Alzheimer's disease Archives - Amazing Health Advances

Homocysteine Imbalance Connected to HIGHER Risk of Alzheimer’s Disease

The AHA! Team — Fri, 20 Dec 2024 06:20:15 +0000

Lori Alton via NaturalHealth365 – Alzheimer’s disease, the most common form of dementia, currently affects about 60-70% of the nearly 55 million people diagnosed worldwide – while heart disease and stroke continue to claim too many lives, every year. As a possible way to help solve this health crisis, scientists are learning that high homocysteine levels can contribute to these life-threatening diseases. For instance, a recent study found that elevated homocysteine is associated with an increased risk of Alzheimer’s disease. Homocysteine is an amino acid, and high levels in the body, often due to deficiencies in vitamin B12 and folate, can lead to cognitive decline. Another study at Temple University highlighted the vital role of B-complex vitamins in controlling homocysteine. With vitamin B deficiencies currently widespread in the United States – and Alzheimer’s disease on the rise – the need for maintaining healthy levels of these essential nutrients has never been more apparent. How vitamin deficiencies and other factors contribute to Alzheimer’s disease In a recent review published in Disease-a-Month, researchers examined how vitamin deficiencies and other factors could be linked to Alzheimer’s disease in humans. They found that low levels of vitamin B12 and folate, along with elevated homocysteine levels, are associated with an increased risk of developing Alzheimer’s. These imbalances can contribute to cognitive decline and neurodegeneration, similar to what’s seen in other studies on dementia. The review also highlighted how oral bacteria, specifically those linked to dental infections like periodontitis, may play a role in Alzheimer’s. These bacteria can trigger inflammation in the nervous system, adding to the damage in the brain. Another key finding is that Alzheimer’s might be related to insulin resistance in the brain, sometimes referred to as “type 3 diabetes,” which disrupts glucose metabolism and worsens brain function. Diet-induced elevations in homocysteine damage the brain Researchers have also uncovered more about how tau tangles form. They found that elevated homocysteine levels trigger an increase in 5-lipoxygenase (5LO), a pro-inflammatory chemical responsible for the formation of tau tangles. The next step is to determine whether blocking the production of 5LO can prevent – or even reverse – the brain damage caused by high homocysteine, which had already been linked to amyloid beta plaques, another hallmark of Alzheimer’s disease. Until now, however, the connection between homocysteine and tau tangles has been unclear. The statistics on elevated homocysteine are alarming Homocysteine, classified as a non-protein amino acid, exists naturally in the human body. It is produced as a byproduct of the metabolism of the amino acid methionine. High homocysteine levels, known as hyperhomocysteinemia, can have a genetic component. But they can also be caused by stress, improper diet – such as eating too many processed foods – and B vitamins and folic acid deficiencies. In addition, although coffee has received high marks lately from researchers for its association with lowered risk of degenerative disease, some experts believe that coffee consumption raises homocysteine levels. Research has shown that high homocysteine levels disrupt fragile arterial linings, promote inflammation and oxidative stress, and reduce blood flow to the heart and brain. All of these destructive processes can “prime the pump” for atherosclerosis and coronary artery disease – to such an extent that blood levels of homocysteine can accurately predict the risk of heart disease. Studies have shown that high homocysteine is associated with a 42 percent increase in the risk of narrowing of the carotid arteries. In addition, people with elevated homocysteine who have had a heart attack are at a 30 percent higher risk of experiencing another adverse event – for example, a second heart attack, stroke, or even death. Finally, high homocysteine doubles the odds of developing dementia (as compared to people with normal levels). Your doctor can check your homocysteine levels with a simple blood test. Levels under 10 umol/L are considered desirable, with 7 umol/L to 8 umol/L considered optimal. How do I avoid vitamin B deficiencies and fight high homocysteine? Unfortunately, vitamin B deficiencies are common, particularly in elderly people. One study showed that 40 percent of heart disease patients aged 80 and over are deficient in vitamin B12. As vitamin B12 is found only in animal products, vegans and vegetarians may be at risk, too. You can boost your intake of B-complex vitamins by eating healthy amounts of organic spinach, wheat germ, beets, and avocados. Wild-caught salmon, 100% grass-fed beef, and organic dairy products are particularly rich in vitamin B12. However, supplementation with B-complex vitamins may be the best approach – especially if you have hyperhomocysteinemia. Naturally, you should consult your holistic doctor before starting a supplement routine. For lowering high homocysteine, natural health experts often recommend taking 25 to 100 mg of vitamin B2 a day – along with 100 to 200 mg a day of vitamin B6, 1,000 to 10,000 mcg a day of vitamin B9 (folate), and 300 to 1,000 mcg of vitamin B12, or methylcobalamin. These B-complex vitamins, which all work together to detoxify homocysteine, should be taken along with the omega-3 fatty acids EPA and DHA found in fish oil. One more bit of encouraging news: In one study, combining B vitamins and omega-3s reduced brain shrinkage by 40 percent! High levels of homocysteine can put you at risk for potentially life-threatening diseases. However, a safe, inexpensive B-complex vitamin routine can help you lower your levels. When preserving the health of your heart and brain, these “B” vitamins are the “A” team. Sources for this article include: NIH.gov ALZ.org Medicalxpress.com Europepmc.org To read the original article click here.

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Discover The Alzheimer’s Treatment You Already Have

The AHA! Team — Fri, 20 Dec 2024 06:06:06 +0000

Al Sears, MD, CNS – New research has revealed that the secret to defeating Alzheimer’s doesn’t come from Big Pharma’s drugs. Instead, it resides deep inside your own body. This will come as a shock to Big Pharma. After all, they’ve been lining their pockets for years pushing drugs that don’t work.1 In fact, tens of billions of dollars, including more than $3.7 billion last year alone, have been poured into Alzheimer’s research over the past decade – and it has all been pointless. Government agencies, tax-payer cash, and countless well-meaning charities have helped fund everything from unfounded genetic theories to all sorts of trial drugs, vaccines, cholinesterase inhibitors, and monoclonal antibodies. None of them have brought us one step closer to finding a cure or stopping the unprecedented global explosion of this epidemic. But now, a team of Israeli scientists have made an astonishing breakthrough discovery. Team of Israeli scientists have made an astonishing breakthrough discovery Researchers at Ben-Gurion University have confirmed that the root of Alzheimer’s lies in your mitochondria, the tiny energy powerhouses found in each one of your cells.2 Piggybacking on the growing body of evidence that has linked mitochondrial dysfunction to Alzheimer’s, the Israeli researchers used mouse models to target a mitochondrial gatekeeper – a protein called VDAC1 – which controls how these little power packs function, as well as the life and death of the cell itself. The scientists found that lab mice that produced excess VDAC1 in their brain cells suffered mitochondrial and cell death, triggering an autoimmune response leading to neuroinflammation. This, in turn, led to the release of neurotoxins that resulted in the amyloid plagues and nerve tangles characteristic of Alzheimer’s disease. But by targeting VDAC1 with a special molecule that binds to the protein, the researchers prevented the changes that led to mitochondrial dysfunction and Alzheimer’s. This is great news because it means you now have the knowledge and ability to prevent this dreadful disease from ever striking. And it helps explain my many successes in treating Alzheimer’s patients at the Sears Institute for Anti-Aging Medicine. I’ve been recommending natural therapies that target the mitochondria for years. Meanwhile, Big Pharma has been caught flat-footed. Despite the recommendations of the Israeli scientists, there are no current Alzheimer’s drug candidates that target mitochondria. But the good news is you don’t need Big Pharma or their expensive drugs to beat Alzheimer’s. Tap Into The Alzheimer’s Treatment Hiding Inside You Here are three powerful nutrients I recommend to my patients for keeping their mitochondria firing on all cylinders. The sooner you start taking them, the better. Acetyl-L-Carnitine (ALC): This amino acid plays a crucial role in making energy in your cells. It transports fatty acids into your mitochondria, where they are burned for fuel. It also carries toxic waste out before it can do any damage. But, as you age, your carnitine levels drop. That’s why you need ALC. Your body converts L-carnitine to ALC. Studies show that when your mitochondria slow down, ALC can fire them up again. Studies also show that ALC reverses the malfunction in mitochondria as you age.3,4 The best source of L-carnitine is grass-fed red meat. But you can also supplement. I suggest taking at least 500 mg of ALC every day on an empty stomach. Look for a formula with only L-carnitine and not D, L-carnitine. D-carnitine is synthetic. N-Acetyl-Cysteine (NAC): This is another amino acid that’s also a powerful antioxidant. NAC helps make glutathione, the body’s most powerful antioxidant. Glutathione is the main line of defense for mitochondria. It helps prevent and repair oxidative damage, thus protecting your mitochondria.5,6 Studies show that it also protects your telomeres from oxidative damage.7 So it throws a one-two anti-aging punch. I advise supplementing with 500 mg per day. Rhodiola Rosea: This tough little yellow flower is native to the arctic mountains of Eastern Siberia, and it’s a great herb for enhancing mitochondrial energy production. I’ve seen the power it has to energize my patients. In just a few months, they are visibly younger and stronger. And they tell me they feel that way, too. You can find rhodiola tea in health food stores. Or you can take it in capsule form. It’s also called golden root or roseroot. But make sure you get a formula with enough of the herb’s active compounds. Look for an extract standardized to contain at least 3% rosavins and 1% salidroside. That’s the same ratio found in the natural root. I recommend taking 250 mg daily on an empty stomach, preferably in the morning, because rhodiola stimulates your brain. To Your Good Health, Al Sears, MD, CNS References: 1. Drake, J. “Dementia drugs may put some patients at risk, Queen’s study shows,” EurekAlert (www.eurekalert.org/news-releases/490531), 5/27/09E 2. Shoshan-Barmatz V, Nahon-Crystal E, Shteinfer-Kuzmine A, Gupta R. VDAC1, mitochondrial dysfunction, and Alzheimer’s disease. Pharmacol Res. 2018;131:87-101.S 3. Opalka, J, et al. “Age and sex dependency of carnitine concentrations in human serum and skeletal muscle.” Clinical Chemistry, 2001; 47: 12: 2150-2153. 4. Kidd PM. “Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management.” Altern Med Rev. 2005; 10(4):268-93 5. Montserrat Marí, Albert Morales, Anna Colell et al. “Mitochondrial Glutathione, a Key Survival Antioxidant.” Antioxid Redox Signal. 2009; 11(11): 2685–2700 6. 5. Kelly GS. “Clinical applications of N-acetylcysteine.” Altern Med Rev. 1998;3(2):114-27. 7. Ludlow A, et al. “Telomeres Shorten in Response to Oxidative Stress in Mouse Skeletal Muscle Fibers.” J Gerontol A Biol Sci Med Sci. 2014;69(7):821-30. To read the original article click here.

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New Study Uncovers the Alzheimer’s Gut Microbiome Connection

The AHA! Team — Thu, 05 Dec 2024 06:33:48 +0000

Recent studies have uncovered a fascinating link between Alzheimer’s disease and a lower risk of developing certain cancers, particularly colorectal cancer.

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How to Care for a Loved One with Dementia

The AHA! Team — Wed, 27 Nov 2024 06:37:37 +0000

University of Miami via Newswise – More than 11 million Americans are tasked with the responsibility of taking care of someone with cognitive decline. A diagnosis of Alzheimer’s disease or related dementias (ADRD) for an aging loved one can be devastating for a family. In 2023, it was estimated that 6.7 million Americans of all ages had the diagnosis of Alzheimer’s disease. More than 11 million people care for a loved one with Alzheimer’s or a related dementia, according to the Centers for Disease Control and Prevention, and about 80 percent of those patients are cared for in the home. Dr. Elizabeth Crocco is a geriatric psychiatrist and the medical director of the Memory Disorders Clinic Center for Cognitive Neuroscience and Aging at the University of Miami Miller School of Medicine. Over the course of her career, she has seen thousands of patients and their families. She reports that for some families, the diagnosis of ADRD can be helpful because it ultimately can explain that the illness is not just due to normal aging. For others, a diagnosis can be scary. “It can be frightening because they know that it is irreversible and that it progresses,” she said. “The idea that the person will lose part of who they are, not just cognitively, but part of their essential personality, brings up a lot of feelings.” Cognitive impairment is the hallmark feature of ADRD, but these illnesses can also have behavioral changes. These include agitation, irritability, depression, and anxiety. It is important for care providers to learn how to handle these situations while also maintaining their own mental health, she said. In her clinic, Crocco and her team work with care providers so that they understand the condition and can better manage its symptoms. This includes how to communicate with the loved one. “The memory issue is not the only problem that is making one’s loved one suffer, and a family member can have a difficult time,” she said. “It is the psychiatric and behavioral symptoms that are often the most difficult to deal with: depression, anxiety, anger issues, agitation, along with resistance to care and help.” Medications, of course, can help, but effective and consistent caregiving is paramount in coping with a patient with ADRD. Crocco offered some helpful tips that can make taking care of an individual with ADRD easier: Establish a routine Consistency is key. Chaotic home situations are not kind to people with cognitive impairment. Traveling is a change of routine that can lead to more behavioral problems and confusion. If they resist a task, try not to force them to do it. Wait an hour or more as their attitude may change later. Keep calm Keeping calm and composed is important when dealing with a loved one with ADRD. Also, remember that your reality might not be theirs, and you need to be respectful. Crocco’s mother had dementia. She tells this story: “One time I was at my mother’s house, and I had left a piece of pizza on the stove. My mother began screaming and cursing because there was a piece of pizza on the stove, and it upset her. I took the pizza off the stove, washed the area down, and I said: ‘I am so sorry, Mom, that I upset you.’ She calmed down immediately.” Sundowning It can happen earlier than expected, in the late afternoon. During this time, for both biological and situational reasons, an ADRD individual may become more confused, disoriented, agitated, and paranoid, as well as anxious and fearful. It is important for loved ones to predict patterns to minimize problems behaviorally without always opting for medications. Therapeutic fibbing Cognitive decline often leaves the person with memories of the past. If a loved one has forgotten that someone is deceased, they may repeatedly ask about them. At times, it might be better to let them believe that they are still alive. “What is the alternative?” asked Crocco. “Letting them relive the death over and over again?” Often arguing with a loved one with Alzheimer’s is a losing proposition and only leads to agitation and discord. “You argue and you lose,” said Crocco. Use music and pets Often introducing preferred music from the loved ones’ era can assist in preventing behavioral problems and be very entertaining and enjoyable. Bringing in pets for ADRD individuals to interact with can also assist. It is well known that having animal or pet interactions can lower ones’ stress level as well as blood pressure, said Crocco. Seek help An adult day care center is a good alternative to help a care provider with the help of a loved one with ADRD, said Crocco. Besides providing social interaction and dementia care during the day, it also affords the caretaker time to work or rest, said Crocco. Learn more about the Memory Disorders Clinic at the University of Miami Health System. 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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Discover The Alzheimer’s Treatment You Already Have

The AHA! Team — Fri, 22 Nov 2024 06:23:28 +0000

Al Sears, MD, CNS – New research has revealed that the secret to defeating Alzheimer’s doesn’t come from Big Pharma’s drugs. Instead, it resides deep inside your own body. This will come as a shock to Big Pharma. After all, they’ve been lining their pockets for years pushing drugs that don’t work.1 In fact, tens of billions of dollars, including more than $3.7 billion last year alone, have been poured into Alzheimer’s research over the past decade – and it has all been pointless. Tens of billions of dollars have been poured into Alzheimer’s research over the past decade Government agencies, tax-payer cash, and countless well-meaning charities have helped fund everything from unfounded genetic theories to all sorts of trial drugs, vaccines, cholinesterase inhibitors, and monoclonal antibodies. None of them have brought us one step closer to finding a cure or stopping the unprecedented global explosion of this epidemic. But now, a team of Israeli scientists have made an astonishing breakthrough discovery. Researchers at Ben-Gurion University have confirmed that the root of Alzheimer’s lies in your mitochondria, the tiny energy powerhouses found in each one of your cells.2 Piggybacking on the growing body of evidence that has linked mitochondrial dysfunction to Alzheimer’s, the Israeli researchers used mouse models to target a mitochondrial gatekeeper – a protein called VDAC1 – which controls how these little power packs function, as well as the life and death of the cell itself. The scientists found that lab mice that produced excess VDAC1 in their brain cells suffered mitochondrial and cell death, triggering an autoimmune response leading to neuroinflammation. This, in turn, led to the release of neurotoxins that resulted in the amyloid plagues and nerve tangles characteristic of Alzheimer’s disease. But by targeting VDAC1 with a special molecule that binds to the protein, the researchers prevented the changes that led to mitochondrial dysfunction and Alzheimer’s. This is great news because it means you now have the knowledge and ability to prevent this dreadful disease from ever striking. And it helps explain my many successes in treating Alzheimer’s patients at the Sears Institute for Anti-Aging Medicine. I’ve been recommending natural therapies that target the mitochondria for years. Meanwhile, Big Pharma has been caught flat-footed. Despite the recommendations of the Israeli scientists, there are no current Alzheimer’s drug candidates that target mitochondria. But the good news is you don’t need Big Pharma or their expensive drugs to beat Alzheimer’s. Tap Into The Alzheimer’s Treatment Hiding Inside You Here are three powerful nutrients I recommend to my patients for keeping their mitochondria firing on all cylinders. The sooner you start taking them, the better. Acetyl-L-Carnitine (ALC): This amino acid plays a crucial role in making energy in your cells. It transports fatty acids into your mitochondria, where they are burned for fuel. It also carries toxic waste out before it can do any damage. But, as you age, your carnitine levels drop. That’s why you need ALC. Your body converts L-carnitine to ALC. Studies show that when your mitochondria slow down, ALC can fire them up again. Studies also show that ALC reverses the malfunction in mitochondria as you age.3,4 The best source of L-carnitine is grass-fed red meat. But you can also supplement. I suggest taking at least 500 mg of ALC every day on an empty stomach. Look for a formula with only L-carnitine and not D, L-carnitine. D-carnitine is synthetic. N-Acetyl-Cysteine (NAC): This is another amino acid that’s also a powerful antioxidant. NAC helps make glutathione, the body’s most powerful antioxidant. Glutathione is the main line of defense for mitochondria. It helps prevent and repair oxidative damage, thus protecting your mitochondria.5,6 Studies show that it also protects your telomeres from oxidative damage.7 So it throws a one-two anti-aging punch. I advise supplementing with 500 mg per day. Rhodiola Rosea: This tough little yellow flower is native to the arctic mountains of Eastern Siberia, and it’s a great herb for enhancing mitochondrial energy production. I’ve seen the power it has to energize my patients. In just a few months, they are visibly younger and stronger. And they tell me they feel that way, too. You can find rhodiola tea in health food stores. Or you can take it in capsule form. It’s also called golden root or roseroot. But make sure you get a formula with enough of the herb’s active compounds. Look for an extract standardized to contain at least 3% rosavins and 1% salidroside. That’s the same ratio found in the natural root. I recommend taking 250 mg daily on an empty stomach, preferably in the morning, because rhodiola stimulates your brain. To Your Good Health, Al Sears, MD, CNS References: 1. Drake, J. “Dementia drugs may put some patients at risk, Queen’s study shows,” EurekAlert (www.eurekalert.org/news-releases/490531), 5/27/09E 2. Shoshan-Barmatz V, Nahon-Crystal E, Shteinfer-Kuzmine A, Gupta R. VDAC1, mitochondrial dysfunction, and Alzheimer’s disease. Pharmacol Res. 2018;131:87-101.S 3. Opalka, J, et al. “Age and sex dependency of carnitine concentrations in human serum and skeletal muscle.” Clinical Chemistry, 2001; 47: 12: 2150-2153. 4. Kidd PM. “Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management.” Altern Med Rev. 2005; 10(4):268-93 5. Montserrat Marí, Albert Morales, Anna Colell et al. “Mitochondrial Glutathione, a Key Survival Antioxidant.” Antioxid Redox Signal. 2009; 11(11): 2685–2700 6. 5. Kelly GS. “Clinical applications of N-acetylcysteine.” Altern Med Rev. 1998;3(2):114-27. 7. Ludlow A, et al. “Telomeres Shorten in Response to Oxidative Stress in Mouse Skeletal Muscle Fibers.” J Gerontol A Biol Sci Med Sci. 2014;69(7):821-30. To read the original article click here.

The post Discover The Alzheimer’s Treatment You Already Have appeared first on Amazing Health Advances.

Do Allergy Medications Increase Your Alzheimer’s Risk?

The AHA! Team — Mon, 10 Jun 2024 09:04:04 +0000

Al Sears, MD, CNS – I love this time of year. But many of my patients dread springtime… They come to my clinic sneezing and sniffling. They have runny noses, and watery, itchy eyes. They can’t sleep or work. You may have the same problems. You need relief fast to get back to your life. So you might be tempted to pop some OTC remedies or ask your doctor for a prescription. But you may be getting more than you bargained for with those allergy drugs. They may make you lose your mind. Let me explain… Many doctors treat allergies with a class of drugs called anticholinergics (ACs). You know them by names like Benadryl and Dimetapp. In a new study, scientists linked ACs to an increased risk of dementia.1 Researchers at the Indiana University School of Medicine looked at 451 people, with an average age of 73. Sixty of the patients were taking at least one AC drug. They gave the whole group memory and cognitive tests. They did PET scans to measure brain activity. They did MRI scans to measure changes in brain structure. The results were worrying… The people taking AC drugs did worse on short-term memory tests. They had worse verbal reasoning, planning skills, and problem-solving. They also had lower levels of brain activity, especially in the hippocampus — the region of the brain linked with memory. And they had reduced brain volume and larger cavities or holes inside their brains. In other words, people taking the drugs had more brain atrophy. And AC drugs cause damage quickly. In fact, using these drugs for as few as 60 or 90 days can cause cognitive problems.2 Allergies are your immune system overreacting to normal dust, pollen, and animal fur. Special cells in the blood vessel linings of the inner eyelids, nasal membranes, and lungs release substances called histamine and inflammatory prostaglandins. These are the real culprits behind all the misery. They release fluids to flush out what your body thinks is a viral or bacterial infection. I don’t prescribe those dangerous AC drugs for allergies. Instead, I help my patients relieve the symptoms naturally. 5 Safe, Natural Allergy Busters You Can Use Today Nasal irrigation. This therapy is a safe and easy way to rinse your sinuses. It flushes allergens and irritants out your nasal passages. You can find nasal rinse applicators, including neti pots and sinus-rinse kits, in most drug stores. Just follow the directions on the box. But one caution… Make sure the water is distilled and as sterile as possible. Tap water isn’t safe because it’s not adequately filtered or treated. And it can increase your risk of infection. Pineapple. This tropical fruit contains an enzyme called bromelain. It counteracts the effects of inflammatory prostaglandins. To help lessen inflammation, you’ll need to eat about a cup of fresh pineapple every day. You can also take a supplement. Look for a capsule that is at or near 2,400 GDU (gelatin dissolving units), the highest standardized potency you can get. I recommend you take 500 mg twice a day. Quercetin. This bioflavonoid targets the special cells that make histamine. Studies show it prevents allergies before they start. It can even stop allergic reactions in progress. And it works instantly.3 Quercetin is found naturally in many fruits and vegetables. Try eating more apples, broccoli, cherries, citrus fruit, cranberries, green tea, leafy greens, raspberries, red grapes, onions, shallots, and tomatoes. If you’re prone to allergies, start eating more of these foods a few weeks before spring arrives. Or you can supplement. I recommend taking 500 mg twice a day. Stinging nettle (urtica dioica). This prickly herb is a natural anti-inflammatory. It can prevent hay fever symptoms if taken as soon as they appear.4 It works by balancing histamine levels and preventing the production of prostaglandins. I recommend drinking nettle tea. You can find dried leaves or tea bags in your local health food store or online. Drink one or two cups a day with a meal. Vitamin C. You already know vitamin C boosts the immune system. But it also halts the production of histamine. And it speeds up the breakdown of histamine already in the blood. One study showed that taking 2,000 mg of vitamin C per day lowered histamine levels by 38% in healthy adults — after just one week.5 To Your Good Health, Al Sears, MD, CNS References: 1. Risacher S, et al. “Association between anticholinergic medication use and cognition, brain metabolism, and brain atrophy in cognitively normal older adults.” JAMA Neurol. 2016;73(6):721-32. 2. Xueya C, et al. “Long-term anticholinergic use and the aging brain.” Alzheimers Dement. 2013;9: 377–385. 3. Middleton, E. et al ” Quercetin: an inhibitor of antigen-induced human basophil histamine release.” J Immunol. 1991;127:546-50. 4. Roschek B Jr, et al. “Nettle extract (Urtica dioica) affects key receptors and enzymes associated with allergic rhinitis.” Phytother Res. 2009;23(7):920-6. 5. Johnston, C. et al ” Antihistamine effect of supplemental ascorbic acid and neutrophil chemotaxis.” J Am Coll Nutr. 1992. II(2):172-76 To read the original article click here.

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Study Reveals Protein Structure Similarities in Alzheimer’s & Down Syndrome

The AHA! Team — Wed, 29 May 2024 08:12:33 +0000

Indiana University School of Medicine via News-Medical – More than 90% of people with Down syndrome, the most common chromosomal disorder in humans and the most frequent genetic cause of intellectual disability, are diagnosed with Alzheimer’s disease by ages 55-60. More than 90% of people with Down syndrome, are diagnosed with Alzheimer’s disease by ages 55-60. A new study recently published in Nature Structural and Molecular Biology uses leading-edge cryo-electron microscopy imaging technology to determine whether differences exist between the protein structures in those with Alzheimer’s disease and those with both Alzheimer’s disease and Down syndrome. Just like in Alzheimer’s disease, the neuropathological phenotype in those with Down syndrome and Alzheimer’s disease is characterized by the presence of amyloid β (Aβ) and by abnormal accumulation of tau protein. The structures of Aβ and tau filaments in Down syndrome have not been previously investigated, and it is unknown whether they are different from those of Alzheimer’s disease.” Ruben Vidal, PhD, the Luella McWhirter Martin Professor of Clinical Alzheimer’s Research at the Indiana University School of Medicine and lead investigator of the study Researchers studied images of Aβ and tau filaments, which occurs in individuals with Down syndrome, and compared with those seen in the most common form of Alzheimer’s disease. They found that the protein structures of Aβ and tau filaments in people with both Down syndrome and Alzheimer’s disease have similarities to those found in Alzheimer’s disease. Vidal said their findings may lead to better treatments for Alzheimer’s disease patients and individuals with Down syndrome. “This study is the first comparison at the near atomic level of Aβ and tau filaments between individuals with both Down syndrome and Alzheimer’s disease and individuals with only Alzheimer’s disease,” Vidal said. “Importantly, the study found variations in the structure of Aβ, but no substantial variation in the structure of tau filaments between individuals with Alzheimer’s disease and both Down syndrome and Alzheimer’s disease. This supports the notion of common mechanisms operating in people with sporadic Alzheimer’s disease and in people with both Down syndrome and Alzheimer’s disease. This knowledge is crucial for understanding Alzheimer’s disease in people with Down syndrome and assessing whether adults with both conditions could be included in Alzheimer’s disease clinical trials. People with Down syndrome are living longer than ever, but almost all of them are dying of Alzheimer’s disease when they get older” Vidal, also an investigator in IU School of Medicine’s Stark Neurosciences Research Institute, said the research team used cryogenic electron microscopy to get a close-up, 3D view of the structure of Aβ and tau filaments in two individuals with both Down syndrome and Alzheimer’s disease. The study revealed two novel types of Aβ filaments in the vascular compartment with structures different from those previously reported in Alzheimer’s disease. Vidal said the study’s findings show it is important to include people with both Down syndrome and Alzheimer’s disease in clinical trials targeting the Aβ or tau filaments. He said there are similarities between the mechanisms at play in amyloid aggregation, but more research is needed to determine whether the differences observed in vascular Aβ deposition are unique to those with Down syndrome. “We are thrilled that our cryo-EM imaging and 3D modeling techniques have facilitated the determination of the atomic structures of amyloid beta and tau fibrils in individuals with Down syndrome, shedding light on the connection between Down syndrome and Alzheimer’s disease,” said Wen Jiang, PhD, professor of biology at Purdue University and co-corresponding author of the study. “We are fortunate to have the Purdue Cryo-EM Facility, which provides exceptional resources and services that have made this research possible. We are grateful to the patients who donated their brains to the research and thankful to the NIH for funding our work.” Other study authors include co-corresponding author Bernardino Ghetti, Anllely Fernandez, Grace Hallinan, Kathy Newell and Holly Garringer, all from the IU School of Medicine; and Rejaul Hoq, Daoyi Li, Sakshibeedu Bharath, Frank Vago, Xiaoqi Zhang and Kadir Ozcan, all from Purdue University. This research was funded by the National Institutes of Health and the IU School of Medicine Department of Pathology and Laboratory Medicine. Source: Indiana University School of Medicine Journal reference: Fernandez, A., et al. (2024). Cryo-EM structures of amyloid-β and tau filaments in Down syndrome. Nature Structural & Molecular Biology. doi.org/10.1038/s41594-024-01252-3. To read the original article click here.

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Dr. Don Colbert Reveals Health Tips for Preventing Alzheimer’s

AHA Publisher — Wed, 30 Nov 2022 08:00:54 +0000

CBN News – Many American families have been touched by the pain of Alzheimer’s disease, and some may be concerned about getting it ourselves as we age. But the good news is scientific studies over the last few decades have led to the discovery of dozens of lifestyle choices that can contribute to Alzheimer’s. On this week’s episode of “Healthy Living” on the CBN News Channel, Dr. Don Colbert discusses some of the health choices we can make to help prevent brain diseases, like choosing more plant-based foods, lowering our intake of unhealthy fats, engaging in intermittent fasting, and tackling homocysteine levels. Dr. Colbert shared practical lifestyle moves you can make to limit your chances of getting Alzheimer’s, dementia, or other cognitive decline. You can check those out on Healthy Living with Lorie Johnson, which is available on the CBN News app. To read the original article click here.

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