about a common antidepressant. It says that this prescribed antidepressant behaves differently in people who are suffering from depression and those who are not. In fact, it says that it can alter brain structures in depressed and non-depressed individuals in very different ways.

For this study, nonhuman primates who have brain structures similar and functions to humans were considered. The study found that the antidepressant sertraline, a selective serotonin reuptake inhibitor (SSRI) which is marketed as Zoloft, did something strange in brain. It decreased the volume of two brain areas in non-depressed subjects and significantly increased the volume of one brain region in depressed subjects. The reason these observations are significant is because Zoloft is widely prescribed not only for depression but for a number of other disorders as well. The study was published in an online issue of the journal Neuropharmacology recently.

Carol A. Shively, Ph.D., professor of pathology-comparative medicine at Wake Forest Baptist and lead author of the study said that the observations made are of great significance for human health as rampant use of Zoloft could do more harm than good.

Researchers experimented on a group of 41 middle-aged monkeys. For 18 months they were fed with a diet which was a replica of what most Americans consume and during this period, the depressive behavior in the animals was recorded. Studies show that women between the ages of 40 to 59 are the most common users of anti-depressants. Since depression is twice as common in women as compared to men, female monkeys were chosen for this study.

This treatment regimen followed for the monkeys is similar to a human taking an antidepressant for approximately five years. After the 18 month pre-study phase was over, the monkeys were divided into two groups balanced for body weight, body mass index and depressive behavior. In the next 18 months, 21 monkeys were given sertraline in daily doses to replicate the dose typically taken by humans while the other group of 20 was given a placebo.

When MRI images were taken at the end of the treatment, it revealed that in depressed subjects the anterior cingulate cortex region of the brain was significantly increased due to the drugs. However, the volume of this region as well as the hippocampus in non-depressed subjects was decreased. Since, these areas are very much connected with other areas of the brain and affects memory, learning, spatial navigation, will, motivation, emotion, etc., – all these are also affected if a person suffers from a major depressive disorder.

Shively opined that in humans it is seen that there is a notable difference in the volume of the neural structures in depressed and non-depressed individuals. Typically it is seen that in depressed people the volume of the cingulate cortex and hippocampus is small. The reason why drugs like Zoloft can be effective in treating depression is likely because they promote neuron growth and connectivity in the affected region of the brain.

However, the problem is SSRIs such as Zoloft are not just prescribed for treating depression but also for a number of other conditions such as obsessive-compulsive disorder, bulimia, hot flashes, post-traumatic stress disorder, stroke recovery and sexual dysfunction. But, there is severe lack of researches which studies the effects of these drugs on brain volumes in individuals who are not suffering from depression.

Shivley said since the present study's findings are compelling, it is important to study the effects of SSRIs on different disorders to find out if these drugs produce similar effects in humans

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References

https://medicalxpress.com/news/2015-09-common-antidepressant-sertraline-brain.html

https://www.wakehealth.edu/News-Releases/2015/Common_Antidepressant_May_Change_Brain_Structures_Differently_in_Depressed_and_Nondepressed_Individuals.htm

A new factor in depression? Brain protein discovery could lead to better treatments

Oct 20, 2015

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People who suffer from depression feel low and down � that is how depression is explained is layman words. Previous researches on depression have indicated that depressed brains often have less key components than non-depressed brains. However, a recent research have indicated that depression can also mean too much of something. It has been found that people suffering from major depression have 32 percent more of a protein called fibroblast growth factor 9 or FGF9 than normal beings, in a part of their brains. When the FGF9 levels were raised artificially in rats, they started exhibiting depression like behavior. Also, when they were made to undergo social stress, the FGF9 levels rose.

This finding can significantly help in the development of better medications to treat depression � an ailment that affect millions of Americans. The role of FGF9 was discovered by a team from the University of Michigan Medical School and the Pritzker Neuropsychiatric Disorders Research Consortium. Their results were reported in the Proceedings of the National Academy of Sciences. Years of detailed comparisons of brain tissue donated by people with and without depression, and multiple studies in rats lead to this discovery.

Elyse Aurbach, a neuroscience doctoral student who is also the paper’s co-first author said that fixing depression is not easy as it is a disorder at the level of the circuits that connect brain cells, and many regions of the brain are involved. However, it is the first time that the role of FGF9 has been linked with depression as it is found to be active in a critical area of the brain for the disorder. The discovery looks promising and further studies will help us in determining what is going on.

Aurbach along with her mentor Huda Akil, Ph.D worked with several universities to make the discovery. The brain bank at the University of California, Irvine, was key to their work. Their study focussed on fibroblast growth factors, molecules involved in cell growth and maintenance in brain and in other parts of the body. For years, they have also studied FGF2 molecules and have tried to figure out why its levels are low in people with depression and other mental health issues. That is why the researchers were surprised when FGF9 levels were found higher in the brains of people who had depression compared to those who had not.

The researchers made the finding using post-mortem brain samples from the Pritzker collection�36 depressed and 56 non-depressed brains in all. It took three different kinds of microarray gene expression studies and a confirming test called quantitative PCR, to look at all the genetic activity that was going on when these brain donors died, specifically in the hippocampus of the brain. Crucial for memory, learning and stress control, this area of the brain is found to be smaller in people with depression. Their experiment showed higher FGF9 levels in the depressed brains. Also, the levels of several other fibroblast growth factors were down when FGF9 was up.

These results intrigued them to experiment further on rats. They tried to determine if FGF9 rises in response to something, like stress, or if levels are naturally higher and predispose someone to depression. When they exposed the rats to social stress for 10 days, the FGF9 level in various regions of the brain’s hippocampus increased and the rats began to exhibit more depression like symptoms. They even experimented by injection FGF9 injections into the rat brains and the rats began showing depression like behavior.

In the next stage of their research, Aurbach, Akil and their colleagues are performing more experiments to find out why FGF9 production rises, how FGF9 levels affect other brain regions and communication among brain cells. Since, the molecule is important in the lungs and blood vessels, caution is very much needed in finding the right for medications to affect FGF9 levels.

A patent application has also been filed and is being managed by the Pritzker Consortium.

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References

https://medicalxpress.com/news/2015-09-factor-depression-brain-protein-discovery.html

https://www.uofmhealth.org/news/archive/201509/new-factor-depression-brain-protein-discovery-could-lead

Scientists Discover Potential Treatment for Parkinson’s Disease

Oct 19, 2015

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Parkinson’s Disease

Parkinson's disease affects an estimated 10 million people worldwide. But, there is no known treatment that can cure or slow down the disease. Therefore, the news that scientists from Singapore’s Nanyang Technological University (NTU Singapore) and McLean Hospital and Harvard Medical School in the United States have found a potential treatment for Parkinson’s disease is particularly heartening. Reports reveal that scientists are positive that an existing anti-malaria drug could be useful in the treatment of this disease. This groundbreaking research was published recently in Proceedings of the National Academy of Sciences of the United States of America (PNAS) online, a prestigious peer-reviewed scientific journal.

Parkinson’s disease, a degenerative disorder of the central nervous system is characterized by a loss of control of motor movements, such as the ability to move hands, arms, and legs. In Singapore, it is one of the most common neurodegenerative conditions that affects three out of every 1,000 persons aged 50 years and above. Since, the population in Singapore is aging, cases of neurodegenerative diseases are very likely to rise.

Professor Kwang-Soo Kim from McLean Hospital and Harvard Medical School in the United States and Associate Professor Yoon Ho Sup from NTU’s School of Biological Sciences partnered together for this multi-year research project. The researchers had discovered that by activating Nurr1, a class of proteins found in the brain, the brain’s ability to generate dopamine neurons is protected.

Nuclear magnetic resonance (NMR) spectroscopy was used by the scientists to identify the compounds which could bind and activate Nurr1 in the brain. We all know dopamine as the chemical in the brain that generates good and pleasurable feelings. In addition to that it is also an important neurotransmitter that affects motor control and movement of muscles in the body. When a person is affected with Parkinson's disease, the production of dopamine is disrupted and it causes progressive loss of motor control.

In their lab experiments, scientists found that when Nurr1 was activated in rats which had Parkinson's disease, there was a marked improvement in their behaviour and they showed no signs of suffering from the disease. Associate Professor Yoon said the team had screened about 1000 FDA-approved drugs before they found two anti-malaria drugs which showed results – Chloroquine and Amodiaquine.

Associate Professor Yoon, an expert in drug discovery and design opined that their discovery brings hope for the millions of people suffering from Parkinson’s disease. These drugs that they have found to have worked in the laboratory tests have already been used to treat malaria in patients for decades. He said that their research also shows that existing drugs can be repurposed to treat other diseases and once several potential drugs are found, they can be redesigned to make them more effective in combating their targeted diseases while reducing the side effects.

Professor Kwang-Soo Kim, a leading expert in Parkinson’s disease, said that presently the dopamine levels in patients are replenished through medication or by using a surgical method to do deep brain stimulation using electric currents. These treatments do address the patient’s symptoms, such as to improve mobility functions in the early stages of the disease to a certain extent, but the treatments are not effective in slowing down or stopping the disease process.

There have been several scientific evidences which have suggested the role Nurr1 can play in treating Parkinson's disease. Even though efforts have been put by pharmaceutical companies and researchers, no breakthrough development happened until now. Both Chloroquine and Amodiaquine are approved by the US Food and Drug Administration and are used treat malaria infections. They are also looking forward to design better drugs for the disease by modifying Chloroquine and Amodiaquine.

For further research, the scientists are now looking into studying more drugs which can halt and reverse the onset of Parkinson’s disease.

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References

https://medicalxpress.com/news/2015-07-scientists-potential-treatment-parkinson-disease.html

https://www.theonlinecitizen.com/2015/07/singapore-scientists-discover-potential-treatment-for-parkinsons-disease/

Researchers Create Model of Early Human Heart Development from Stem Cells

Oct 18, 2015

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Breakthrough results in early human heart development from stem cells have been achieved by the scientists at the University of California, Berkeley in association with researchers at the Gladstone Institute. The results of the experiment have been published in the Journal of Nature Communications. A template for growing beating cardiac tissue from stem cells has been developed; thus, creating a system that could serve as a model for early heart development and a drug-screening tool to make pregnancies safer. Biochemical and biophysical cues were used by researchers to prompt stem cells to differentiate and self-organize into micron-scale cardiac tissue, including micro chambers.

Kevin Healy, a UC Berkeley professor of bioengineering, and a co-senior author of the study said that it is the first example illustrating the process of a developing human heart chamber in vitro. He is positive about this technology and is hopeful that it would help in quickly screen for drugs that are likely to generate cardiac birth defects, and thereby help doctors in pointing out the drugs that can be potentially dangerous during pregnancy.

In order to test the potential of the system as a drug screening tool, differentiating cells were exposed to thalidomide � a drug that is known to cause severe birth defects. It was found that even at normal therapeutic doses, the drug led abnormalities in the hearts micro chambers like decreased size, problems with muscle contraction and lower beat rates.

Dr. Bruce Conklin, a senior investigator at the Gladstone Institute of Cardiovascular Disease, a professor of medical genetics and cellular and molecular pharmacology at UC San Francisco and a co-author of the study said that drug cardiac developmental toxicity screening was specifically chosen to demonstrate a clinically relevant application of the cardiac micro chambers. He opined that every year about 280,000 pregnant women are exposed to drugs with evidence of potential fetal risk. Birth defects involving the heart are the most common, and that is the reason why drug safety during pregnancy is of utmost importance.

For this new study, the scientists mimicked human tissue formation by starting with stem cells that were genetically reprogrammed from adult skin tissue to form small chambers with beating human heart cells. The undifferentiated stem cells were then placed onto a circular-patterned surface that served to physically regulate cell differentiation and growth. After 2 weeks, the cells that had started on a two-dimensional surface environment started taking on a 3D structure as a pulsating micro chamber. Also, the cells had self-organized based upon whether they were positioned along the perimeter or in the middle of the colony. It was also observed that cells along the edge experienced greater mechanical stress and tension, and appeared more like fibroblasts, which form the collagen of connective tissue as compared to the cells in the center. The center cells on the other hand developed into cardiac muscle cells. This spatial organization was observed as soon as the differentiation started. Center cells lost the expression of octamer-binding transcription factor 4 (OCT4) and epithelial cadherin (E-cadherin) faster than perimeter cells, which are important to the development of heart tissue.

Zhen Ma, a UC Berkeley postdoctoral researcher in bioengineering and study's lead author said that such spatial differentiation happens in biology naturally, but it was demonstrated by them through this process in vitro. The confined geometric pattern provided biochemical and biophysical cues that directed cardiac differentiation and the formation of a beating micro chamber.

Healy opined that since patient-derived human pluripotent stem cells were used in this experiment, it made a huge difference in the results. Previous similar studies used harvested rat cardiomyocytes, which is not a suitable model for human disease. This technology holds great potential to study other organ development as well.

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References

https://medicalxpress.com/news/2015-07-early-human-heart-stem-cells.html

https://news.berkeley.edu/2015/07/14/early-human-heart-development-stem-cells-model/

New Findings Hint toward Reversing Hearing Loss

Oct 17, 2015

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When it comes to recovering lost hearing ability, birds and amphibians have more advantages than mammals. In humans, the cells present in the inner ear endowed with the responsibility of detecting sound and transmitting those signals to brain develop during very early stage of development. If due to any reason � say injury, illness or aging, the hearing ability is lost it cannot be replaced.

Scientists at the Washington University School of Medicine in St. Louis have identified two signaling molecules that are important for the right development of cochlea � a part of the inner ear. If these signaling molecules are not present, the embryo doesn't produce enough cells which eventually form the adult cochlea. That can result in shortened cochlear duct and impaired hearing. This study is a step towards understanding inner ear development, which will take us near towards the goal of being able to recover lost hearing. One can check the study online in the journal eLife.

David M. Ornitz, MD, PhD, the Alumni Endowed Professor of Developmental Biology and senior author of the study said that in order to eventually be able to restore hearing, regeneration of the sensory hair cells of the cochlea is important. In case of birds and fishes, if the cells in the inner ear are damaged, those cells are naturally turned back into progenitor cells that are capable of replacing the sensory cells. But, mammals are more complex organisms. They boast of a better sense of hearing over a wider range of sounds, but they do not have the ability to regenerate sensory hair cells.

In this new study, Ornitz and his colleagues shave found that proper inner ear development in mice depends on the presence of two signaling molecules called FGF9 and FGF20. In mice, the normal signaling of these molecules in the inner ear turns on at about day 11 of the mouse embryo’s typical 20-day development. It takes another two to three days for these two molecules to direct the progenitor cells to multiply. By embryonic day 14, the progenitor cells stop multiplying and begin to differentiate to become functional adult sensory cells. At this point, the cellular population that comprises the adult ear is largely complete. It has been deduced that if the FGF signals are not present during inner ear development, shortened cochlea and impaired hearing are likely.

Study's first author Sung-Ho Huh, PhD, instructor in developmental biology added that in mammals, including mice and people, the number of sensory progenitor cells is fixed. This number is determined by cell division or cell death in early stages of development. Between embryonic days 11 and 14 is the period when it happens in mice. When that developmental window closes, the number of cells that are formed is all you get. There is no compensation if the number of these cells is low.

This new study reveals that FGF9 and FGF20 send signals to their receptors, located in nearby cells surrounding the developing sensory cells. Through signaling to these surrounding cells, FGF9 and FGF20 promote the growth of the sensory progenitor cells. A feedback loop is activated through this signaling that helps to direct proper development of the cochlea. Ornitz and Huh are of the opinion that future work will be focused on identifying the molecules involved in the feedback mechanism.

Ornitz said that it has been discovered by us that an FGF signal is instructive in forming the cochlea. These are the signals that tell the surrounding tissue to make a factor which regulates the progenitor cell growth. We need to find out what this factor is � it is crucial to finding the key to restoring hearing.

References:

https://medicalxpress.com/news/2015-07-hint-reversing-loss.html

https://news.wustl.edu/news/Pages/New-findings-hint-toward-reversing-hearing-loss.aspx

Chemists Develop Novel Drug to Fight Malaria

Oct 16, 2015

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Malaria � a mosquito borne disease is one of the deadly diseases to affect mankind; it kills more than 500,000 people annually. A team of researchers led by scientists from the University of Washington and two other institutions has some great news to share. They have created a new compound that can strengthen the fight against malaria and the compound is ready for human trials.

The research paper was published in Science Translational Medicine recently. The news revealed that this compound has the capacity to cripple a critical protein which is essential for the malaria parasite to survive at different stages of its complex life cycle. If the said clinical trials on humans are successful, the compound known by its acronym DSM265�could equip the doctors with a new tool to prevent and treat infection by the microscopic parasites that cause malaria. This novel anti-malarial drug is the team's first major breakthrough for use in humans.

The team made great efforts to identify and optimize chemical compounds that show promise against malaria parasites. The scientists in this research belong to various international institutes�spanning 20 institutions on three continents. They pooled their collective expertise and accelerated the pace of discovery and validation.

UW chemistry professor Pradipsinh Rathod, one of the founders and leaders of this research project said that this is the first of a new class of molecules that’s going into humans. Till date, everything used against malaria had been variations of the drugs that were developed in the distant past.

DSM265 acts on a cellular protein – known by its acronym DHODH- made by the malaria parasite. This protein is critical for the malaria parasite to express their genes and copy them when it’s time to divide. Since, the role of DHODH is a critical one for these parasites; this drug could impair the parasite at multiple stages of its life cycle � one of the most important being when it hides in the human host’s liver.

All the enabling chemistry work was done at Rathod's UW lab and all the tests on malaria parasite cells and human cells started and have continued there. Scientists had long sought drugs that would inactivate DHODH. The Texas researchers studied the malaria DHODH protein, and worked on identifying a chemical compound that would cripple it. When they found a chemical that seemed promising, Rathod’s lab undertook validation, modification, and fine-tuning. With additional able guidance and collaboration from advisors at the Medicines for Malaria Venture, Rathod’s group altered the chemical compound to increase its potency against DHODH. Rathod's group made more than 500 versions of the initial compound and the found the 265^th � DSM265 � to be most promising.

‘DSM’ stands for ‘Dallas-Seattle-Melbourne,’ the three cities where the founding teams were working on this project. The DSM265 and related compounds were then passed onto their collaborators at Monash University, who tested how human cells might modify or metabolize the compound. They carried out experiments to ensure that a drug based on DSM265 would last long enough in our bodies for a single-dose anti-malarial treatment. Rathod’s lab also developed and performed experiments to test how well the malaria parasite might evolve to become resistant against DSM265. If the conditions that permit the malaria parasite to develop resistance to DSM265 are known, the drug’s use can be tailored in a clinical setting to lower that risk.

Rathod has high hopes that the development and discovery pipeline for DSM265 will make the way for a faster and more collaborative drug development process in the long war against the deadly disease.

References

https://medicalxpress.com/news/2015-07-chemists-drug-malaria.html

https://www.washington.edu/news/2015/07/15/uw-chemists-help-develop-a-novel-drug-to-fight-malaria/

Antidepressants And Pain Killers—Should We Be Worried?

Oct 15, 2015

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Is the combined use of antidepressants and pain killers risky? Well, the answer may well surprise you. According to new research there is an increased risk of brain hemorrhage when painkillers like ibuprofen and antidepressant medicines are used together. With the increased use of pain killers and antidepressants, it seems there is really something that we need to be worried about. Dr. Rupert Payne from the Cambridge Centre for Health Services Research delves deeper into the evidence.

Popping in those pain killer pills to get relief from headache, or to soften those sore joints is fairly common. We often take these pills to reduce the symptoms of common cold. Some of these drugs commonly used by people � like ibuprofen belong to a class of drugs called NSAIDS – non-steroidal anti-inflammatory drugs. The use of these medicines is widespread; in fact, they are amongst the top-twenty most frequently prescribed medications in UK primary care. Many of these medicines are non-prescription and can easily be bought from supermarket shelves � where there is no pharmacists to keep a check on it.

Similarly, antidepressants are also commonly used in the UK; although these medicines are prescription only. One interesting thing to note here is that often depression and chronic pain co-exist in people. By a rough estimate a third of those suffering from a painful condition also experience depression, and over a quarter of those suffering depression also report of having chronic pain.

A recent study published in British Medical Journal has identified that there in an increase in the risk of brain hemorrhage when antidepressants and NSAIDS are used together. That surely raises concerns � but the question remains is that really so straightforward?

It is already known that combined used of antidepressants and NSAIDS can cause gastrointestinal bleeding � this already established risk is likely greater than the newly identified risk of brain haemorrhage. Despite that many GPs remain unaware of this problem, and their prescribing behaviour is not influenced by this study.

One point which must be taken into account is the fact that the risk of brain haemorrhage is relatively low: if both antidepressants and NSAIDS are taken daily for a period of 30 days, only one person in every 2,000 would be likely affected. Again, the absolute benefits of antidepressants and NSAIDs cannot be easily quantified, and are typically assessed in the context of the individual’s personal psychological and social circumstances. So, it is very difficult to find out the balance of harm and benefits.

If antidepressants and NSAIDs cannot be prescribed together, then doctors will understandably ask for alternatives. And the bad news is there are only limited options left. The crux of the matter is patients’ quality of life will be significantly diminished by stopping these medicines.

These are several other important questions which this recent study doesn't answer.

What are the longer-term risks? Are the risks same when the drugs are used separately? Can these findings be generalized when the study is based on an East-Asian population? Of course, there is a need for further research before concluding the risks. This new paper does identify a potential small risk of adverse consequences of combining two common drugs, but several queries still remain unresolved. If you are one among those who is prescribed both of these medicines, do discuss your concerns with your doctor.

Nevertheless, the issues raised by this study are important and quite relevant to safe and rational use of medicines. It is not uncommon for a person to be suffering from more than one ailment- so they may need to take a combination of drugs. So, further research to understand the challenges associated with using combinations of medicines in people with multiple health conditions is much needed.

Taking too many pain killers to banish joint pain? Try this natural pain killer.

References

https://medicalxpress.com/news/2015-07-antidepressants-pain-killersshould.html

https://www.washingtonpost.com/news/to-your-health/wp/2015/07/15/study-mixing-antidepressants-and-painkillers-associated-with-elevated-risk-of-bleeding/

Study Reveals New Clues to Help Understand

Oct 12, 2015

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For people who suffer from various psychiatric and neurological conditions, brain stimulation has become an increasingly important treatment option in the recent decades.

Deep Brain Stimulation

Brain simulation techniques can be divided into two broad categories, invasive and noninvasive. Both of them work by targeting specific sites in the brain to adjust the overall brain activity. Among the most well-known invasive techniques is the deep brain stimulation (DBS) which requires a brain surgery and is approved by the U.S. Food and Drug Administration (FDA). This process is typically used for treated Parkinson's disease and this process requires an electrode to be inserted in the brain. Among the noninvasive techniques is the transcranial magnetic stimulation (TMS) which can be administered from outside the head. This treatment is currently approved for treating depression.

Brain stimulation has resulted in dramatic benefits to patients with such disorders, which has motivated researchers to test if it can be useful in treated patients suffering from other diseases. The problem is that doctors have been unable to pinpoint which are the ideal sites to administer simulation in a given patient for a given condition.

A new study led by investigators at Beth Israel Deaconess Medical Center (BIDMC) in the Proceedings of the National Academy of Sciences (PNAS) suggest that brain networks which consists of the interconnected pathways that link brain circuits to one another can assist in selection of ideal spot for brain stimulation therapies.

Michael D. Fox, MD, PhD, First author of the study, an investigator in the Berenson-Allen Center for Noninvasive Brain Stimulation and in the Parkinson’s Disease and Movement Disorders Center at BIDMC remarked that although different types of brain stimulation are currently applied in different locations, it has been found that the targets used to treat the same disease are nodes in the same connected brain network. This can have a direct implication on how brain stimulations are administered to treat diseases.

For example, in order use brain stimulation to treat Parkinson’s disease or tremor an electrode need to be inserted deep in the brain. Getting the same effect with noninvasive stimulation is difficult, as the spot is deep in the brain. However, by looking at the brain’s network connectivity, sites can be identified on the surface of the brain that is connected with the deep spot site. Hence, that deep spot can also be stimulated noninvasively.

For this study Fox's team conducted a large-scale literature search to find out all neurological and psychiatric diseases where brain stimulation via both invasive and non-invasive techniques had shown improvement. The search found 14 such conditions namely addiction, Alzheimer’s disease, anorexia, depression, dystonia, epilepsy, essential tremor, gait dysfunction, Huntington’s disease, minimally conscious state, obsessive compulsive disorder, pain, Parkinson disease and Tourette syndrome. In the next step, they listed the stimulation sites, both deep in the brain or on the surface of the brain that was found to have been effective for the treatment of each of the 14 diseases.

In order to test the hypothesis that the various stimulation sites in the brain are different spots within the same brain network, Fox's team used a data base of functional MRI images and a technique that enabled them to see correlations in spontaneous brain activity. These correlations helped the investigators in creating a map of connections from deep brain stimulation sites to the surface of the brain. When this map was compared to sites for noninvasive brain stimulation on the brain surface, the two matched.

The study suggest that understanding the brain networks can help in understanding why brain stimulation works and how these therapies can be improved by identifying the best place to stimulate the brain for a given patient suffering from a given disease. These findings also suggest that resting-state functional connectivity can be useful for translating therapy between treatment modalities, optimizing treatment and identifying new stimulation targets.

References

https://www.eurekalert.org/pub_releases/2014-09/bidm-srn092514.php

https://www.sciencedaily.com/releases/2014/09/140929153935.htm

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