Parkinson's disease Archives - Amazing Health Advances

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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Brain Cell Grafts in Monkeys Jump-Start Human Trial for New Parkinson’s Treatment

The AHA! Team — Mon, 28 Oct 2024 05:21:55 +0000

University of Wisconsin–Madison via Newswise – People with Parkinson’s disease are receiving a new treatment in a clinical trial started after University of Wisconsin–Madison scientists demonstrated the safety and feasibility of the therapeutic delivery method in a study of non-human primates. People with Parkinson’s disease are receiving a new treatment in a clinical trial started after University of Wisconsin–Madison scientists demonstrated the safety and feasibility of the therapeutic delivery method in a study of non-human primates. Parkinson’s disease damages neurons in the brain that produce dopamine, a brain chemical that transmits signals between nerve cells. The disrupted signals make it progressively harder to coordinate even simple movements and cause rigidity, slowness and tremors that are the disease’s hallmark symptoms. Patients are typically treated with drugs like L-DOPA to increase dopamine production. Although the drugs help many patients, they present complications and lose their effectiveness over time. Parkinson’s disease damages neurons in the brain that produce dopamine Researchers at the Wisconsin National Primate Research Center successfully grafted brain cells called dopaminergic neuronal progenitor cells into the brains of cynomolgus macaque monkeys. California-based Aspen Neuroscience provided the cells, grown from multiple lines of human induced pluripotent stem cells, along with key pieces of the equipment for delivering them to specific parts of the brain. “By the time of diagnosis, it is common for people with Parkinson’s to have lost the majority of dopaminergic neurons, leading to progressive loss of motor and neurological function,” explains Edward Wirth III, an expert in cell therapies, study co-author and Aspen’s chief medical officer. “To replace these lost cells, we must target a very specific area of the brain with a high degree of surgical precision. Utilizing the latest advances in intraoperative MRI guided techniques, the patient’s new cells are transplanted, a few microliters at a time, to the exact area where they are most needed.” Working with potential cell therapies in pursuing treatments for Parkinson’s disease is a particular specialty of the team at Marina Emborg’s lab and their primate center colleagues. “Using autologous cells, a patient’s own cells, avoids the need to use immunosuppression to keep the patient’s body from rejecting or attacking the graft,” says Emborg, a UW–Madison professor of medical physics. “Aspen has developed the technological methods for manufacturing, for quality control, that makes it feasible at scale to make autologous cells and get them to the patients.” The researchers’ results in non-human primates, which supported Aspen’s successful Investigational New Drug application to the Food and Drug Administration to begin human trials, were published today in the Journal of Neurosurgery. “This study was an important step in our work to bring the promise of a cell-replacement therapy to people with Parkinson’s disease” “This study was an important step in our work to bring the promise of a cell-replacement therapy to people with Parkinson’s disease,” says Andrés Bratt-Leal, study co-author, Aspen Neuroscience co-founder and senior vice-president of research and development. “The results were instrumental in opening our first-in-human trial and informing how we deliver patients’ own cells to them in the study.” The UW–Madison scientists, led by Parkinson’s researcher Emborg, took up the Aspen-funded work fresh off their own success (published in 2021) reversing Parkinson’s symptoms in monkeys by grafting neurons grown from the monkeys’ own cells, called an autologous transplant. The 2021 study, using cells grown by UW–Madison stem cell researcher Su-Chun Zhang, added new dopamine-producing neurons to each animal’s brain through injections guided in real time by MRI to an area of the brain called the putamen. Dopamine production increased dramatically, as did the monkeys’ motor skills. At the same time, symptoms of depression and anxiety were reduced. The new study was designed to test the delivery of Aspen’s human cells. Wirth and Aspen scientists worked with Emborg’s team to bridge the monkey-to-human application. While Emborg’s previous study administered cells to the putamen through the top of the skull, the Aspen study examined cell administration through the back of the skull — an angle that could allow surgeons to reach their target with fewer insertions of the apparatus that delivers the new cells into the brain. “The core idea is to decrease the risk of infection, the trauma, the surgical time the patient spends under anesthesia,” Emborg says. “The fewer tracks you have to follow through the brain, the better for all of that.” Six monkeys received grafts of the human neurons Six monkeys received grafts of the human neurons through two paths in each side, or hemisphere, of their brains, with more cells deposited on one side of the brain than the other. A control group of three animals underwent the procedure without the cell delivery. “In tissue samples taken seven and 30 days after the procedures, we found the grafted cells persisted in five of the animals,” Emborg says. The researchers confirmed the presence of Aspen’s human neurons in the monkeys’ brains, finding more cells in the hemispheres that were injected with a higher dose, more cells in the 30-day tissue samples compared to the seven-day samples and the presence of a protein produced by young neurons working to integrate with neighboring cells — all signs the cells grafts were successful. It was a true collaboration, according to Emborg — between the Aspen scientists, her lab and the Wisconsin National Primate Research Center veterinarians and staff — to validate the company’s procedures and equipment before study co-author Paul Larson, a neurosurgeon at Banner – University Medical Center Tucson and professor of neurosurgery at the University of Arizona College of Medicine – Tucson, began Aspen’s first-in-human trial with people with Parkinson’s in April. The work done to refine the logistics, surgical equipment and techniques in the animal procedures will inform the way patients in the human trial receive and recover from the new therapy, providing hope for those struggling with a debilitating disease. “Our results were all so exciting,” Emborg says. “And then, when I saw they had been able to begin with a human patient this spring, I just had tears in my eyes.” 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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These Harmful Pesticides Linked to Type 2 Diabetes

AHA Publisher — Mon, 21 Nov 2022 08:00:59 +0000

Al Sears, MD, CNS – A couple of weeks ago, I told you the EPA and the FDA gave Bayer Pharmaceuticals the greenlight to keep selling the weed killer Roundup… They did this even though multiple studies show that chemical herbicides and pesticides are linked to Alzheimer’s, Parkinson’s disease, and cancer. And now, a recent study has clearly linked these toxins to type 2 diabetes. In a brand-new study that examined farmers who use organophosphates — the most commonly used pesticides — the results couldn’t be more clear… “The prevalence of diabetes was positively associated with exposure to all types of pesticides and insecticides.”1 Another study proved that chemicals found in common insecticides and pesticides are also key diabetes triggers and may be responsible for hundreds of thousands of diabetes-related deaths every year. The researchers found that two chemicals, in particular, carbaryl and carbofuran, bind to the receptors on your cells that govern your biological clock. And this can lead directly to diabetes.2 Let me explain… Although it’s illegal in several countries, carbaryl is the third most widely used insecticide in the U.S. Carbofuran, the most toxic carbamate insecticide has been banned in the U.S. since 2009. But it’s still widely used in places where we import a lot of our produce, like Mexico and Brazil. Carbaryl and carbofuran are what are known as “POPs” — persistent organic pollutants. These chemicals don’t biodegrade easily, so they stay in the environment for a long time. But here’s where the diabetes connection comes into play… Researchers found that both carbaryl and carbofuran are structurally similar to melatonin. That’s the hormone that controls your body’s circadian rhythm – or internal clock. And your circadian rhythm does much more than controlling your sleep cycles. It also controls the metabolism of some brain-wave activity, hormone production, cell regeneration, and other biological activities, including glucose levels and insulin secretion — key factors in type 2 diabetics. There’s a very delicate balance between the release of insulin from your pancreas and glucose levels in your blood, at very specific times of the day. Studies show that if the balance gets disrupted for long periods of time, it can trigger the development of diabetes.3 That’s exactly what the insecticides carbaryl and carbofuran do. They mimic melatonin and wreak havoc with your circadian rhythms. This disruption of your body’s natural circadian rhythm substantially raises your risk of diabetes. Along with a whole host of other diseases including: Heart disease Stroke Respiratory problems Depression Breast, prostate, and colon cancer Obesity Eat These 3 Superfoods to Flush Pesticides From Your Body In a recent letter, I shared how to protect yourself from the deadliest pesticide of all time. The next step in protecting yourself is to get rid of the toxic accumulation of chemicals in your body. One great way to do this is by detoxifying superfoods. Foods rich in vitamin C like fruits, berries, and fresh vegetables will help do the trick, along with fiber-rich nuts and seeds. But some foods are superstars when it comes to flushing the toxins from your system: Make grapefruit your citrus of choice. Grapefruit contains naringenin, a potent antioxidant that decreases your body’s insulin resistance to help prevent diabetes and reprogram your liver to melt excess fat, instead of storing it. This is extremely important for detoxification because insecticide toxins like carbaryl and carbofuran tend to collect in the fat around your tissues. Eating grapefruit will help you stop this process. Eat the oldest food on earth. Spirulina is a kind of blue-green algae and the world’s richest source of vitamins, minerals, iron, protein, and a host of other nutrients. But, it’s also a powerful detoxifier. Go green with barley grass. This superfood is made up of unique amino acid chains. And it’s so well balanced, it has the EXACT blend of amino acids, proteins, enzymes, vitamins, and minerals that you need for optimum health. The major contributors behind its detoxification powers are the trace elements zinc, selenium, and copper. High levels of beta-carotene energize the cleansing of waste materials such as mucus and crystallized acids, and it has a powerful detoxifying effect on your liver. To Your Good Health, Al Sears, MD, CNS References: 1. Juntarawijit, C, et al. “Association between diabetes and pesticides: a case-control study among Thai farmers.” Environ Health Prev Med. 2018; 23: 3 2. Popovska-Gorevski M, Dubocovich ML, et al. “Carbamate Insecticides Target Human Melatonin Receptors.” Chem Res Toxicol. 2017. 3. Bouatia-Naji N,, Bonnefond A, et al. “A variant near MTNR1B is associated with increased fasting plasma glucose levels and type 2 diabetes risk.” Nat Gen. 41, 89 – 94; 7 Dec 2008. To read the original article click here.

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New Research May Yield Treatment to Halt Parkinson’s

AHA Publisher — Mon, 19 Sep 2022 07:24:21 +0000

Abigail Klein Leichman via Israel21c – Scientists from the University of Haifa reported in the journal NJP Parkinson’s Disease a groundbreaking discovery that could lead to treatments stopping the spread of Parkinson’s disease. Parkinson’s patients suffer from massive loss of nerve cells in a brain region that’s normally packed with dopaminergic neurons. Dopamine allows brain cells to transfer messages and orchestrate motor actions. One of the problems in developing drugs for the disease is that only 15 percent of Parkinson’s cases are caused by known genetic factors. The other 85% are defined as “sporadic” and it is not possible to create a model for sporadic Parkinson’s in animals. The international research team, led by Prof. Shani Stern of the university’s Sagol Department of Neurobiology, used an innovative cell reprogramming technique to identify malfunctioning neural processes common to both types of the progressive brain disease. “We managed to show for the first time the presence of impaired neural and cellular mechanisms in a similar manner across all the types of disease we examined,” explained Stern. She explained that these changes exist in Parkinson’s patients long before they are aware of a problem. “If we perform this sequencing in a young person and find a similar picture to that found among people who have developed Parkinson’s disease, we can assume that this individual will develop the disease at a later stage,” she said. “Currently, most of the treatments are intended to prevent the exacerbation of the disease rather than to prevent it. If we can identify the potential to develop Parkinson’s disease at an early stage and develop treatments that can halt the advancement of the disease, we will be able to start preventative treatment at a stage when the nerve cell mortality is limited. This will allow us to significantly slow down the progression of the disease,” she concluded. Stern’s team included Prof. Fred Gage from the Salk Institute; Prof. Alexis Brice from ICM, Paris; Prof. Juergen Winkler from FAU, Germany; and Prof. Irit Sagi from the Weizmann Institute of Science. To read the original article click here.

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Oxidized Cholesterol and Alzheimer’s Disease

AHA Publisher — Fri, 13 May 2022 07:00:51 +0000

Michael Greger M.D. FACLM via NutritionFacts – Oxidized cholesterol can be a hundred times more toxic than regular cholesterol, raising additional concerns about foods such as ghee, canned tuna, processed meat, and parmesan cheese. Too much cholesterol in the blood “has long been considered to act as a primary risk factor for developing Alzheimer’s disease and, possibly, Parkinson’s disease.” Striking images on autopsy show that the brain arteries of Alzheimer’s victims are clogged with fat and cholesterol, compared to non-demented elderly controls, as you can see at 0:16 in my video Oxidized Cholesterol as a Cause of Alzheimer’s Disease. But “cholesterol cannot be directly exported across the blood-brain barrier,” so it can’t get directly into—or out of—the brain. What if the brain has too much cholesterol and needs to get rid of some? As a safety valve, an enzyme in the brain can oxidize cholesterol. So, in that form, it can exit the brain and eventually the body. There’s a catch, though. “Although this fact means that the brain can eliminate excess amounts of these oxidation products,” it could be a two-way street. “[I]t could conversely allow toxic amounts of oxysterols [oxidized cholesterol], present in the blood stream, to accumulate in the brain”—that is, to go the other way. This is not just a theoretical concern. An elegant study showed that by measuring oxidized cholesterol levels in the blood coming off the brain, collected from the jugular vein in the neck, compared to the levels going into the brain through the artery, you could determine the difference. The researchers found that if you have too much oxidized cholesterol in your bloodstream, it can end up in your brain. This is a problem, because research shows the accumulation of oxysterols can be “cytotoxic, mutagenic, atherogenic and possibly carcinogenic”—in other words, toxic to cells, toxic to DNA, and contributing to heart disease and maybe also cancer. Yes, samples from atherosclerotic plaques on autopsy contain 20 times more cholesterol than normal arteries, but they contain 45 times higher levels of oxidized cholesterol. Cholesterol oxidation products may be up to a hundred times more pathological, more toxic, than unoxidized cholesterol, contributing not only to heart disease, but potentially also to a variety of different major chronic diseases, including Alzheimer’s, as you can see at 2:03 in my video. How can we cut down on the amount of these oxysterols in our body? One way is by not eating them. Oxidized cholesterol is found in “milk powders, meat and meat products (including fish), cheese, eggs and egg products.” “Until recently, our understanding…has been limited by the lack of analytical procedures [testing methods] to analyse foods with sufficient sensitivity and accuracy”—until now, that is. As you can see at 2:39 in my video, oxidized cholesterol can be found throughout animal products. Canned tuna was surprisingly high, but ghee takes the cake. Ghee, clarified or boiled butter, is commonly used in Indian cooking. Its method of preparation appears to multiply oxidized cholesterol levels tenfold. This dietary exposure to oxidized cholesterol may help explain why the subcontinent of India is ravaged by such heart disease, even though a significant proportion of the population stays away from meat and eggs. (A number of Indian dairy-based desserts are also made in a similar way to ghee.) Oxidized cholesterol in the diet is a source of oxidized cholesterol in the human bloodstream, where it can readily cross the blood-brain barrier into the brain. This could then trigger inflammation inside the brain and the buildup of amyloid “years before the impairment of memory is diagnosed.” Early studies showing the buildup of oxidized cholesterol in the blood of those fed meals rich in oxidized cholesterol, causing a spike in the bloodstream a few hours after eating, as you can see at 3:45 in my video, were done with things like powdered egg, which can be found in a lot of processed foods, but you typically don’t sit down to a meal of it. You get the same types of spikes, though, from eating “ordinary foodstuff.” Give folks some salami and parmesan cheese, which are naturally rich in cholesterol oxidation products (COPs), and later that day, COP is circulating throughout their bodies, as you can see at 4:04in my video. Higher levels are not only associated with mild cognitive impairment, but they’re linked to Alzheimer’s disease as well. “Increased oxysterol concentrations in the brain may promote cellular damage, cause neuron [nerve cell] dysfunction and degeneration, and could contribute to neuroinflammation [brain inflammation] and amyloidogenesis,” the formation of amyloid plaques. You can show the boost in inflammatory gene expression right in a petri dish, as you can see at 4:30 in my video. You can grow human nerve cells in vitro and drip on a little cholesterol, which causes a bump in inflammation. According to a blog on neuropathycure.org, if you add the same amount of oxidized cholesterol, it gets much worse. What’s more, if you look at the changes in brain oxysterols at different stages of Alzheimer’s disease on autopsy, you can see how the three main cholesterol oxidation products appear to be building up, as I show at 4:48 in my video. Levels have been shown to dramatically increase in Alzheimer’s disease brains, adding to the evidence that oxidized cholesterol may be “the driving force behind the development of Alzheimer’s disease.” Cholesterol gets oxidized when animal products are exposed to heat. Are there some cooking methods that are less risky than others? Find out in my video How to Reduce Cholesterol Oxidation. KEY TAKEAWAYS A primary risk factor for the development of Alzheimer’s and possibly Parkinson’s diseases is too much cholesterol in the blood. Although cholesterol can’t be exported directly across the blood-brain barrier, it can be oxidized by an enzyme in the brain and, in that form, exit the brain. However, oxidized cholesterol present in the bloodstream may be able to enter the brain through this two-way street. Accumulation of these oxysterols can be toxic to cells and DNA, as well as contribute to heart disease and possibly cancer. Samples from atherosclerotic plaques on autopsy contain 20 times more cholesterol than normal arteries and 45 times higher levels of oxidized cholesterol, which can be 100 times more toxic than regular unoxidized cholesterol. Oxysterols are found throughout animal products, including dairy, meat (including fish), and eggs, and one way to cut down on the amount of them in our body is by not consuming them. The preparation of ghee, clarified or boiled butter that is commonly used in Indian cooking, appears to multiply oxysterol levels tenfold, which may help explain why heart disease is so rampant on the Indian subcontinent despite a significant percentage of Indians avoiding meat and eggs. The presence of oxidized cholesterol in the brain can trigger inflammation inside the brain and the buildup of amyloid, far before memory impairment is diagnosed. To read the original article click here.

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The Answer to Parkinson’s and Alzheimer’s Is All in Your Eyes

AHA Publisher — Wed, 12 Jan 2022 08:00:46 +0000

Brian Blum via Israel21c – “Look into my eyes. What do you see?” the man says to his wife. “I see Parkinson’s, Alzheimer’s and MS,” she replies. Not the most romantic interchange. But imagine if gazing into someone’s eyes were the key to diagnosing neurological disorders, which are the world’s leading cause of disability and cost some $800 billion a year in direct treatment expenses. The correlations between “oculometrics” (the biometric measurement of the movement and condition of the eyes) and neurological conditions is a much-researched area of study, with over 750 papers published in journals such as The Lancet, Nature and Neurology. Developing a technology that can decode the data from the eyes has proven to be challenging, however. No one has successfully made strides toward commercializing an oculometric approach. Until now. In October 2021, Tel Aviv and Austin, Texas-based startup Neuralight launched out of stealth with a $5.5 million seed investment and a goal of digitizing and even automating neurological evaluation and care. You Can Only Improve What You Can Measure Neurological exams have traditionally relied on a subjective, manual assessment of symptoms. “The physician will ask 50 questions, like how hard is it to button your shirt? Or the doctor asks the patient to walk across the room so they can assess their gait,” explains Neuralight CEO Micah Breakstone. The lack of objective criteria has prevented pharmaceutical companies from developing effective drugs. Breakstone notes that for dementia, studies have shown that two physicians looking at the same patient on the same day could have a 35 percent variable in diagnosis. “We need a statistically significant result,” Breakstone says. Neuralight’s technology is not a cure or a treatment for neurological disease. Rather, the platform is meant mainly to accelerate pharmaceutical development, with an initial focus on Parkinson’s, Alzheimer’s and multiple sclerosis. The platform automatically extracts microscopic eye movement measurements that serve as “digital endpoints” for neurological disorders. A physician will record a short, five-minute video of a patient’s eyes. Neuralight’s imaging tools clean up the video, then artificial intelligence and machine learning get to work at deciphering what’s behind the eye movements. Once Neuralight has extracted ocular metrics on a patient, it plans to sell the data to pharma companies. As Breakstone tells ISRAEL21c, “You can’t improve what you don’t measure.” “Digital endpoints are the future of neurology,” adds Rivka Kreitman, the company’s chief innovation officer and the former head of global innovative research and development at Israeli pharmaceutical giant Teva. “This technology has been the missing piece pharma has needed to make drug development for neurological diseases effective and ultimately more successful.” Privacy Compliant In Breakstone’s ideal world, all the data extracted from videos by Neuralight would be processed on the Neuralight cloud, which he says is HIPAA compliant with all data de-identified (“We don’t need to see a patient’s face, only his or her eyes”). Some organizations do want to keep the data in-house for privacy reasons; in those cases, Neuralight brings its own server. Neuralight does not require eye-trackers, making the process simpler for patients because they don’t have to sit still for a relatively long period of time. Instead, a simple iPhone or even Zoom recording is fine. A Neuralight video recording takes 10 minutes vs. 40 minutes when working with an eye-tracker. Neuralight’s AI “amplifies and augments standard video resolution so you can glean from standard video signals what you could traditionally do only with professional lab equipment,” Breakstone explains. He likens the resolution to how satellites in space can make out the numbers on a car’s license plate using a similar kind of “super-resolution.” Neuralight analyzes close to 100 parameters, including blinking rate, how quickly the patient can fix on a specific object, and the speed of pupil dilation (the latter is highly correlated with Parkinson’s). Digital Biomarkers Breakstone cofounded Neuralight with CTO Edmund Benami after Breakstone sold his previous startup, Chorus.ai, to ZoomInfo for $575 million. “I could have retired, but that would have been a little empty,” he says. His grandfather suffered from Alzheimer’s, and that led Breakstone to want “to do something to make the world a better place, something I deeply believed in,” he tells ISRAEL21c. “Digital biomarkers are very much in vogue,” he says, and investors agreed. Initial funding for Neuralight came from VSC Ventures, Operator Partners, Clover Health CEO Vivek Garipalli and Noam Solomon, the CEO of Immunai. While most of the 19-person team is in Israel, where R&D is based, Breakstone relocated to Austin to build up the company’s connections in the United States. Neuralight has a working MVP (tech speak for “minimum viable product”) and Breakstone hopes to receive initial FDA clearance by the end of 2022 with the first commercial contracts signed in 2023. Clinical trials are due to kick off in the next few months. Neuralight is in conversations with three large pharma companies. Although neurotechnology is a booming industry, Breakstone says most of Neuralight’s competition “is doing things with devices, not with the eyes.” Boston-based Beacon Biosignals, for example, uses EEG data to create biomarkers for neurological disorders, which he says “will be harder to be adopted as a universal solution.” Fortunately for the billion people suffering from neurological disorders, Breakstone feels that Neuralight is “on an urgent mission. We are building a value-driven company.” For more on Neuralight, click here. To read the original article click here.

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How to Use the Mind to Improve Your Physical Performance

AHA Publisher — Mon, 03 Jan 2022 08:00:51 +0000

Abigail Klein Leichman via Israel21c – Most of us can conjure up a vivid mental image of our favorite food. Just thinking about it can make our mouths water. Israeli physical therapist Amit Abraham heads a lab at Ariel University that’s translating this phenomenon into innovative training protocols to enhance dancers’ and gymnasts’ performance and improve rehab results for people with Parkinson’s disease. Over the past year, he worked with Israel’s Olympic rhythmic gymnastics team, which finished the Tokyo Games in sixth place. “Mental imagery by itself has been extensively used and researched. Even ancient Egypt used mental imagery,” Abraham tells ISRAEL21c. “Our lab is one of very few in the world studying the neurocognitive aspects and integrating it into training and rehabilitation. Some of the things we are doing in this field for the very first time internationally.” Following his postdoc research at Emory University School of Medicine in Atlanta with movement scientist Madeleine Hackney, Abraham returned to Israel in 2020 and established the Mental Imagery & Human Embodied Potential Lab in Ariel University’s Department of Physical Therapy. Not Child’s Play The lab’s goal is to provide scientific evidence for the motor and cognitive benefits of creating experiences in the mind. “We do group and one-on-one sessions in a specific process of bringing to life the mind-body connection,” he explains. “A lot of athletes visualize before competing. But they are not trained in how to use this efficiently as a tool to its fullest potential. That is my goal.” In his initial session, he often needs to overcome participants’ hesitancy. “People think mental imagery is childish and feel embarrassed to use it, especially in a group setting,” Abraham says. “So we start from scratch by explaining how to use it, what are its possibilities and limitations, the science behind it, and how to address lack of belief in it. Once people get excited about it, they can step out of their comfort zone and then it’s easier.” Imagine Motion Without Moving Abraham explains that just as it’s possible to imagine the taste of coffee without drinking it, you can imagine moving your arm without moving it. “Or you can lift your arm slightly while imaging your arm doing a full range of motion,” he says. “If you want to improve your quality of movement, you can imagine your arm as light as a feather. That’s called ‘metaphorical imagery’ and it’s a core component of the Franklin Method, developed my mentor and colleague, Eric Franklin, for teaching body alignment.” This is not always simple. For someone has lower back issues, for example, it is challenging to image the spine moving fluidly without pain. “We are confronting a reality that doesn’t always match the imaging,” Abraham says. “However, this is exactly the huge potential of mental imagery — to overcome the reality with the goal of changing it.” The final step is individualized interventions or training protocols, whether for a rhythmic gymnast or an individual with Parkinson’s disease. “My training as a musculoskeletal physical therapist helps because we can address a problem mechanically as well as with mental imagery,” says Abraham. “We’re trying to be less dependent on the therapist or on technology and more focused on the individual’s potential for self-empowerment.” Openminded Coaches Abraham finds that if the team trainer or coach is open to trying this evidence-based approach it’s more likely to catch on with the athletes. In the case of Israel’s rhythmic gymnastics team, head coach Ira Vigdorchik was quite enthusiastic to try this approach. Abraham did group training in collaboration with Vigdorchik’s coaching team, individual training to address specific areas for improvement, and an assessment of how the trainings impacted performance. “We started with traditional motor imagery: They lie on their back and mentally image the entire sequence of an exercise. We made it more codified, feeling the sensations and perspectives of first and third person,” he says. Abraham also does metaphorical imagery. For example, while balancing on one leg the gymnast visualizes that leg as a tree rooted in the mat. Team member Bar Shapochnikov tells ISRAEL21c: “The mental imagery work with the Franklin Method and Dr. Abraham helped me enhance my performance. My range of motion increased, my confidence in performing increased, and the training became more efficient.” Abraham admits that achieving further improvements at this high level of expertise is extremely difficult. “Therefore, we’re constantly looking for novel approaches that can help the gymnasts and athletes without putting them under even greater physical stress.” Neurocognitive Imagery for Parkinson’s At Emory, Abraham did the first research on integrating dynamic neurocognitive imagery into Parkinson’s disease rehab. He tailored a pilot intervention, based on the Franklin Method, to correct distorted mental representations of the body that can worsen motor and cognitive functioning. “Parkinson is a multifaceted condition, mostly known for slowness of movement, rigidity, balance dysfunctions and resting tremor. But about 60 percent of individuals also have sensory and cognitive deficits that are less talked about. We thought mental imagery could address these deficits,” he explains. This unique embodiment approach taught people to connect imagery with physical sensations. This intervention eased both motor and non-motor symptoms of the disease, as described in a paper Abraham and colleagues published earlier this year in a special issue of Brain Science exploring novel therapies for movement disorders. “We have to develop protocols in this and other neurological and orthopedic populations,” says Abraham. “It’s kind of out of the box to focus on different populations but I see mental imagery as connecting them all.” Abraham aims to become an international leader in the field of mental imagery for rehabilitation and performance. “We collaborate with various researchers in the US and Europe, but this is more than just research. We are looking to really make an impact on dance and gymnastics performance. We are constantly looking for teams and dance companies worldwide willing to try it to enhance performance and wellbeing,” he says. “Shoot me an email amitab@ariel.ac.il if our research intrigues you.” To read the original article click here.

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Drinking THIS Popular Beverage Slashes Depression and Suicide Risk by Half, According to Study

AHA Publisher — Fri, 27 Aug 2021 07:00:30 +0000

Karen Sanders via NaturalHealth365 – In the song “9 to 5,” from the 1980 movie of the same name, singer Dolly Parton refers to coffee as a “cup of ambition.” Now, emerging research indicates that coffee’s potential benefits extend far beyond increasing motivation; according to one study, coffee may even help prevent suicide. Other recent studies show that coffee can help protect against dementia, Parkinson’s disease, as well as a host of other serious conditions. The research is quite interesting. Coffee Consumption Cuts Risk of Suicide Almost in Half Although the results may sound like a coffee advertising executive’s dream come true, the research on coffee and suicide was conducted by professors of epidemiology and nutrition at the highly credible Harvard School of Public Health, and published in July 2013 in The World Journal of Biological Psychiatry. The study, which took over two decades to complete and involved nearly a quarter of a million participants, showed that people who drank two to three cups of coffee a day are at much lower risk of killing themselves than drinkers of decaffeinated coffee and non-coffee drinkers. In fact, daily, moderate coffee consumption slashed suicide rates by almost 50 percent – a truly astounding figure. One can’t help but think that if a pharmaceutical antidepressant achieved this type of dramatic benefit, manufacturers would be shouting it from the rooftops. Of course, it almost goes without saying, we are not suggesting that people drink any of the popular brands – sold in coffee shops – loaded with horrible (added) sweeteners and other junk ingredients. As with anything you choose to consume, it should be of the highest quality sources to reduce the risk of toxicity from chemicals. Back to the study: the results, although surprising, didn’t come out of the blue; past epidemiological studies have shown lower rates of depression among coffee drinkers. Researchers believe that coffee’s mood-lifting effects stem from the way it increases the production of neurotransmitters such as serotonin, dopamine, and noradrenaline. WARNING: Ingesting Excessive Caffeine Can Still Be Problematic The researchers stopped short of advising that people suffering from depression increase their coffee intake. Noting that most people naturally adjust their caffeine levels to an amount that is optimal for them, the team added that drinking more than three cups of coffee a day – or ingesting over 400 milligrams of caffeine – carries no additional benefit, and can cause unpleasant side effects. In fact, a Finnish study showed that individuals who drank large quantities of coffee – eight and nine cups a day – actually had a higher suicide risk than moderate coffee drinkers. According to just-released research, caffeine in coffee can actually help to prevent Parkinson’s disease According to a Swedish study published in July 2014 in the scientific journal PLoS One, coffee – along with the presence of a certain genetic mutation – can help prevent Parkinson’s disease. While both genetic and environmental factors play a role in the development of the neurodegenerative condition, researchers have found that variations in one specific gene – a glutamate receptor gene known as GRIN2A – can help to protect against it. Caffeine, which integrates with the dopamine receptor, works in conjunction with the genetic mutation to lower Parkinson’s risk. Organic Coffee Has More to Offer Than Just Its Caffeine Content Coffee has extremely high levels of potent antioxidants, including trigonelline, catechol, and N-methylpyrinidium. In fact, researchers say that an ordinary cup of coffee contains 1,000 different compounds. Further study is needed to explore the full effects of these beneficial substances. Meanwhile, evidence of the link between coffee and longer life continues to accumulate. In a study of 400,000 participants conducted by the National Cancer Institute and the American Association of Retired People and published in 2012 in New England Journal of Medicine, researchers found that older adults who drank multiple cups of coffee (every day) – whether decaf or “high-test” – had lower risks of death overall than non-coffee drinkers. Participants were less likely to die from heart and respiratory disease, stroke, infection, and diabetes, as well as less likely to suffer fatal injuries and accidents. Other studies have linked coffee drinking to better blood vessel health and to reduced risk of certain cancers, including oral cancer, liver cancer, and a lethal form of prostate cancer. Coffee May Not Be Appropriate for Everyone According to Mayo Clinic, up to 400 milligrams of caffeine, a day is safe for most healthy adults. However, children should not ingest caffeine at all, and teens should not consume more than 100 milligrams a day. Caffeine, which is classified as a stimulant, can cause adverse effects in some individuals, including anxiety, insomnia, irritability, stomach upset, and muscle tremors. Taking certain medications or herbs along with coffee can intensify the effects of caffeine. And, of course, people with anxiety disorders should avoid caffeinated coffee. If you are in doubt about safe caffeine consumption, talk to a trusted integrative physician. Finally, again, for maximum health benefit – look for fair trade, organic coffee that is free of pesticides and chemicals. Then, enjoy your cup of “joe.” From what the latest research tells us, a cup of fresh-brewed, flavorful organic coffee really is good to the last drop. Sources for this article include: NIH.gov ScienceDaily.com ScienceDaily.com NIH.gov MayoClinic.org To read the original article click here.

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