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World’s Most Popular Diet Boosts Brain Power

The AHA! Team — Mon, 30 Dec 2024 06:36:52 +0000

Al Sears, MD, CNS – A ketogenic diet can preserve your brain power and even reverse memory loss in old age, according to an exciting new study. The high-fat keto diet, which encourages your body to burn fat instead of carbs, is the world’s most popular meal plan. Users report shedding excess pounds quickly and getting a “second wind” with more energy. I’ve been recommending my fat-based, zero-carb “Primal Power Meal Plan” to patients for more than two decades. And while the impact of this diet on balanced blood sugar and weight loss is clear, there’s more to it… When you eat this way, you’ll immediately notice that your brain is firing on all cylinders. So, I wasn’t surprised to see studies that reveal what this diet can do for your memory. Memory Loss Reversed The latest study is a follow-up to a previous study that revealed the ketogenic diet can improve cognitive performance in older male mice. This time, the research team uncovered the specific mechanism that makes it possible. Scientists put 19 male mice aged between 20 and 23 months – which counts as “old age” for the animals – on either a cycled keto diet or a standard, control diet. Mice in the experimental group switched between a ketogenic diet and a standard diet every other week. Researchers measured metabolic changes for the first 12 weeks. For five weeks after that, the team examined differences in behavior. That’s when they found out what was really happening… Upon further testing, the scientists found that ketone bodies – which are produced by the liver when your body breaks down fat for energy instead of glucose – boosted the connection between the synapses in the brain.1 This has incredible implications for your brain and memory. As you may know, synapses make up the space between nerve cells. This is how chemicals are passed along between neurotransmitters. A better connection between the synapses in your brain helps neurons send signals more effectively – increasing your capacity to recall old memories and enhance your ability to store new ones.2 An earlier study noted that ketone bodies “decrease oxidative stress, increase antioxidants, and scavenge free radicals.” These processes are essential for promoting the healing of the brain.3 The researchers say this is what restored cognitive function in the mice. And they have every reason to believe it would have the same effect on humans. Ketones can be used by most cells of the brain to make energy. When insulin resistance blocks glucose from brain cells, this energy source for the brain can help restore function. Your body produces ketones when you eat a diet high in fat and very low in carbs. Your body enters a state called “ketosis.” Because your body doesn’t have carbs to burn for energy, you burn ketones instead. And ketones burn clean. They make fewer waste products, keeping the stress off the damaged brain cells. Studies show a ketogenic diet can slow and even help reverse dementia symptoms. In a recent study, 23 people with mild cognitive impairment were put on a high- or low-carb ketogenic diet. After just six weeks, the low-carb group showed improved memory compared to the high-carb group.4 Ketogenic diets have also been linked to reduced risk of type-2 diabetes,5 Alzheimer’s,6 Parkinson’s disease,7 autism,8 multiple sclerosis,9 and certain cancers, especially brain cancer.10 As I mentioned, I’ve been recommending a high-fat, low-carb meal plan for many years. In fact, I have a catered keto-friendly lunch for my staff every other week. Unlike other diet fads that have come and gone, a ketogenic meal plan doesn’t ask you to give up much — some of your favorite foods may already be on the menu. To Your Good Health, Al Sears, MD, CNS References: Acuna-Catalan D, et al. “Ketogenic diet administration later in life improves memory by modifying the synaptic cortical proteome via the PKA signaling pathway in aging mice.” Cell Reports Med. 2024;5(6):101593. Kennedy M. “Synaptic signaling in learning and memory.” Cold Spring Harb Perspect Biol. 2016;8(2):a016824. Greco T, et al. “Ketogenic diet decreases oxidative stress and improves mitochondrial respiratory complex activity.” J Cereb Blood Flow Metab. 2016 Sep; 36(9): 1603–1613. Krikorian R, et al. “Dietary ketosis enhances memory in mild cognitive impairment.” Neurobiology Aging. 012;33(2):425.e19-425.e27. University of Michigan. “Liquid low-calorie or low-carb keto diet can reverse type 2 diabetes, research shows.” (https://news.umich.edu/liquid-low-calorie-or-low-carb-keto-diet-can-reverse-type-2-diabetes-research-shows.) Accessed on July 17, 2024 Dillmore A, et al. “Effects of a ketogenic and low-fat diet on the human metabolome, microbiome, and foodome in adults at risk for Alzheimer’s disease.” Alzheimers Dement. 2023 Nov;19(11):4805-4816. Grochowska K and Przeliorz P. “The effect of the ketogenic diet on the therapy of neurodegenerative diseases and its impact on improving cognitive functions.” Dement Geriatr Cogn Dis Extra. 2022 May-Aug; 12(2): 100–106. Evangeliou A, et al. “Application of a ketogenic diet in children with autistic behavior: pilot study.” J Child Neurol. 2003 Feb;18(2):113-8. Bock M, et al. “Ketogenic diet and prolonged fasting improve health-related quality of life and lipid profiles in multiple sclerosis – A randomized controlled trial.” 2015. Varshneya K, et al. “The efficacy of ketogenic diet and associated hypoglycemia as an adjuvant therapy for high-grade gliomas: a review of the literature.” Cureus. 2015 Feb 27;7(2):e251. To read the original article click here.

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Promising New Drug Could Slow Progression of ALS

The AHA! Team — Mon, 25 Nov 2024 06:46:21 +0000

John Jeffay via Israel21c – A chance encounter with an inspiring ALS patient, prompted Alon Ben-Noon to set up NeuroSense Therapeutics, a startup developing a drug combo that aims to slow progression of ALS and other neurodegenerative diseases. It was a life-changing moment for Alon Ben-Noon when he first met Shay Rishoni. Rishoni, once a keen runner and cyclist, had been robbed of all movement by the devastating and degenerative disease ALS. It was 2016 and Rishoni was by then immobile, only able to communicate by staring at an eye-tracking computer screen. But that didn’t stop him working as CEO of Prize4Life, a nonprofit founded by other ALS patients to help find a treatment for the disease. Ben-Noon was profoundly moved by the meeting. “I looked at myself and I thought: You’re completely functioning, but you’re not doing half of what he’s doing. He’s completely paralyzed and he’s moving mountains.” Ben-Noon was already working in the pharmaceutical industry, as a consultant, but decided to change track and do everything he could to allow ALS patients to live longer and live better. And so NeuroSense Therapeutics was born. The pharmaceutical startup, based in Herzliya, central Israel, aims to slow the progress of ALS (amyotrophic lateral sclerosis) as well as Alzheimer’s and Parkinson’s, which are also neurodegenerative disorders. PrimeC ALS is a rare and incurable disease caused by the death of motor neurons, the nerve cells that send messages from the brain and spinal cord to our muscles and glands. ALS (also known as Lou Gehrig’s disease) leads to complete paralysis, followed by death, usually with two to five years. Rishoni, married with two sons, was diagnosed when he was 45 and survived another seven years, which is longer than most. At the time, the only medication available was a drug called Riluzole, approved for use in 1995, which extended patients’ lives by around three months. Ben-Noon was determined to do better. He gathered a team of experts to identify molecules in existing drugs that could be combined to attack multiple targets associated with ALS. Previous attempts to treat the disease had focused on single targets. The team succeeded in addressing a number of distinct problems, including the degeneration of motor neurons. In clinical trials in Israel, Canada and Italy, the drug that NeuroSense developed has been shown to give ALS patients, on average, an extra 18 months. Patients experienced a 36% slower disease progression and a 43% better survival rate over 12 months compared to control subjects. The drug is named PrimeC – “prime” is English for “Rishoni” — and could be available for patients within three and a half years. The patented drug combines the antibiotic ciprofloxacin and the anti-inflammatory agent celecoxib, both already approved by the US Food and Drug Administration (FDA) for unrelated conditions. Fast progression ALS is a highly aggressive and complex disease that affects around one in 10,000 people. Initial symptoms are mild, such a weakness in a finger, or dragging a leg, but it can progress at an alarming rate. “Quality of life in terms of functionality is usually quite good at the beginning and then it declines as the disease progresses,” says Ben-Noon. “One day a patient can still eat by himself; the next day they’ll need assistance. One day a patient can walk independently and the next day they’ll have difficulties walking without a cane and soon they’ll need a wheelchair. “We understood quite quickly that we cannot reverse the disease, but we can stop it and make a meaningful change to people’s lives.” But he hopes to do even more. “Eventually, we will create a world where ALS is a non-fatal disease. Patients will live life to the full, happily, maybe with a very small dysfunction. That’s it, that’s the vision,” Ben-Noon says. Orphan drug designation NeuroSense has received orphan drug designation in the US and Europe, recognizing its potential to treat a rare condition (which means tax breaks and other benefits for the company) though it still needs to gain regulatory approval pending further clinical trials. The company, which went public on NASDAQ in December 2021, has so far attracted $30 million in funding and has a US office in Cambridge, Massachusetts. “We are only 16 employees but we work with dozens of consultants and vendors who are assisting us in advancing our programs,” says Ben-Noon. Dr. Vivian Drory, director of the ALS clinic at Tel Aviv Sourasky Medical Center, said that promising results from the company’s 12-month clinical study highlight the significant potential of PrimeC as a disease-modifying drug for ALS. “These findings underscore the importance of early intervention, which can lead to more substantial benefits, and provide valuable insights that will inform the design of the company’s Phase 3 study, increasing the likelihood of success,” she said. It’s often small companies, like NeuroSense, that pioneer new drugs, Ben-Noon notes. “Nowadays the ratio is about 60/40 — 60 for the small companies 40 for big pharma,” says Ben-Noon. “In many cases it starts in a very small company like ours and then a big pharma looks at the outcomes and decides to buy out the company and continue the development.” Looking back to his first meeting with Rishoni, back in 2016, does he feel he’s done what he set out to achieve? “Yes, absolutely,” he says. “We always keep in touch with Tami [Rishoni’s widow]. We talk, we meet and every time we reach a new milestone is very fulfilling.” “If I hadn’t bumped into Shay,” he reflects, “I probably would still be doing medical consulting work. But now I’m very proud to say we’re creating change in the world.” For more information, click here. To read the original article click here.

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Eyelid Wearable Can Predict and Alert to Epileptic Seizure

The AHA! Team — Tue, 10 Sep 2024 09:00:10 +0000

John Jeffay via Israel21c – Blink Energy’s tiny device, fitted to one eyelid, monitors and analyzes blink patterns to detect or diagnose a wealth of health conditions. A tiny patch is fixed to your eyelid. It monitors your blink pattern and sends a warning to your smartphone that you’re about to have an epileptic seizure. Or that you’re about to fall asleep at the wheel. Or else it measures your REM (rapid eye movement) to help diagnose sleep disorders or Parkinson’s disease or a range of neurological conditions. This isn’t science fiction. This is the next step forward in the world of wearable technology. And according to Yariv Bar-On, CEO at Israel-based Blink Energy, it’s a gamechanger. The wearables market has been dominated, so far, by smartwatches and fitness trackers. The first Apple Watch was launched in April 2015, and wearable technology now includes jewelry that tracks your steps and notifies you of an incoming call, VR headsets for gamers, earbuds, smart glasses with Internet access, smart clothing integrated with electronic devices and a range of health monitors. But the world’s first eyelid wearable device opens up a whole new world of opportunity. Blink patterns Blink Energy’s device weighs just 0.4 grams (0.014 ounces) — less than half the weight of a paperclip – and is fitted to one eyelid. You barely notice it, says Bar-On. “After two minutes you forget it’s there.” But it’s performing an important function by monitoring blink patterns, which provides AI with a wealth of data. “There is one type of muscle that closes the eye, and another that opens it,” says Bar-On, an optometrist and entrepreneur. “There’s a ratio between those two muscles when they are working, and we can, with AI machine learning, identify abnormalities in the patterns of blinks.” Smartwatches and other devices measure eye movement indirectly, by collecting related data. Bar-On says they are only 80 percent accurate. His blink patch provides, for the first time, a way of readily measuring eye movement directly. He says he hopes to launch the company’s first product commercially within two years, at what he describes as an “affordable” price. Starting with epilepsy The possibilities for such technology, developed with his small team of engineers in Haifa, northern Israel, are many. The patch, held onto the eyelid with a disposable adhesive strip that lasts for 10 or 20 uses, can provide data about eye health or eye strain during the course of everyday activities. It can detect drowsiness at the wheel and has other possible uses in health and wellbeing. But the company had to start somewhere. And that somewhere is epilepsy. Bar-On wants to lessen the anxiety that people with epilepsy suffer. “My goal would be to bring epileptic patients more confidence in their daily life,” he tells ISRAEL21c. “You just wear it outside the house, knowing you don’t have to think about when the next seizure might be. The Blink device will indicate a few seconds before a seizure. But it’s not so much the detection as the fact that the wearer doesn’t have to worry about when the next seizure will be,” he says. “Knowing that the device will do that, instead of you having to, makes a big difference. Epileptic patients feel when the seizure is coming, but we can dramatically reduce the anxiety levels, which in themselves contribute to a seizure.” Blink Energy has yet to test its device on epileptic patients. The patch exists as a prototype, but there are still refinements needed before it’s ready for market. Eye mavens Bar-On cofounded Blink Energy four years ago with Nadav Cohen, a specialist in optics and vibrations, and Ziv Rotfogel, an ophthalmologist at Kaplan Medical Center in Rehovot, central Israel. “We wanted to see how we can look at the eye movement or the physiological signals that can be detected from the eye and develop a product that is beyond what it is on the market today,” he says. At first their focus was on using the blink movement to power the patch – which is why they chose the name Blink Energy. “We made a pivot almost two years ago and we developed our own sensor biomarker [which measures biological activity] with communication capabilities but without generating its own power,” he says. The product will recharge inside its own box, just like a pair of earbuds. “It’s not a me-too technology. It’s more like a really game-changing technology. I believe that in the next five to 10 years to come you’ll see many people walking down the street wearing an eyelid patch,” Bar-On predicts. “The adoption rate of wearable tech or smart wearables is already immense. This is just the start.” Blink Energy has received funding from the Israel Innovation Authority and by Israel-based MindUP, which invests in healthcare innovation. For more information, click here. To read the original article click here.

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Nanoplastics Promote Conditions for Parkinson’s Across Various Lab Models

The AHA! Team — Mon, 26 Aug 2024 03:47:42 +0000

Duke Health – DURHAM, N.C. – A novel study sounds the alarm on the need for a new area of research. Nanoplastics interact with a particular protein that is naturally found in the brain, creating changes linked to Parkinson’s disease and some types of dementia. In a Duke-led study appearing Nov. 17 in Science Advances, the researchers report that the findings create a foundation for a new area of investigation, fueled by the timely impact of environmental factors on human biology. Improperly disposed plastics have been shown to break into very small pieces “Parkinson’s disease has been called the fastest growing neurological disorder in the world,” said principal investigator, Andrew West, Ph.D., professor in the Department of Pharmacology and Cancer Biology at Duke University School of Medicine. “Numerous lines of data suggest environmental factors might play a prominent role in Parkinson’s disease, but such factors have for the most part not been identified.” Improperly disposed plastics have been shown to break into very small pieces and accumulate in water and food supplies, and were found in the blood of most adults in a recent study. “Our study suggests that the emergence of micro and nanoplastics in the environment might represent a new toxin challenge with respect to Parkinson’s disease risk and progression,” West said. “This is especially concerning given the predicted increase in concentrations of these contaminants in our water and food supplies.” West and colleagues in Duke’s Nicholas School of the Environment and the Department of Chemistry at Trinity College of Arts and Sciences found that nanoparticles of the plastic polystyrene — typically found in single use items such as disposable drinking cups and cutlery — attract the accumulation of the protein known as alpha-synuclein. West said the study’s most surprising findings are the tight bonds formed between the plastic and the protein within the area of the neuron where these accumulations are congregating, the lysosome. Researchers said the plastic-protein accumulations happened across three different models performed in the study – in test tubes, cultured neurons, and mouse models of Parkinson’s disease. West said questions remain about how such interactions might be happening within humans and whether the type of plastic might play a role. And were found in the blood of most adults in a recent study “While microplastic and nanoplastic contaminants are being closely evaluated for their potential impact in cancer and autoimmune diseases, the striking nature of the interactions we could observe in our models suggest a need for evaluating increasing nanoplastic contaminants on Parkinson’s disease and dementia risk and progression,” West said. “The technology needed to monitor nanoplastics is still at the earliest possible stages and not ready yet to answer all the questions we have,” he said. “But hopefully efforts in this area will increase rapidly, as we see what these particles can do in our models. If we know what to look out for, we can take the necessary steps to protect ourselves, without compromising all the benefits we reap every day from plastics.” The study was funded by in part by The Michael J. Fox Foundation for Parkinson’s Research and the Aligning Science Across Parkinson’s initiative (ASAP-020527). In addition to West, study authors include Zhiyong Liu, Arpine Sokratian, Addison M. Duda, Enquan Xu, Christina Stanhope, Amber Fu, Samuel Strader, Huizhong Li, Yuan Yuan, Benjamin G. Bobay, Joana Sipe, Ketty Bai, Iben Lundgaard, Na Liu, Belinda Hernandez, Catherine Bowes Rickman, and Sara E. Miller. To read the original article click here.

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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.

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The Parkinson’s Disease Gut Has an Overabundance of Opportunistic Pathogens

AHA Publisher — Mon, 29 Jun 2020 07:00:35 +0000

University of Alabama at Birmingham via Newswise – Parkinson’s disease is a common, progressive and debilitating neurodegenerative disease. It currently cannot be prevented or cured. In 2003, Heiko Braak proposed that non-inherited forms of PD are caused by a pathogen in the gut. He hypothesized that the pathogen could pass through the intestinal mucosal barrier and spread to the brain through the nervous system. Up to now, there has been no evidence of a specific pathogen that may trigger PD. Now Haydeh Payami, Ph.D., professor of neurology at the University of Alabama at Birmingham, and colleagues report for the first time a significant overabundance of a cluster of opportunistic pathogens in the guts of persons with PD, compared to control subjects. “The exciting question is whether these are Braak’s pathogens capable of triggering PD, or are they irrelevant to PD but able to penetrate the gut and grow, because the gut lining is compromised in PD,” Payami said. “We emphasize that no claims can be made on function based solely on association. The identity of these microorganisms will enable experimental studies to determine whether and how they play a role in PD.” Payami and colleagues at UAB, Emory University, Albany Medical College and the University of Washington were able to identify these microorganisms because they performed the largest microbiome-wide association study of persons with PD and controls to date. Many previous studies have found altered gut microbiomes in persons with PD but did not detect an increase in opportunistic pathogens. Opportunistic pathogens are often harmless, but they can grow and cause infections if the immune system is compromised or if they penetrate into sterile sites of the body. “We suspect the reason we were able to detect these microorganisms is that they are rare and we had a much larger sample size and power than prior studies,” Payami said. Her researchers re-analyzed their 2017 study that had 197 cases and 130 controls, using a more advanced bioinformatics pipeline. They also analyzed a new, independent dataset with 323 cases of PD and 184 controls, in parallel to the first dataset. This allowed internal replication and the power to detect both rare and common signals. Previous PD microbiome studies have ranged from 10 to 197 PD cases and 10 to 130 controls. A microbiome-wide association study uses advances in DNA sequencing and computational tools to look for microbial communities that may be associated with disease. There is emerging understanding that the gut microbiome — which includes 500 to 1,000 bacterial species that have a mainly beneficial influence — plays an important role in human health and disease. Payami and colleagues also used hypothesis-free correlation network analysis to identify communities of co-occurring microorganisms. Network analysis is an important new tool in biology. An easily understood example of networks is a social network like Facebook, where one can map the connections between followers or friends. A few people will have a huge number of connections, some will have many, and a vast majority will have much fewer. A map of these connections is akin to an airline route map. Using network analysis, Payami and colleagues found three polymicrobial clusters, and also found that each cluster shared functional characteristics. The first cluster was that of opportunistic pathogens overabundant in PD cases, a novel finding. The other two clusters were confirmatory of previous studies. In comparison to controls, persons with PD had reduced levels of a cluster of microbes that produce short-chain fatty acids. In the third cluster, the persons with PD had elevated levels of two genera that are carbohydrate-metabolizing probiotic microbes. Payami says the current study had a precise focus and an intentionally strict analytic execution. The rigor of the study included showing that the altered gut microbiomes in the PD cases were independent of sex, age, BMI, constipation, gastrointestinal discomfort, geography and diet. The 15 PD-associated genera that achieved microbiome-wide significance in both datasets were identified using two methods, and with or without covariate adjustment. “There is more to be learned,” Payami said, “with larger sample sizes with greater power, longitudinal studies to track change from prodromal to advanced disease, and by next-generation metagenome sequencing to broaden the scope from bacteria and archaea to include viruses and fungi, and improve the resolution to strain and gene level.” Co-authors with Payami for the study, “Characterizing dysbiosis of gut microbiome in PD: evidence for overabundance of opportunistic pathogens,” published in the Nature partner journal Parkinson’s Disease are Zachary D. Wallen, Mary Appah, Marissa N. Dean, Cheryl L. Sesler and David G. Standaert, UAB Department of Neurology; Stewart A. Factor, Emory University School of Medicine, Atlanta, Georgia; Eric Molho, Albany Medical College, Albany, New York; and Cyrus P. Zabetian, Veterans Administration Puget Sound Health Care System and University of Washington, Seattle, Washington. Support came from National Institutes of Health grants NS036960, NS062684, NS108675 and NS095775. The U.S. Army Medical Research Acquisition Activity, 820 Chandler Street, Fort Detrick, Maryland 21702-5014, is the awarding and administering acquisition office. This work was also supported by the U.S. Army Medical Research Materiel Command endorsed by the U.S. Army, through the Parkinson’s Research Program, under Award Nos. W81XWH1810508 and W81XWH1810509. Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the U.S. Army. In conducting research using animals, the investigator(s) adheres to the laws of the United States and regulations of the Department of Agriculture. In the conduct of research utilizing recombinant DNA, the investigator adhered to NIH Guidelines for research involving recombinant DNA molecules. In the conduct of research involving hazardous organisms or toxins, the investigator adhered to the CDC-NIH Guide for Biosafety in Microbiological and Biomedical Laboratories. To read the original article click here.

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