neurons Archives - Amazing Health Advances

The Decision to Eat May Come Down to These Three Neurons

The AHA! Team — Wed, 13 Nov 2024 06:38:18 +0000

Rockefeller University via Newswise – Speaking, singing, coughing, laughing, yelling, yawning, chewing—we use our jaws for many purposes. Each action requires a complex coordination of muscles whose activity is managed by neurons in the brain. But it turns out that the neural circuit behind the jaw movement most essential to survival—eating—is surprisingly simple, as researchers from Rockefeller University recently described in a new paper in Nature. Christin Kosse and other scientists from the Laboratory of Molecular Genetics, headed by Jeffrey M. Friedman, have identified a three-neuron circuit that connects a hunger-signaling hormone to the jaw movements of chewing. The intermediary between these two is a cluster of neurons in a specific area of the hypothalamus that, when damaged, has long been known to cause obesity. Strikingly, inhibiting these so-called BDNF neurons not only leads animals to consume more food but also triggers the jaw to make chewing motions even in the absence of food or other sensory input that would indicate it was time to eat. And stimulating them has the opposite effect, reducing food intake and putting a halt to the chewing motions, resulting in an effective curb against hunger. The simple architecture of this circuit suggests that the impulse to eat may be more similar to a reflex than has been considered—and may provide a new clue about how the initiation of feeding is controlled. “It’s surprising that these neurons are so keyed to motor control,” says study first author Christin Kosse, a research associate in the lab. “We didn’t expect that limiting physical jaw motion could act as a kind of appetite suppressant.” More than a feeling? The impulse to eat is driven not just by hunger but by many factors. We also eat for pleasure, community, ritual, and habit; and smell, taste, and emotions can impact whether we eat too. In humans, eating can also be regulated by the conscious desire to consume more or less. The causes of obesity are equally complex, the result of a dynamic interplay of diet, environment, and genes. For example, mutations in several genes—including those coding for the hunger-controlling hormone leptin and brain-derived neurotrophic factor (BDNF)—lead to gross overeating, metabolic changes, and extreme obesity, suggesting that both factors normally suppress appetite. When Friedman’s team began this study, they sought to pinpoint the location of the BDNF neurons that curtail overeating. That’s eluded scientists for years, because BDNF neurons, which are also primary regulators of neuronal development, differentiation, and survival, are widespread in the brain. In the current study, they homed in on the ventromedial hypothalamus (VMH), a deep-brain region linked to glucose regulation and appetite. It’s well-documented that damage in the VMH can lead to overeating and eventually obesity in animals and people, just as mutated BDNF proteins do. Perhaps the VMH played a regulatory role in feeding behavior. They hoped that by documenting BDNF’s impact on eating behavior, they could find the neural circuit underpinning the process of transforming sensory signals into jaw motions. They subsequently found that BDNF neurons in the VMH—but not elsewhere—are activated when animals become obese, suggesting that they are activated when weight is gained in order to suppress food intake. Thus, when these neurons are missing, or there is a mutation in BDNF, animals become obese. Chewing without food In a series of experiments, the researchers then used optogenetics to either express or inhibit the BDNF neurons in the ventromedial hypothalamus of mice. When the neurons were activated, the mice completely stopped feeding, even when they were known to be hungry. Silencing them had the opposite effect: the mice began to eat—and eat and eat and eat, wolfing down nearly 1200% more food than they normally would in a short period of time. “When we saw these results, we initially thought that perhaps BDNF neurons encode valence,” Kosse says. “We wondered if when we regulated these neurons, the mice were experiencing the negative feeling of hunger or maybe the positive feeling of eating food that’s delicious.” But subsequent experiments disproved that idea. Regardless of the food given to the mice—either their standard chow or food packed with fat and sugar, like the mouse equivalent of a chocolate mousse cake—they found that activating the BDNF neurons suppressed food intake. And because hunger is not the only motivation to eat—as anyone unable to skip dessert can attest—they also offered high-palatable food to mice that were already well fed. The animals chowed down until the researchers inhibited the BDNF neurons, at which point they promptly stopped eating. “This was initially a perplexing finding, because prior studies have suggested that this ‘hedonic’ drive to eat for pleasure is quite different from the hunger drive, which is an attempt to suppress the negative feeling, or negative valence, associated with hunger by eating,” Kosse notes. “We demonstrated that activating BDNF neurons can suppress both drives.” Equally striking was that BDNF inhibition caused the mice to make chewing motions with their jaw, directed at any object in their vicinity even when food was not available. This compulsion to chew and bite was so strong that the mice gnawed on anything around them—the metal spout of a water feeder, a block of wood, even the wires monitoring their neural activity. The circuit But how does this motor-control switch connect to the body’s need or desire for food? By mapping the inputs and outputs of the BDNF neurons, the researchers discovered that BDNF neurons are the linchpin of a three-part neural circuit linking hormonal signals that regulate appetite to the movements required to consume it. At one end of the circuit are special neurons in the arcuate nucleus (Arc) region of the hypothalamus that pick up hunger signals such as the hormone leptin, which is produced by fat cells. (A high amount of leptin means the energy tank is full, while a low leptin level indicates it’s time to eat. Animals with no leptin become obese.) The Arc neurons project to the ventromedial hypothalamus, where their signals are picked up by the BDNF neurons, which then project directly to a brainstem center called Me5 that controls the movement of jaw muscles. “Other studies have shown that when you kill Me5 neurons in mice during development, the animals will starve because they’re unable to chew solid foods,” says Kosse. “So it makes sense that when we manipulate the BDNF neurons projecting there, we see jaw movements.” It also explains why damage in the VMH causes obesity, Friedman says. “The evidence presented in our paper shows that the obesity associated with these lesions is a result of a loss of these BDNF neurons, and the findings unify the known mutations that cause obesity into a relatively coherent circuit.” The findings suggest something deeper about the connection between sensation and behavior, he adds. “The architecture of the feeding circuit is not very different from the architecture of a reflex,” says Friedman. “That’s surprising, because eating is a complex behavior—one in which many factors influence whether you’ll initiate the behavior, but none of them guarantee it. On the other hand, a reflex is simple: a defined stimulus and an invariant response. In a sense, what this paper shows is that the line between behavior and reflex is probably more blurred than we thought. We hypothesize that the neurons in this circuit are the target of other neurons in the brain that convey other signals that regulate appetite.” This hypothesis is consistent with the work of early 20th century neurophysiologist Charles Sherrington, who pointed out that while cough is regulated by a typical reflex, it can be modulated by conscious factors, such as the desire to suppress it in a crowded theater. Kosse adds, “Because feeding is so essential to basic survival, this circuit regulating food intake may be ancient. Perhaps it was a substrate for ever-more complex processing that occurred as the brain evolved.” To that end, in the future the researchers want to explore the brainstem area known as Me5 with the idea that the jaw’s motor controls might be a useful model for understanding other behaviors, including compulsive, stress-related mouth actions such as gnawing on a pencil eraser or strands of one’s hair. “By examining these premotor neurons in the Me5, we might be able to understand whether there are other centers that project into the region and influence other innate behaviors, like BDNF neurons do for eating,” she says. “Are there stress-activated or other neurons that project into there as well?” Journal Link: Nature To read the original article click here.

The post The Decision to Eat May Come Down to These Three Neurons appeared first on Amazing Health Advances.

NEW Research Links 3 More Pesticides to Parkinson’s Disease

The AHA! Team — Mon, 06 May 2024 18:41:51 +0000

Patrick Tims via NaturalHealth365 – The call to restrict or ban pesticide use is not mere alarmism; it’s grounded in substantial evidence and urgent necessity. Paraquat – a highly toxic herbicide – has long been linked to Parkinson’s disease. Now, a recent report has shed alarming light on the dire consequences associated with the use of three more pesticides. This latest analysis unequivocally demonstrates that these harmful chemicals, when applied to crops, are directly linked to the onset of Parkinson’s disease – a debilitating neurological disorder that robs individuals of their quality of life and independence. Pesticides used throughout the United States are now in the crosshairs The three pesticides currently under scrutiny are widely utilized in crop cultivation across the United States despite their potential to cause Parkinson’s disease. Despite being relatively unnoticed by many, there has been a concerning surge in the prevalence of Parkinson’s disease, mirroring the upward trend observed in several other neurological conditions. Research indicates that these toxic pesticides pose significant harm to brain neurons. While 14 pesticides have been associated with an elevated risk of Parkinson’s disease, the connection appears most pronounced with three specific pesticides. Parkinson’s disease manifests as the progressive loss of neurons in the brain, leading to debilitating immobility among patients. These neurons play a pivotal role in producing dopamine, a neurotransmitter crucial for transmitting signals throughout the brain. The decline or loss of such signaling capability profoundly compromises an individual’s motor control. Accumulation of the alpha-synuclein peptide within the neurons of Parkinson’s patients exacerbates neuron damage and impedes dopamine production, which is essential for signal transmission. Living in areas of high pesticide use increases risk of Parkinson’s disease Though the idea that chemicals might damage neurons in the brain was floated as early as the 1980s, it hasn’t been proven until recently. The research linked above will be formally presented this April at Denver’s American Academy of Neurology’s 76th annual meeting. Though the study has not been published in a peer-reviewed journal, it is only a matter of time until it reaches academic circles and mainstream society. The research, conducted by scholars from Washington University and Amherst College, sheds light on how the risk of Parkinson’s disease is closely tied to the extent of exposure to pesticides. These researchers delved into data concerning 21,549,400 individuals living in the USA and mapped the usage of pesticides across counties from 1992 to 2008. The findings showed that 14 pesticides were associated with a greater risk of Parkinson’s disease in the wide open spaces of America’s Great Plains and the rugged terrain of the Rocky Mountains. In particular, the pesticides atrazine, lindane, and simazine had the strongest link to heightened Parkinson’s risk. Simazine is an herbicide primarily used to control broadleaf weeds and grasses in various crops such as corn, sugarcane, citrus fruits, and ornamental plants. It can also be used to control weeds in non-crop areas such as highways, railways, and industrial sites. Lindane is an organochlorine insecticide – used to control pests in agriculture, forestry, and veterinary medicine. Lindane has also been used to treat lice and scabies infestations in humans and animals and to treat wood and seeds. Atrazine is a widely used herbicide primarily applied to control weeds in crops such as corn, sugarcane, sorghum, and other crops. It is also used in non-agricultural settings such as golf courses and residential lawns for weed control. The results of the study are deeply concerning: Those in areas with the highest atrazine use were 31% more likely to be diagnosed with Parkinson’s Those in areas with the highest lindane use were 25% more likely to be diagnosed with Parkinson’s Those in areas with the highest simazine use were 36% more likely to be diagnosed with Parkinson’s Though these three pesticides have been restricted in other countries, they are allowed in the United States. Strategies to reduce your exposure to toxic pesticides It’s crucial for every American to recognize that Parkinson’s disease has doubled in prevalence over the past 25 years. This condition is now the fastest-growing brain disorder worldwide, but you have the power to prevent yourself from becoming a statistic. Avoid fruits and vegetables that have been treated with pesticides. Instead of patronizing Big Box stores and corporate supermarkets that stock produce grown with pesticides, opt to shop locally at farmers’ markets, locally owned stores, and roadside stands that sell organic produce. Simply put, our food choices have the power to make this world less toxic and better for all of us. Sources for this article include: Aanfiles.bob.core.windows.net Medicalnewstoday.com Medpagetoday.com To read the original article click here.

The post NEW Research Links 3 More Pesticides to Parkinson’s Disease appeared first on Amazing Health Advances.

Saturated Fatty Acid Levels Increase When Making Memories

AHA Publisher — Tue, 06 Jul 2021 07:00:02 +0000

University of Queensland via EurekAlert – Saturated fatty acid levels unexpectedly rise in the brain during memory formation, according to research, opening a new avenue of investigation into how memories are made. Dr Tristan Wallis, from Professor Frederic Meunier’s laboratory at UQ’s Queensland Brain Institute (QBI), said traditionally, polyunsaturated fatty acids were considered important to health and memory, but this study highlighted the unexpected role of saturated fatty acids. “We tested the most common fatty acids to see how their levels changed as new memories were formed in the brain,” Dr Wallis said. “Unexpectedly, the changes of saturated fat levels in the brain cells were the most marked, especially that of myristic acid, which is found in coconut oil and butter. “In the kitchen, saturated fats are those which are solid at room temperature while unsaturated fats are normally liquid. “The brain is the fattiest organ in the body, being 60 per cent fat, which provides energy, structure and assists in passing messages between brain cells. “Fatty acids are the building blocks of lipids or fats and are vital for communication between nerve cells, because they help synaptic vesicles — microscopic sacs containing neurotransmitters–to fuse with the cell membrane and pass messages between the cells. “We have previously shown that when brain cells communicate with each other in a dish, the levels of saturated fatty acids increase.” Researchers have found that fatty acid levels in the rat brain, particularly saturated fatty acids, increase as memories are formed, but when they used a drug to block learning and memory formation in rats, the fatty acid levels did not change. The highest concentration of saturated fatty acids was found in the amygdala — the part of the brain involved in forming new memories specifically related to fear and strong emotions. Study contributor and QBI Director Professor Pankaj Sah said the work opened a new avenue on how memory was formed. “This research has huge implications on our understanding of synaptic plasticity — the change that occurs at the junctions between neurons that allow them to communicate, learn and build memories,” Professor Sah said. To read the original article click here.

The post Saturated Fatty Acid Levels Increase When Making Memories appeared first on Amazing Health Advances.

How Trauma Causes Inflammation & How to Begin Healing

AHA Publisher — Mon, 16 Nov 2020 08:00:00 +0000

Dr. Caroline Leaf – In Western thought, we see mental and physical health as two separate things, but this is not the case. Our thoughts and emotions, choice, life events, trauma and so on affect both our mental AND physical wellbeing. In this podcast (episode #225) and blog, I speak with leading functional medicine practitioner Dr. Will Cole about this mind-body connection, ways to reduce stress-induced inflammation, what adaptogens we should be taking to strengthen the mind and body, the best supplements for brain health, how to recognize and heal orthorexia, and more! When it comes to the mind-body connection, how we handle stress is incredibly important. Stressful life events and situations amplify our fight or flight state, which impacts the body’s adaptation to stress (through the HPA axis) and can negatively affect our health if not dealt with. In fact, although the stress hormone cortisol is designed to help regulate inflammation, if we are constantly stressed out, the flight or fight state upsets our natural cortisol cycles. This, in turn, can have many health repercussions because it throws the body into a state of disordered inflammation. Our body essentially starts working against us instead of for us! One example of this is adrenal fatigue. Adrenal fatigue does not just have to do with our adrenal glands; it is a brain-based issue, and it is related to our stress response and the HPA axis. It is related to how stressed we are, and for how long. If we want to start combating the negative effects of toxic stress on the body, we need to look at our lifestyle choices, including what we eat. As Dr. Cole notes in his book, The Inflammation Spectrum, every food we eat either fuels inflammation or fights it. This means that our ability to handle stress and deal with trauma will be affected by our diet. Food is medicine, yes, but this also means you should find out what your body loves—what is medicine for you? There is no cookie-cutter approach for everyone. Processed and refined sugar, for example, is an inflammatory food for everyone, but we will react to sugar in different ways and at different levels. There is an inflammation spectrum—everyone’s body is different. Just because it is your experience, doesn’t mean it is someone else’s experience. One thing that everyone can benefit from is adding adaptogens to their diet. As Dr. Cole describes in both Ketotarian and The Inflammation Spectrum, adaptogens are plant and earth medicines that are found all over the world. They have been used in traditional medicine to help bring balance to the body and promote healing and longevity. Science is only now starting to study adaptogens and showing how many of these plants (like holy basil and rhodiola) can bring back homeostasis in the brain and body by balancing the HPA axis and reducing toxic stress-induced inflammation. They are accessible, easy to use and are a great complement to any wellbeing regimen, as Dr. Cole noted in a recent guest blog on our site. They also help with memory formation and can improve our ability to handle anxiety. Adaptogens like chaga and lion’s mane mushrooms, for example, can boost brain-derived neurotrophic factor (BDNF), which helps grow new neurons and improve neuroplasticity (the ability of the brain to change, adapt and grow). They essentially make us more resilient physically, which helps us deal with our issues mentally! Certain supplements can also help boost our diet and ability to handle stress: 1. Methylated B vitamins, which are needed for a healthy brain, hormone levels, immune system and so on. How much you need will depend on your unique health needs and biology, so see your health professional before taking any B vitamin supplements. In fact, methylation helps support good genetic function in the brain and body. How? As we now know, our genetics are not our destiny. They are light switches that are being constantly regulated by the choices we make every day and the environment we live in. Methylation is one way to make sure these light switches function as they should by switching on more good genes and switching off more bad genes. 2. Vitamin D3 and K2 is very important for the brain and immune system. D3 acts like a hormone and helps regulate many biological functions. K2 is also important and helps regulate inflammation and keep the body running well. Many people can’t get K1 from the plant foods they eat because their gut microbiome is comprised, so adding K2 to the diet through foods like organ meats, ghee, certain fermented foods and supplements can be helpful. 3. Curcumin, which helps balance inflammation levels. This gives turmeric its rich, yellow color. 4. Omega fish oil. You can get shorter train omegas from nuts and seeds, but the conversion is not always great. Fish or Krill oil supplements and wild-caught fish contain longer chain omegas, which are more bioavailable. 5. Probiotics, which help balance the microbiome and make sure the gut-brain connection functions as it should. Prebiotics, which are fibers in plant food that help feed the healthy bacteria in your gut, are also important. All these supplements are available on Dr. Cole’s website. Remember, when it comes to supplements and health products, you often get what you pay for. Mass-produced, cheaper health products generally do not always work or give you all the health benefits you expect. Some may even cause more harm than good, so always try find reputable companies that sell tested and good-quality products. And make sure to consult your health professional before taking any supplements, as everyone’s physical needs are different. We also need to remember that we cannot supplement our way out of a poor diet or toxic mindset. What we eat affects how we think, and what we think affects how we eat and our overall health, as I discuss in my book Think and Eat Yourself Smart. Mind management and self-regulating our thinking is essential when it comes to our health! We can go several weeks without eating, but we cannot go a few seconds without thinking. How we think about food is also important when dealing with disordered eating patterns like orthorexia. As Dr. Cole describes in his guest blog for our site, orthorexia is related to healthy eating—someone with orthorexia is hyper-focused and obsessed with healthy eating. Some of the warning signs (in context) are: A fear of food and how the body reacts to food Constantly judging others for eating a certain way Feeling isolated and avoiding going out to eat with friends If you or someone you know is battling with orthorexia, remember that you cannot stress and obsess your way into wellness. Just start where you are and at your specific capacity. Start low and slow, and don’t feel like you must solve all your problems over night. Try make incremental changes over time. The more you feel healthy, the more you will be healthy and make good lifestyle changes to sustain your sense of wellbeing. It is also important to remover that any wellness practice can be abused if your mind is not in a good place. So, always examine your intentions. Why are you doing this? What is your goal? How is it affecting you? Is this practice benefiting, or harming, your mental health?

The post How Trauma Causes Inflammation & How to Begin Healing appeared first on Amazing Health Advances.

New Gut-Brain Link: How Gut Mucus Could Help Treat Brain Disorders

AHA Publisher — Sat, 30 May 2020 07:00:29 +0000

RMIT University via EurekAlert – Changes in gut mucus could be contributing to bacterial imbalance and exacerbating core symptoms of brain disorders like autism, Parkinson’s disease, Alzheimer’s and Multiple Sclerosis. Mucus is the first line of defence against bad bacteria in our gut. But could it also be part of our defence against diseases of the brain? Bacterial imbalance in the gut is linked with Alzheimer’s disease, autism and other brain disorders, yet the exact causes are unclear. Now a new research review of 113 neurological, gut and microbiology studies led by RMIT University suggests a common thread – changes in gut mucus. Senior author Associate Professor Elisa Hill-Yardin said these changes could be contributing to bacterial imbalance and exacerbating the core symptoms of neurological diseases. “Mucus is a critical protective layer that helps balance good and bad bacteria in your gut but you need just the right amount – not too little and not too much,” Hill-Yardin said. “Researchers have previously shown that changes to intestinal mucus affect the balance of bacteria in the gut but until now, no-one has made the connection between gut mucus and the brain. “Our review reveals that people with autism, Parkinson’s disease, Alzheimer’s and Multiple Sclerosis have different types of bacteria in their gut mucus compared with healthy people, and different amounts of good and bad bacteria. “It’s a new gut-brain connection that opens up fresh avenues for scientists to explore, as we search for ways to better treat disorders of the brain by targeting our ‘second brain’ – the gut.” Gut mucus is different depending on where it’s found in the gastrointestinal tract – in the small intestine it’s more porous so nutrients from food can be easily absorbed, while in the colon, the mucus is thick and should be impenetrable to bacteria. The mucus is full of peptides that kill bacteria, especially in the small intestine, but it can also act as an energy source, feeding some of the bacteria that live inside it. Gut Neurons and Brain Disorders Scientists are learning that brain disorders can affect neurons in the gut. For example, RMIT researchers have shown that neurons in both the brain and the gut nervous systems are affected in autism. The new review suggests that reduced gut mucus protection may make patients with neurological diseases more susceptible to gastrointestinal problems. Hill-Yardin said severe gut dysfunction could exacerbate the symptoms of brain disorders, significantly affecting quality of life for patients and their families. “If we can understand the role that gut mucus plays in brain disease, we can try to develop treatments that harness this precise part of the gut-brain axis,” she said. “Our work shows that microbial engineering, and tweaking the gut mucus to boost good bacteria, have potential as therapeutic options for neurological disorders.” To read the original article click here.

The post New Gut-Brain Link: How Gut Mucus Could Help Treat Brain Disorders appeared first on Amazing Health Advances.

Scientists Create Artificial Neurons that Help Cure Chronic Diseases

AHA Publisher — Wed, 11 Dec 2019 08:00:47 +0000

Angela Betsaida B. Laguipo, BSN via News Medical-Net – Artificial brain cells could now be implanted in the brain to repair the damage caused by chronic diseases, such as Alzheimer’s disease and other neurodegenerative conditions, thanks to a team of scientists who created bionic neurons that work like the real thing. A team of scientists at the University of Bath created artificial neurons that could potentially help overcome paralysis, connect minds to machines, and restore failing brain circuits. The new technology can help patients who have degenerative diseases affecting the brain. Just like real neurons, the bionic neurons, which were described in a study published in Nature Communications, receive electrical signals from healthy neurons, process them, and send new signals to other neurons, muscles or organs in the body. Challenging But Worth the Wait Aside from working like real neurons, the artificial brain cells require only 40 nanowatts of power, which is one-billionth the power of a microprocessor. The invention is the fruit of years of collaboration and hard work, which faced many struggles along the way. It took decades for scientists to design artificial neurons that respond to electrical signals from the nervous system. The new technology could open new possibilities in the cure and treatment of conditions wherein the neurons are faulty and are not properly working. Using artificial neurons, the scientists believe that can repair diseased bio-circuits by duplicating their proper functioning and responding properly to biological feedback to restore body functions. For instance, in people with heart failure, the neurons in the brain base do not respond appropriately to the nervous system feedback and do not send the correct signals to the heart, unable to pump properly as well. If the patients have artificial neurons, their hearts will normally work again. The scientists plan to replicate the artificial neurons since they can be used in the treatment of brain illnesses that are characterized by brain cell death, including Alzheimer’s disease. “Until now, neurons have been like black boxes, but we have managed to open the black box and peer inside. Our work is paradigm-changing because it provides a robust method to reproduce the electrical properties of real neurons in minute detail,” Professor Alain Nogaret, from the University of Bath’s department of physics, said. Neuron Response to Electrical Stimuli The researchers derived equations that shed light on how nerve cells respond to electrical stimuli from other nerves. Though the process is complicated since the responses are non-linear, they might be three times bigger or more. Further, the team devised silicon chips that accurately modelled biological ion channels, imitating real and live neurons that can respond to a broad range of stimulations. After successfully replicating the processes and dynamics of respiratory and hippocampal in laboratory mice, the researchers believe that they are a step closer to creating the world’s first artificial neurons to help curb many diseases and help thousands of people. “Until now neurons have been like black boxes, but we have managed to open the black box and peer inside. Our work is paradigm changing because it provides a robust method to reproduce the electrical properties of real neurons in minute detail,” Prof. Nogaret said. He explained that the team’s approach incorporates many breakthroughs, and now, they can estimate the accurate parameters that control any nerve cell behavior with high precision. “We have created physical models of the hardware and demonstrated its ability to successfully mimic the behaviour of real living neurons. Our third breakthrough is the versatility of our model which allows for the inclusion of different types and functions of a range of complex mammalian neurons,” he added. The team is hopeful that they can finally use their model. The study opens up a broad range of possibilities in repairing the nerve cell that have been lost or had died due to degenerative disease, such as Alzheimer’s and heart disease. The study was carried out with the help of the University of Bristol, University of Zurich, and University of Auckland. To read the original article click here.

The post Scientists Create Artificial Neurons that Help Cure Chronic Diseases appeared first on Amazing Health Advances.

Dealing a Therapeutic Counterblow to Traumatic Brain Injury

AHA Publisher — Mon, 07 Oct 2019 07:00:00 +0000

New Jersey Institute of Technology via EurekAlert – To date, there is no effective treatment for restoring damaged neurons. The body’s protective mechanisms also make it difficult to penetrate the blood-brain barrier, which hampers the delivery of medications. A blow to the head or powerful shock wave on the battlefield can cause immediate, significant damage to a person’s skull and the tissue beneath it. But the trauma does not stop there. The impact sets off a chemical reaction in the brain that ravages neurons and the networks that supply them with nutrients and oxygen. It is the secondary effects of traumatic brain injury (TBI), which can lead to long-term cognitive, psychological and motor system damage, that piqued the interest of a team of NJIT biomedical engineers. To counter them, they are developing a therapy, to be injected at the site of the injury, which shows early indications it can protect neurons and stimulate the regrowth of blood vessels in the damaged tissue. The challenge, researchers say, is that brain cells don’t regenerate as well as other tissues, such as bone, which may be an evolutionary strategy for preserving the synaptic connections that retain memories. To date, there is no effective treatment for restoring damaged neurons. The body’s protective mechanisms also make it difficult to penetrate the blood-brain barrier, which hampers the delivery of medications. “Nerve cells respond to trauma by producing excessive amounts of glutamate, a neurotransmitter that under normal conditions facilitates learning and memory, but at toxic levels overexcites cells, causing them to break down. Traumatic brain injury can also result in the activation and recruitment of immune cells, which cause inflammation that can lead to short- and long-term neural deficits by damaging the structure around cells and creating a chronic inflammatory environment,” says Biplab Sarkar, a post-doctoral fellow in biomedical engineering and member of the team that presented this work at a recent American Chemical Society conference. The team’s treatment consists of a lab-created mimic of ependymin, a protein shown to protect neurons after injury, attached to a delivery platform – a strand of short proteins called peptides, contained in a hydrogel – that was developed by Vivek Kumar, director of NJIT’s Biomaterial Drug Development, Discovery and Delivery Laboratory. After injection, the peptides in the hydrogel reassemble at the localized injury site into a nanofibrous scaffold that mimics extracellular matrix, the supporting structure for cells. These soft materials possess mechanical properties similar to brain tissue, which improves their biocompatibility. They promote rapid infiltration by a variety of stem cells which act as precursors for regeneration and may also provide a biomimetic niche to protect them. Now in preclinical animal trials, rats injected with the hydrogel retained twice as many functioning neurons at the injury site as compared to the control group. They also formed new blood cells in the region. “The idea is to intervene at the right time and place to minimize or reverse damage. We do this by generating new blood vessels in the area to restore oxygen exchange, which is reduced in patients with a TBI, and by creating an environment in which neurons that have been damaged in the injury are supported and can thrive,” Kumar says. “While the exact mechanism of action for these materials is currently under study, their efficacy is becoming apparent. Our results need to be expanded, however, into a better understanding of these mechanisms at the cellular level, as well as their long-term efficacy and the resulting behavioral improvements.” Collaborators James Haorah, an associate professor of biomedical engineering, and his graduate student Xiaotang Ma at NJIT’s Center for Injury Biomechanics, Materials and Medicine have shown how a number of TBI-related chemical effects can disrupt and destroy integral brain vasculature in the blood-brain barrier, the brain’s protective border, promoting chronic inflammation that can lead to symptoms such as post-traumatic stress disorder and anxiety, among others. Their current work provides insights into the potential neuroprotective and regenerative response guided by the Kumar lab’s materials, while future studies will attempt to analyze other mediators of inflammation and blood flow in the brain. Kumar’s delivery mechanism is a customizable, Lego-like strand made of short proteins called peptides, which are composed of amino acids, with a biological agent attached at one end that can survive in the body for weeks and even months, where other biomaterials degrade quickly. Its self-assembling bonds are designed to be stronger than the body’s dispersive forces; it forms stable fibers, with no signs of inducing inflammation, that rapidly incorporate into specific tissues and collagen, recruiting native cells to infiltrate. The hydrogel, which is also composed of amino acids, is engineered to trigger different biological responses depending on the payload attached. These platforms can deliver drugs and other small cargo over day-, week- or month-long periods. Kumar’s lab has recently published research on applications ranging from therapies to prompt or prevent the creation of new blood vessel networks, to reduce inflammation and to combat microbes. “The ultimate hope is that that localized delivery of regenerative materials may provide significant benefits for a number of pathologies,” he notes. For example, the team recently developed a class of materials that may be useful against infection. These novel anti-microbial peptides are capable of disrupting dense bacterial colonies and have shown promise against a number of yeasts. Additionally, they promote human cell proliferation and are currently being studied for wound healing. That work was published this summer in the journal ACS Biomaterials Science and Engineering. Kumar and his lab have created another hydrogel designed to recruit autologous (a person’s own) dental pulp stem cells directly to the disinfected cavity after root canal therapy. The tooth would be regenerated in part by prompting growth of the necessary blood vessels to support the new tissue. Yet another peptide-based therapy, armed with antiangiogenic capabilities, targets diabetic retinopathy, an ocular disease affecting more than 90 million people worldwide. People with the disease form immature blood vessels in the retina, obstructing their vision. The hydrogel can be injected directly into the vitreous gel of the eye, where the peptide interacts with the endothelial cells in the aberrant blood vessels, causing them to die. “Conventional biomaterials used in tissue regeneration suffer from a variety of problems with delivery, retention and biocompatibility, which can lead to rejection by the host,” Kumar says. “We’re trying to address these issues with a technology designed to be universal in its application, delivering materials that persist in the tissue and promote their biologic effects for long periods of time.” To read the original article click here.

The post Dealing a Therapeutic Counterblow to Traumatic Brain Injury appeared first on Amazing Health Advances.

Neurons Promote Growth of Brain Tumor Cells

AHA Publisher — Sat, 28 Sep 2019 02:48:35 +0000

German Cancer Research Center via EurekAlert – Glioblastomas invade the healthy brain in a diffuse pattern like a fungal network. As a result, they cannot be completely removed by surgery, and they also survive intensive chemotherapy and radiotherapy. Glioblastomas are thus among the most dangerous tumors in humans; the average survival time is 15 months following the initial diagnosis. Joint press release by Heidelberg University Hospital and the German Cancer Research Center In a current paper published in the journal “Nature”, Heidelberg-based researchers and physicians describe how neurons in the brain establish contact with aggressive glioblastomas and thus promote tumor growth / New tumor activation mechanism provides starting points for clinical trials. Neurons transmit their signals to each other via synapses, fine cell projections with terminals that contact another neuron. Researchers and physicians at Heidelberg University Hospital, Heidelberg Medical Faculty, and the German Cancer Research Center (DKFZ) have now discovered that neurons in the brain form these kinds of direct cell-to-cell contacts with tumor cells of aggressive glioblastomas too, thus transmitting impulses to the cancer cells. The tumor benefits from this “input”: The activation signals are probably a driving force behind the tumor growth and the invasion of healthy brain tissue by tumor cells, as Frank Winkler, Thomas Kuner, and their teams discovered using special imaging methods. But there is also some good news: Certain substances can block the signal transmission in animal experiments. The results have just been published online in the journal “Nature”. Networks of Neurons and Tumor Cells Glioblastomas invade the healthy brain in a diffuse pattern like a fungal network. As a result, they cannot be completely removed by surgery, and they also survive intensive chemotherapy and radiotherapy. Glioblastomas are thus among the most dangerous tumors in humans; the average survival time is 15 months following the initial diagnosis. In 2015, the team led by Frank Winkler, head of the Research Group Experimental Neurooncology in the Clinical Cooperation Unit Neurooncology, discovered a cause of this resistance to treatment: The glioblastoma cells are connected to one another through long cell protrusions. They communicate through these connections, exchange substances that are relevant for their survival, and thus protect themselves from treatment-related damage. The current findings add a further piece of the puzzle to our understanding of this type of cancer: “The tumor cells are not only interconnected in the brain like neurons; they also receive direct signals from them,” explained Winkler, whose research group is affiliated with the University Hospital and the DKFZ. The researchers observed the growth of human glioblastomas that they had transferred to mice, and studied cell cultures with human neurons and tumor cells, and tissue samples from patients. To do so, they used a wide range of modern microscopy methods, which provide detailed three-dimensional images of the connections – only micrometers large – between neurons and tumor cells as well as showing their molecular structure and signals within the cells. Electrical recordings from tumor cells revealed electrical currents generating from the synaptic connections, which form the starting point for further processing of these signals in the tumor cells. “We were able to show that signal transmission from neurons to tumor cells does in fact work like stimulating synapses between the neurons themselves,” added Thomas Kuner, Director of the Department of Functional Neuroanatomy at the Institute for Anatomy and Cell Biology, where the synaptic connections were first discovered by Varun Venkataramani. “This project began with an observation in basic research. In close cooperation with our clinical partners, it has led to conceptually new insights which will allow new treatment approaches to be developed using targeted translational research.” A Fatal Mechanism – But One That Opens Up New Avenues for Treatment How exactly activation of the tumor cell ultimately leads to increased tumor growth and invasion of healthy areas of the brain by the glioma cells has yet to be clarified. It is clear that this mechanism can be blocked in animals, however. Possible methods include a significant reduction of brain activity (for example under general anesthesia), pharmacological interventions that interrupt binding of the neurotransmitters on the AMPA receptor, or blocking the AMPA receptor using genetic engineering. In all these cases, tumor spread became slower in animal experiments. “This mechanism is therefore an extremely interesting approach for drug development and future drug treatments,” neurooncologist Winkler emphasized. “Suitable substances have in fact already been approved that block the AMPA receptor and are used to treat other neurological diseases. These substances are promising candidates for clinical trials.” “The new results not only show what makes glioblastomas so aggressive, but also how they could be stopped. That is highly relevant from a translational point of view and paves the way for clinical studies,” commented Wolfgang Wick, Medical Director of the Neurology Department at Heidelberg University Hospital and head of the Clinical Cooperation Unit Neurooncology at DKFZ. “We are also extremely pleased that the work of our junior researcher Varun Venkataramani, who also works in clinical practice, has been acknowledged by a publication in such a prestigious journal as, Nature’.” The relevance of the results from Heidelberg has been confirmed by a paper from Stanford University, California, USA: Michelle Monje and her research team also found synaptic connections between neurons and tumor cells in currently untreatable pediatric brain tumors and also observed the treatment effects reported by the Heidelberg-based researchers. Both papers are being published in “Nature” simultaneously. To read the original article click here.

The post Neurons Promote Growth of Brain Tumor Cells appeared first on Amazing Health Advances.