Preventing Dementia A Major Challenge

New Report Offers Little Hope In Battle Against Neurodegenerative Disease

By Sharon Begley, STAT

Alzheimer’s disease drug treatments have met failure after failure. Many people have decided that prevention is the only hope. Unfortunately, a U.S. panel of experts claims that prevention might be just as elusive as a cure.

From physical activity to avoiding high blood pressure to brain training, a 17-member committee assembled by the National Academies of Sciences concluded, no interventions are “supported by high-strength evidence.” Instead, some high-quality studies found that one or another intervention worked, but other equally rigorous studies found they didn’t.

Alzheimer's disease diagnosisThe three prevention strategies that the report focused on were cognitive training, blood pressure control, and physical activity. (Unfortunately, it didn’t track dietary factors.)

  1. Cognitive training: The evidence for programs aimed at boosting reasoning, problem-solving, memory, and speed of processing does include randomized trials that reported benefits from brain training, but the report calls that evidence “low to moderate strength.” One problem: There seemed to be benefits for two years, but not after five or 10. Results in other randomized studies were even more equivocal. There are also data from studies that are less rigorous, leading the committee to conclude that brain training (computer-based or not) can delay or slow age-related cognitive decline — but not Alzheimer’s.
  2. Blood pressure: Evidence that this helps is weaker still. It’s mostly not based on randomized controlled trials, but the committee decided there is “sufficient” evidence from other kinds of studies as well as from understanding how the brain works to conclude that managing hypertension (especially from ages 35 to 65) can prevent, delay, or slow Alzheimer’s disease, and therefore to include it in public health messages. But there’s no good evidence on how best to reduce high blood pressure; of all the kinds of drugs that do so, however, angiotensin receptor blockers seem to be the best for cognition, for unknown reasons.
  3. Physical activity: Evidence for this is on a par with that for blood pressure: “evidence is insufficient to conclude whether increasing physical activity” prevents or slows Alzheimer’s disease. Randomized controlled trials only sometimes showed benefit, though there is some evidence from other kinds of studies shows that exercise delays or slows age-related cognitive decline (but not Alzheimer’s disease).

“Even though clinical trials have not conclusively supported the three interventions,” Alan Leshner, chair of the committee and CEO emeritus of the American Association for the Advancement of Science, said in a statement, “the evidence is strong enough to suggest the public should at least have access to these results to help inform their decisions.”

The disappointing conclusion comes in the wake of a review published last month of the 105 experimental anti-Alzheimer’s compounds in development. It concluded that their immediate prospects are so poor that the U.S. is unlikely to meet its goal of having a “meaningful” therapy for Alzheimer’s by 2025. That makes the need for prevention strategies greater than ever.

Some experts outside the committee said it had set too high a bar. Henry Mahncke, CEO of brain-training company Posit Science, criticized the committee for lumping together all kinds of cognitive training. That diluted the results showing that the kind that taps into neuroplasticity, the brain’s ability to change its structure and function, “consistently works,” while other forms have “poor to mixed results.”

prevent Alzheimer's disease

The Alzheimer’s Association said it is sticking with its “10 Ways to Love Your Brain” and reduce the risk of dementia. The 10 include physical activity, lifelong learning, heart health, and sound sleep.

“No one is promising this is going to prevent Alzheimer’s,” said spokesman Niles Frantz, “but we think there is enough evidence to say it can reduce your risk.” Unlike the committee, he said, “we believe it is worth talking publicly about these things.”

The neurobiology of dementia suggests that “a multifaceted approach [to prevention] may be most effective,” the report notes. But it is fiendishly complicated to do randomized controlled trials on more than one intervention at a time.

However, STAT has learned, a large-scale, U.S.-based lifestyle intervention study to prevent cognitive decline and dementia will be introduced at the Alzheimer’s Association International Conference in London in July. It is expected to be modeled on a Finnish study that found that a kitchen sink approach — healthy eating, brain training, exercise, and managing diabetes and cardiovascular risk — slows cognitive decline.

Neurodegenerative Disease News via STAT https://www.statnews.com/2017/06/22/preventing-dementia-strategies/

Alzheimer's disease public relations firm

Crossbow Communications specializes in issue management and public affairs. Alzheimer’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and the prion disease epidemic is an area of special expertise. Please contact Gary Chandler to join our coalition for reform gary@crossbow1.com.

Alzheimer’s Disease Research Targets Prions

More Evidence That Prions Cause Alzheimer’s Disease

ProMIS Neurosciences highlighted the growing mountain of research, which calls out Amyloid-beta and Tau prions (proteins), as the root cause for Alzheimer’s disease. The company released a white paper today compiling the scientific data as the basis for new treatments.

Prions and Alzheimer's disease

In the white paper, the company provided a concise overview of empirical evidence from a number of leading researchers, much of it recent, that supports the methodology of selectively targeting the prion variants of Amyloid-beta and Tau.

Amyloid-beta (Aβ) acts as a causative agent in the progression of Alzheimer’s disease. Researchers also have discovered that depletion of Aβ reversed cerebral amyloidosis and associated pathology in susceptible mice.

Other research points to the likelihood that prion-like oligomers of misfolded Aβ mediate neurotoxicity and progression of Alzheimer’s disease. In the Cleary et al 2004; Jin et al 2011 studies, scientists concluded that while the presence of Aβ plaque was the calling card of Alzheimer’s disease, the synaptic loss and neurodegenerative spread of the disease were primarily mediated by soluble oligomers of misfolded Aβ rather than plaque.

Alzheimer's disease research

Even more research contends that the progressive nature of Alzheimer’s disease comes from the formation and spread of Aβ prions. As found in the Khan et al 2014 study, the self-propagation of these Aβ prions follows the stereotypical progression of AD. The prion-like spread is well-documented in animal models.

A growing body of data also indicates that the selective targeting of Aβ prions offers distinct advantages over the broadly reactive Aβ antibodies currently in clinical testing. This specificity of Aβ prion neutralization is expected to increase efficacy by mitigating “target distraction.” This means that treating physicians can preserve normal Aβ function in the patient as well as decreasing the risk of edema and vascular adverse effects.

To achieve this precision medicine approach to Alzheimer’s therapy, ProMIS employed two proprietary computational discovery technologies, ProMIS™ and Collective Coordinates to predict regions of protein most likely to unfold based on thermodynamic stability. This means the company was able to identify six predicted disease-specific epitopes of Aβ prions that would act as homing beacons for antibody therapy. Antibodies have been raised from five of the epitopes and are currently undergoing screening and validation for prion-specific binding and functional activity.

Read more at http://www.stockhouse.com/news/newswire/2016/06/23/promis-t-pmn-white-paper-affirms-a%CE%B2-and-tau-prions-as-alzheimer-s-root-cause#u1wxD4DCfkxcIGMw.99

Brain Disease The Fastest Growing Cause Of Death

More Than 50 Million People Have Alzheimer’s Disease

Neurodegenerative disease is now a global epidemic among many mammals, including humans. Advocates claim that mismanagement and misinformation around the world are fanning the flames and putting millions of people in harm’s way.

Anywhere from 50-100 million people around the world are dying of brain disease. Millions more will contract it this year, while just as many will go undiagnosed and misdiagnosed. Adding to the madness is the fact that physicians are withholding millions of other diagnoses.

Alzheimer's disease epidemic

Death rates from heart disease, cancer and other leading causes of death are steady, if not dropping, in most countries due to advances in nutrition, medicine and disease management. Unfortunately, neurodegenerative disease is the one glaring exception. It’s spreading exponentially. If we had accurate mortality statistics, we would likely find that brain disease is already the leading cause of death around the world. Some countries are at a higher risk than others.

“This will be the most important documentary ever produced about brain disease,” said Gary Chandler, president of Crossbow Communications. “Thanks to mismanagement and the widespread contamination of our food and water, brain disease has more to do with neurotoxins than it does with normal aging and genetics.”

The most common forms of neurodegenerative disease include Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease–the most aggressive and infectious of them all. According to Nobel Prize Laureate Stanley Prusiner, they are all part of the same disease spectrum—prion disease. It’s also known as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.”

Prions and Alzheimer's disease

Prions are unstoppable. The pathogen spreads through the bodily fluids and cell tissue of its victims. The blood, saliva, mucus, milk, urine and feces of victims are infectious. Once unleashed on the environment, prions remain infectious. In fact, they migrate, mutate and multiply.

Not only are homes and hospitals exposed to the prion pathogen, so are entire sewage treatment systems and their by-products. Wastewater treatment plants are prion incubators. The sewage sludge and wastewater released are spreading disease far and wide.

Alzheimer's disease prevention and treatment

Sewage treatment plants can’t detect or stop prions. Dumping sewage sludge (biosolids) from billions of people on land and at sea spreads prions far and wide. It also spreads heavy metals, radioactive waste, carcinogens, pharmaceuticals and more. The risk assessments for biosolids and wastewater reuse don’t mention prions because there is no answer.

“Although there are many factors contributing to the global epidemic, millions of these deaths could have been prevented,” said Chandler. “In addition to dietary risks, it appears that Alzheimer’s disease is just as infectious as Creutzfeldt-Jakob disease. There’s no evidence to the contrary.”

  • Women are contracting neurodegenerative disease at twice the rate of men;
  • Caregivers are six times more likely to contract brain disease;
  • People from Finland, Iceland, Sweden and the United States have the highest death rates from Alzheimer’s; and
  • Smart nutrition is the best strategy to avoid brain disease and the only way to effectively treat its symptoms.

biosolids land application sewage sludge

There are many more questions than answers, but we know that neurotoxins, head trauma and genetics can all trigger neurodegenerative disease. Unfortunately, that’s where much of the knowledge gets fuzzy. Diagnoses, for example, are barely more than a shot in the dark.

According to Chandler, truth and targeted nutrition are the best defense against environmental contamination and brain disease. His company is producing a documentary that will help promote food safety, wellness and reform. It’s called “Food For Thought.” It offers the most comprehensive guidance available about prevention, aversion and treatment, including vital advice for caregivers and family members.

brain disease treatment

Preview and order the eBook now. It will:

  • Help you avoid neurotoxins in food, water and the circles of life;
  • Offer targeted nutritional guidance that can save lives;
  • Offer nutritional therapies that can make a difference. It’s the most logical and comprehensive nutrition for neurological disease available. It also has critical aversion strategies;
  • Inform caregivers about misinformation and misdiagnoses that put them in harm’s way;
  • Blow the whistle on industry practices that are contaminating food, water and other pathways; and
  • Advocate for food safety, water quality, wellness and reforms that can save millions of lives.

According to Chandler, pharmaceutical remedies are nonexistent, but nutritional strategies and tactics provide hope and relief from many symptoms. Unfortunately, there is no cure for brain disease, so prevention is paramount.

The film will be produced in both Denver and Phoenix. The producers are looking for testimonials and commentary from a variety of stakeholders, including family, caregivers, providers and advocates. For more information, please contact Gary Chandler at 602-999-7204 or visit our home page at http://alzheimerdisease.tv/

Crossbow Communications is a public affairs and issue-management firm headquartered in Denver, Colorado. The company is expanding to Phoenix, Arizona. The firm specializes in health and environmental issues. It has helped influence public opinion and public policy around the world. For more information, please visit http://crossbowcommunications.com/phoenix-pr-firm-alzheimers-disease/

Alzheimer’s Symptoms Impacted By Antioxidant

Fisetin Helps Maintain Brain Function In Tests

An antioxidant found in fruits and vegetables appears to stop memory loss that accompanies Alzheimer’s disease in mice, scientists at the Salk Institute for Biological Studies have discovered. In experiments on mice that normally develop Alzheimer’s symptoms less than a year after birth, a daily dose of the compound—a flavonol called fisetin—prevented the progressive memory and learning impairments. The drug, however, did not alter the formation of amyloid plaques in the brain, accumulations of proteins which are commonly blamed for Alzheimer’s disease. The new finding suggests a way to treat Alzheimer’s symptoms independently of targeting amyloid plaques.

treat Alzheimer's disease

“We had already shown that in normal animals, fisetin can improve memory,” says Pamela Maher, a senior staff scientist in Salk’s Cellular Neurobiology Laboratory who led the new study. “What we showed here is that it also can have an effect on animals prone to Alzheimer’s disease.”

More than a decade ago, Maher discovered that fisetin helps protect neurons in the brain from the effects of aging. She and her colleagues have since—in both isolated cell cultures and mouse studies—probed how the compound has both antioxidant and anti-inflammatory effects on cells in the brain. Most recently, they found that fisetin turns on a cellular pathway known to be involved in memory.

“What we realized is that fisetin has a number of properties that we thought might be beneficial when it comes to Alzheimer’s disease,” says Maher.

So Maher—who works with Dave Schubert, the head of the Cellular Neurobiology Lab—turned to a strain of mice that have mutations in two genes linked to Alzheimer’s disease. The researchers took a subset of these mice and, when they were only three months old, began adding fisetin to their food. As the mice aged, the researchers tested their memory and learning skills with water mazes. By nine months of age, mice that hadn’t received fisetin began performing more poorly in the mazes. Mice that had gotten a daily dose of the compound, however, performed as well as normal mice, at both nine months and a year old.

“Even as the disease would have been progressing, the fisetin was able to continue preventing symptoms,” Maher says.

In collaboration with scientists at the University of California, San Diego, Maher’s team next tested the levels of different molecules in the brains of mice that had received doses of fisetin and those that hadn’t. In mice with Alzheimer’s symptoms, they found, pathways involved in cellular inflammation were turned on. In the animals that had taken fisetin, those pathways were dampened and anti-inflammatory molecules were present instead. One protein in particular—known as p35—was blocked from being cleaved into a shorter version when fisetin was taken. The shortened version of p35 is known to turn on and off many other molecular pathways. The results were published December 17, 2013, in the journalAging Cell.

Alzheimer's disease treatment

Studies on isolated tissue had hinted that fisetin might also decrease the number of amyloid plaques in Alzheimer’s affected brains. However, that observation didn’t hold up in the mice studies. “Fisetin didn’t affect the plaques,” says Maher. “It seems to act on other pathways that haven’t been seriously investigated in the past as therapeutic targets.”

Next, Maher’s team hopes to understand more of the molecular details on how fisetin affects memory, including whether there are targets other than p35.

“It may be that compounds like this that have more than one target are most effective at treating Alzheimer’s disease,” says Maher, “because it’s a complex disease where there are a lot of things going wrong.”

They also aim to develop new studies to look at how the timing of fisetin doses affect its influence on Alzheimer’s.

“The model that we used here was a preventive model,” explains Maher. “We started the mice on the drugs before they had any memory loss. But obviously human patients don’t go to the doctor until they are already having memory problems.” So the next step in moving the discovery toward the clinic, she says, is to test whether fisetin can reverse declines in memory once they have already appeared.

Other researchers on the paper were Antonio Currais, Marguerite Prior, Richard Dargusch, Jennifer Ehren, and David Schubert of the Salk Institute and Aaron Armando and Oswald Quehenberger of the University of California at San Diego.

The work was supported by grants from the Alzheimer’s Association, Paul Slavik, the National Institutes of Health, the Alzheimer’s Drug Discovery Foundation, and the George E. Hewitt Foundation.

Source: http://www.healthcanal.com/brain-nerves/brain-diseases/alzheimer%E2%80%99s/47065-natural-plant-compound-prevents-alzheimer-s-disease-in-mice.html

Vitamin E Treats Alzheimer’s Disease

Alzheimer’s Disease Symptoms Managed Best By Nutrition

According to a new report in JAMA, vitamin E can help people cope with symptoms of Alzheimer’s disease. Researchers also found that the treatment reduced burden on caregivers.

Alzheimer's disease treatment

Both Vitamin E and memantine, an FDA-approved drug, have been shown to slow the rate of progression of moderately severe Alzheimer’s disease. But Veterans Administration researchers across the country wanted to know if Vitamin E and memantine could also slow the rate of Alzheimer’s progression in patients with mild to moderate forms of the disease. Different patient groups received Vitamin E alone, memantine alone, a combination of the two or a placebo pill daily.

“Patients had to have a caregiver present who could manage the medications,” explained Dr. Maurice Dysken, a geriatric phsychiatrist at the Minneapolis VA Health Care System.

Caregivers also answered questionnaires about how ordinary activities were affected by the patients’ illness, including using the telelphine, shopping, cooking, dressing and bathing.

“Vitamin E slowed the rate of progression of Alzheimer’s disease on this measure of functional impairment and resulted in a delay of about six months over an average of two years,” Dysken said.

Adults require about 15 mg (22.4 IU) of vitamin E per day, according to the Office of Dietary Supplements. The vitamin (alpha tocopherol) is found in vegetable oils like wheat germ, sunflower, and safflower oils.

treat Alzheimer's disease

In the present study, researchers have found that higher levels of the vitamin (2000 IU/d of alpha tocopherol) can help Alzheimer’s patients cope with the symptoms of the disease.

For the study, researchers analyzed data obtained from 613 people with mild to moderate AD.

Participants were divided into groups and they either received a daily dose of vitamin E; memantine; combination of vitamin E and the drug, or a placebo, according to BBC.

Memantine belongs to the category of drugs called NMDA receptor antagonists and is used to slow AD progression in patients who are at the advanced stages of the disease.  The drug works by decreasing abnormal activity in the brain. However, the drug doesn’t cure the condition.

Researchers found that people on vitamin E had lower functional decline when compared with others. They were able to perform daily activities (washing or dressing) better than people on the dummy pill.  Also, participants getting the combo treatment were less dependent on caretakers.

“This is a well done study by a solid research group,” said Maria Carrillo, vice president of Medical and Scientific Relations at the Alzheimer’s Association, in a statement, CNN reported. “The results are positive enough to warrant more research to replicate and confirm these findings, but should not change current medical practice. No one should take vitamin E for Alzheimer’s except under the supervision of a physician.”

Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking, according to National Institute on Aging. Latest data from the Alzheimer’s Association shows that over 5 million people in the U.S. have AD, a number that is expected to explode to 13. 8 to 16 million people by 2050. There is no cure for the disease.

However, people should consult their doctors before increasing vitamin E levels in the diet as the vitamin is also linked to a higher chance of developing prostate cancer. The risk stays even after people stop taking the supplements.

Source: http://www.natureworldnews.com/articles/5494/20140102/vitamin-e-slows-down-alzheimers-disease-progression.htm

Alzheimer’s Researchers In Japan Make Breakthrough

Protein Formations Key In Preventing Alzheimer’s Disease

Japanese researchers claim to have developed a compound to suppress the formation of a protein that causes Alzheimer’s disease. Satoru Funamoto, associate professor of neuropathology at the Doshisha University and colleagues, said they hoped the substance, which inhibits the formation of beta amyloid, might help establish preventive measures against the disease or treatment methods with fewer side effects, Kyoto reported.

Alzheimer's disease research

The findings, published in the online-only Nature Communications, said it might be possible to treat Alzheimer’s disease by suppressing the action of enzymes involved in the formation of beta amyloid. The protein formations seem to be both cause and effect of Alzheimer’s. As the proteins accumulate, the disease accelerates.

Read more: http://www.upi.com/Health_News/2013/10/11/Possible-Alzheimers-disease-breakthrough/UPI-35191381471218/#ixzz2hQakADkB

Antioxidant Slows Progression Of Alzheimer’s Disease

Alpha-Lipoic Acid Might Delay Disease Onset

Oxidative stress and neuronal energy depletion are characteristic hallmarks of Alzheimer’s disease. It has been hypothesized that, because of this, pro-energetic and antioxidant drugs such as alpha-lipoic acid might delay the onset or slow down the progression of the disease.

Alzheimers disease epidemic

In one study, alpha-lipoic acid was given daily to nine patients with Alzheimer’s disease. The treatment led to a stabilization of cognitive functions in the study group. According the study:

“… [T]he progression [of Alzheimer’s for patients taking alpha-lipoic acid] appears dramatically lower than data reported for untreated patients or patients on choline-esterase inhibitors in the second year of long-term studies … [O]ur data suggest that treatment with alpha-lipoic acid might be a successful ‘neuroprotective’ therapy option.”

Separate research also revealed that alpha lipoic acid, in combination with vitamin E and acetyl-l-carnitine, led to improvements in potential biomarkers for Alzheimer’s disease and showed promise for slowing the progression of the disease.

Alpha lipoic acid (ALA) is a powerful antioxidant and one of the most effective free radical scavengers. Perhaps more importantly, it’s the only one known to be easily transported into your brain, where it offers dramatic benefits for people with brain diseases like Alzheimer’s disease.

Alzheimer’s Progression Impaired

In one study of patients with Alzheimer’s disease, those given 600 mg of alpha lipoic daily for 12 months had a stabilization of cognitive function. A follow-up study, which increased the number of patients in the study and extended the observation period to 48 months, the progression of the disease was “dramatically lower” among those taking alpha lipoic acid, compared to those with no treatment or those taking choline-esterase inhibitor drugs.

Researchers noted:

” … treatment with alpha-lipoic acid might be a successful ‘neuroprotective’ therapy option for AD [Alzheimer’s disease].”

This study was not double-blinded, randomized or placebo-controlled, which is generally the “gold standard” of medical research, however it still shows promise as a treatment for a disease that conventional medicine offers little in the way of treatment.

A separate animal study published last year did find similar benefits; rats with Alzheimer’s disease given a combination of alpha lipoic acid, vitamin E and acetyl-l-carnitine showed improvements in several markers of the disease, including total homocysteine, insulin, insulin-like growth factor and tumor necrosis factor.

treat Alzheimer's disease

Further, in a review of research into alpha lipoic acid for the treatment of Alzheimer’s disease, researchers noted several mechanisms by which it appears to show benefit, including scavenging free radicals, chelating metals, and reducing oxidative stress and inflammation. Researchers noted:

  • “LA [lipoic acid] increases acetylcholine (ACh) production by activation of choline acetyltransferase and increases glucose uptake, thus supplying more acetyl-CoA for the production of ACh.” (Those suffering from Alzheimer’s disease typically have a marked shortage of acetylcholine.)
  • “LA chelates redox-active transition metals, thus inhibiting the formation of hydroxyl radicals and also scavenges reactive oxygen species (ROS), thereby increasing the levels of reduced glutathione.” (Glutathione deficiency has been linked to age-related diseases such as Alzheimer’s.)
  • “LA down-regulates the expression of redox-sensitive pro-inflammatory proteins … ” (People with Alzheimer’s tend to have higher levels of inflammation in their brains.)

They also pointed out a potential benefit of combining ALA with other nutraceuticals like curcumin, EGCG from green tea, and docosahexaenoic acid (DHA) from krill oil to provide a synergistic treatment.

Conventional Alzheimer’s Treatments Offer Little Benefit

In the United States, someone develops Alzheimer’s disease every 69 seconds, and by 2050 this is expected to increase to a new case every 33 seconds, according to the Alzheimer’s Association’s 2011 Alzheimer’s Disease Facts and Figures. The disease is currently at epidemic proportions, with 5.4 million Americans — including one in eight people aged 65 and over — living with Alzheimer’s disease. By 2050, this is expected to jump to 16 million, and in the next 20 years it is projected that Alzheimer’s will affect one in four Americans.

Unfortunately, existing treatments are often of little to no benefit whatsoever.

Memantine, brand name Namenda, is a widely used Alzheimer’s drug that is approved for moderate to severe cases. Despite this, doctors often prescribe it off-label for mild Alzheimer’s cases and even for mild cognitive impairment (MCI), which is frequently the prelude to Alzheimer’s.

However, a reanalysis of data from three clinical trials showed that patients with mild Alzheimer’s who took Namenda had no improvement in mental function or their ability to perform everyday tasks compared to placebo. Even among moderate to severe Alzheimer’s patients, for which the drug is approved to treat, the researchers found only “meager” improvements.

Namenda paired with a cholinesterase inhibitor, a type of drug that may help prevent the breakdown of certain memory-influencing neurotransmitters, is the go-to treatment for Alzheimer’s, but the study shows it likely offers little to no benefit to patients.

What Else Can Alpha Lipoic Acid Benefit?

One of the positive aspects of using alpha lipoic acid as a treatment is that it offers other potential benefits as well, whereas Alzheimer’s drugs are linked with side effects like confusion, hip fractures and slower heart rate.

For instance, ALA has the ability to regenerate other antioxidants such as vitamins C, E, and glutathione. So, when your body has used up these antioxidants, if there’s ALA around, it helps regenerate them. Alpha lipoic acid also recycles coenzyme Q10 and NAD (nicotinamide adenine dinucleotide) and is:

  • A great modifier of gene expression to reduce inflammation
  • A very potent heavy metal chelator
  • An enhancer of insulin sensitivity

According to Dr. Burt Berkson, Russia has even successfully used ALA intravenously to reverse ischemia reperfusion injuries by injecting it right after a heart attack or a stroke. And people with diabetes or metabolic syndrome tend to do much better when taking lipoic acid, as it enhances insulin sensitivity.

There’s even been quite a bit of research showing it can restore T cell function. T cells are a type of white blood cells that are of key importance to your immune system, and are at the core of adaptive immunity, the system that tailors your body’s immune response to specific pathogens. ALA may even help slow down the aging process itself through its reduction in free radicals.

For more science behind the benefits of ALA, GreenMedInfo has indexed 79 studies showing its influence on 84 conditions (six of these are on Alzheimer’s disease and 10 are related to ALA’s neuroprotective properties).

Alzheimer’s Prevention Basics

If you have Alzheimer’s disease or know someone who does, ALA may be a useful supplement to consider that could potentially offer benefit. But, because of the very limited treatments, and no available cure as of yet, for Alzheimer’s, I strongly suggest you take every step you can to prevent it from happening to you in the first place.

In order to effectively prevent a disease, you must address its underlying causative factors. Although we do not have definitive “proof” of what, specifically, causes Alzheimer’s, a number of factors have been linked to an increased risk of dementia, and we know enough about those to in turn make educated recommendations for preventing this type of brain deterioration.

Some of the best strategies for Alzheimer’s prevention include:

  • Fructose. You simply MUST keep your level below 25 grams per day. This toxic influence is serving as the master regulator of brain toxicity. Since the average person is exceeding this recommendation by 300% this is a pervasive and serious issue. I view this as the MOST important step you can take.
  • Keep your fasting insulin levels below 3. This is indirectly related to fructose, as it will clearly lead to insulin resistance. However other sugars, grains and lack of exercise are also factors here.
  • Vitamin B12: According to a small Finnish study recently published in the journal Neurology, people who consume foods rich in B12 may reduce their risk of Alzheimer’s in their later years. For each unit increase in the marker of vitamin B12 (holotranscobalamin) the risk of developing Alzheimer’s was reduced by 2 percent.Very high doses of B vitamins have also been found to treat Alzheimer’s disease and reduce memory loss.
  • Vitamin D: In 2007 researchers at the University of Wisconsin uncovered strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests. Scientists launched the study after family members of Alzheimer’s patients who were treated with large doses of prescription vitamin D reported that they were acting and performing better than before.Researchers believe that optimal vitamin D levels may enhance the amount of important chemicals in your brain and protect brain cells.Vitamin D receptors have been identified throughout the human body, and that includes in your brain. Metabolic pathways for vitamin D exist in the hippocampus and cerebellum of the brain, areas that are involved in planning, processing of information, and the formation of new memories.Sufficient vitamin D is also imperative for proper functioning of your immune system to combat inflammation, and other research has discovered that people with Alzheimer’s tend to have higher levels of inflammation in their brains.
  • Eat a nutritious diet, rich in folate, such as the one described in my nutrition plan. Ideally you’ll want to design your diet around your nutritional type. Everyone, however, regardless of nutritional type will want to avoid fructose as much as possible.Strict vegetarian diets have been shown to increase your Alzheimer’s risk, whereas diets high in omega-3’s lower your risk. However, vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day.
  • High-quality animal based omega-3 fats, such as krill oil. (I recommend avoiding most fish because although fish is naturally high in omega-3, most fish stocks are now severely contaminated with mercury.)High intake of the omega-3 fatty acid DHA helps by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression, and lowering your risk of developing the disorder. Researchers have also said DHA “dramatically reduces the impact of the Alzheimer’s gene.”
  • Avoid and remove mercury from your body. Dental amalgam fillings are one of the major sources of mercury, however you should be healthy prior to having them removed. Once you have adjusted to following the diet described inmy optimized nutrition plan, you can follow the mercury detox protocol and then find a biological dentist to have your amalgams removed.
  • Avoid aluminum, such as antiperspirants, non-stick cookware, etc.
  • Exercise regularly. I would strongly recommend reviewing the Peak Fitness Technique for specific recommendations.
  • Avoid flu vaccinations as most contain both mercury and aluminum!
  • Eat plenty of blueberries. Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against Alzheimer’s and other neurological diseases.
  • Challenge your mind daily. Mental stimulation, especially learning something new, such as learning to play an instrument or a new language, is associated with a decreased risk of Alzheimer’s. Researchers suspect that mental challenge helps to build up your brain, making it less susceptible to the lesions associated with Alzheimer’s disease.
  • Avoid anticholinergic drugs. Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain night-time pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence, and certain narcotic pain relievers. A study found that those who took drugs classified as ‘definite anticholinergics’ had a four times higher incidence of cognitive impairment. Regularly taking two of these drugs further increased the risk of cognitive impairment.

Source: http://articles.mercola.com/sites/articles/archive/2011/07/23/this-antioxidant-dramatically-inhibits-alzheimers-disease-progression.aspx

Top Alzheimer’s Drug Deemed Ineffective

Treatment For Alzheimer’s Disease Elusive

A popular drug used to treat Alzheimer’s patients appears to provide no benefit to those who may be in the early stages of the disease, CNN reports. Although the drug is approved by the FDA for only moderate to severe cases, many physicians have been prescribing it off-label for milder cases. But their efforts are in vain, according to a study reported by CNN. “We conclude that there is a lack of efficacy in mild Alzheimer’s,” says the study’s lead researcher, Lon Schneider, M.D., a professor of psychiatry, neurology, and gerontology at the University of Southern California, in Los Angeles. “We think physicians, patients, and caregivers should simply know this.” 

(Even so), nearly one-fifth of all people with mild Alzheimer’s received the drug in 2006, and the rates may be far higher in some hospitals and practices, according to the study, which appears in the journal Archives of Neurology.Many neurologists — 40 percent, by one estimate — even prescribe the drug for mild cognitive impairment, a condition that may or may not progress to full-blown dementia.” 

Alzheimer's disease treatment

In the United States, someone develops Alzheimer’s disease every 69 seconds, and by 2050 this is expected to increase to a new case every 33 seconds, according to the Alzheimer’s Association’s 2011 Alzheimer’s Disease Facts and Figures.

The disease is currently at epidemic proportions, with 5.4 million Americans — including one in eight people aged 65 and over — living with Alzheimer’s disease. By 2050, this is expected to jump to 16 million, and in the next 20 years it is projected that Alzheimer’s will affect one in four Americans. If that turns out to be true, it would then be more prevalent than obesity and diabetes is today!

Alzheimer’s is a devastating disease that develops slowly and gets worse over time. The first stages involve mild memory loss, but as the disease progresses it can make you unable to carry on a conversation or respond to your external environment. On average, 40 percent of the time a person spends with Alzheimer’s disease is spent in the most severe advanced stages of the disease, making it truly devastating.Worse yet, there is no known cure and very few treatments, and as this latest study shows, existing treatments are often of little to no benefit whatsoever.

More Evidence That Alzheimer’s Drugs Don’t Work

Memantine, brand name Namenda, is a widely used Alzheimer’s drug that is approved for moderate to severe cases. Despite this, doctors often prescribe it off-label for mild Alzheimer’s cases and even for mild cognitive impairment (MCI), which is frequently the prelude to Alzheimer’s.However, a new reanalysis of data from three clinical trials showed that patients with mild Alzheimer’s who took Namenda had no improvement in mental function or their ability to perform everyday tasks compared to placebo. Even among moderate to severe Alzheimer’s patients, for which the drug is approved to treat, the researchers found only “meager” improvements.

The researchers concluded:”Despite its frequent off-label use, evidence is lacking for a benefit of memantine in mild AD [Alzheimer’s disease], and there is meager evidence for its efficacy in moderate AD.”

Namenda paired with a cholinesterase inhibitor, a type of drug that may help prevent the breakdown of certain memory-influencing neurotransmitters, is the go-to treatment for Alzheimer’s, but the new study shows it likely offers little to no benefit to patients.Along with dizziness and headache, confusion is listed as one of the most common side effects of Namenda, and this is certainly the last thing a person with Alzheimer’s needs.Furthermore, cholinesterase inhibitor drugs such as Aricept, Exelon and Reminyl may do more harm than good.

treat Alzheimer's disease

This class of drugs is known to provoke slower heart rates, significantly increasing your chances of getting a permanent pacemaker, as well as increasing your risk of hip fracture.Because of the very limited treatments, and no available cure as of yet, that leaves you with just one solid solution, and that is to prevent it from happening to you in the first place.

Source: http://articles.mercola.com/sites/articles/archive/2011/05/02/popular-alzheimers-drug-proven-ineffective.aspx