Tau protein

Tau protein is essential for stress-induced brain pathology

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Significance

Exposure to stressful events is a well-known inducer of neuronal atrophy implicated in the development of neuropsychiatric and neurological pathologies (e.g., depression and Alzheimer’s disease), although the underlying molecular mechanisms remain elusive. The current study demonstrates that absence of the cytoskeletal protein Tau blocks stress-evoked hippocampal synaptic signaling and morphofunctional damages related to both neuronal structure and connectivity as well as subsequent behavioral deficits. These findings suggest, for the first time to our knowledge, that Tau protein is a key regulator of neuronal malfunction found in stress-driven hippocampal pathology.

Abstract

Exposure to chronic stress is frequently accompanied by cognitive and affective disorders in association with neurostructural adaptations. Chronic stress was previously shown to trigger Alzheimer’s-like neuropathology, which is characterized by Tau hyperphosphorylation and missorting into dendritic spines followed by memory deficits. Here, we demonstrate that stress-driven hippocampal deficits in wild-type mice are accompanied by synaptic missorting of Tau and enhanced Fyn/GluN2B-driven synaptic signaling. In contrast, mice lacking Tau [Tau knockout (Tau-KO) mice] do not exhibit stress-induced pathological behaviors and atrophy of hippocampal dendrites or deficits of hippocampal connectivity. These findings implicate Tau as an essential mediator of the adverse effects of stress on brain structure and function.

Bolstering a Link Between Alzheimer’s Disease and Lead Exposure.

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Lifelong hazard. Infants exposed to lead from peeling paint and other sources may be more susceptible to Alzheimer’s-like brain abnormalities as adults, according to a study in macaques spanning 23 years.Shaiith/iStockphoto/Thinkstock; (inset) Paul StevensonLifelong hazard. Infants exposed to lead from peeling paint and other sources may be more susceptible to Alzheimer’s-like brain abnormalities as adults, according to a study in macaques spanning 23 years.

Researchers striving to understand the origins of dementia are building the case against a possible culprit: lead exposure early in life. A study spanning 23 years has now revealed that monkeys who drank a lead-rich formula as infants later developed tangles of a key brain protein, called tau, linked to Alzheimer’s disease. Though neuroscientists say more work is needed to confirm the connection, the research suggests that people exposed to lead as children—as many in America used to be before it was eliminated from paint, car emissions, water, and soil—could have an increased risk of the common, late-onset form of Alzheimer’s disease.

Even in small doses, lead can wreak havoc on the heart, intestines, kidneys, and nervous system. Children are especially prone to its pernicious effects, as it curbs brain development. Many studies have linked early lead exposure with lower IQs. Researchers estimate that one in 38 children in the United States still have harmful levels of the metal in their systems, but evidence linking this exposure to dementia later in life has been tenuous.

A team led by toxicologist Nasser Zawia, however, has vigorously pursued the lead hypothesis. In one early study, from 2008, the group showed that plaques, insoluble globs of a protein called β-amyloid, marred the brains of five macaques that had consumed a lead-enriched formula as infants. The researchers had compared the preserved brain tissues from those macaques, sacrificed in 2003 at age 23 in a National Institutes of Health lab, with four similarly aged monkeys who had had lead-free formula. The amyloid plaques closely resembled those in the brains of adults with Alzheimer’s disease that are thought to contribute to the dementia.

Now, Zawia’s team has used brain samples from the same five macaques that received lead-enriched formula to find clear evidence of another structural change strongly linked to Alzheimer’s: tangles of tau protein. It’s not certain how, or even if, these tangles promote dementia, but when tau proteins decompose into crumpled strands inside a neuron, the cell’s vital transport system can become blocked. The researchers analyzed frontal cortex tissues to show that the lead-exposed monkeys had three times more irregular tau protein in their brain cells than the monkeys who drank normal formula as infants. Moreover, the genetic instructions that assemble the tau proteins were altered, suggesting that early lead exposure epigenetically reprogrammed the monkeys’ DNA.

“This is very strong evidence that early [lead] exposure can determine what happens in old age,” says Zawia, of the University of Rhode Island, Kingston. The team’s results appear in the December issue of NeuroToxicology.

The brain physiologies of macaques and humans are close enough that dementia researchers should pay attention to the findings, says neuroscientist Marc Weisskopf of the Harvard School of Public Health in Boston. “This study adds another important piece to this link between early-life lead exposure and Alzheimer’s-like pathology.”

While Weisskopf says he is “intrigued” that the researchers could find macaques that lived a full life after infant lead exposure, he is cautious. “As far as I can tell, there’s only one group putting this story out,” he says. “We [would] like to see that this is replicable, but that’s hard. It’s just a difficult study to wait that long and have that kind of data.”

Understanding how lead might interfere with DNA’s instructions to promote brain degeneration later in life will take much more work, Weisskopf adds. Correlating the lead exposure of human infants to a disease that doesn’t manifest until people are in their 60s, 70s, and 80s is challenging, he says.

Current lead regulations in the United States should suffice to prevent such long-term neurological harm, Zawia believes. However, children in many other countries still face this hazard—as do adults in the United States who grew up in densely populated areas much more contaminated by lead. “This study is a good indicator to not forget people who were exposed in the past before [lead] awareness and regulations,” he says. “Their risk [of developing dementia] might have been increased.”

 

Functional Brain Imaging May Spot Alzheimer’s Early.

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Two hallmark cerebrospinal fluid (CSF) biomarkers of early Alzheimer’s disease (AD) correlate with decay in the default mode network (DMN) seen on resting-state functional connectivityMRI (rs-fcMRI), a new study suggests.

Beau M. Ances, MD, PhD, and colleagues from the Knight Alzheimer’s Disease Research Center at Washington University, St. Louis, Missouri, say rs-fcMRI may be an effective noninvasive way to detect early asymptomatic AD.

Earlier research by Dr. Ances and others has shown that AD disrupts connections in the DMN and other brain networks, asreported at that time by Medscape Medical News. “Our study is one the first that links resting-state functional connectivity and CSF biomarkers,” Dr. Ances told Medscape Medical News.

“We are excited about this work,” Dr. Ances said. “We hope in the future that resting-state functional connectivity markers will be added to our arsenal for evaluation of early AD. While these results are only cross-sectional in nature they help place changes in resting-state functional connectivity in context with other measures.”

Still, he added, “we do not advocate for using this technique yet at the individual patient level, but our work creates a stepping stone for helping justify the use of this method. We think that resting-state functional connectivity will provide additional spatial information for areas involved in early AD.”

The study was published online August 19 in JAMA Neurology.

Best Chance of Success

The ability to diagnose AD early is crucial as many researchers now believe that treating patients before symptoms of dementia appear offers the best chances of success.

Patients with symptomatic AD typically have reduced amyloid β42 (Aβ42) and increased phosphorylated tau181 (ptau) in CSF. Cognitively healthy individuals can also exhibit these CSF biomarkers of AD pathology.

Emerging evidence, Dr. Ances and colleagues note, suggests that functional scans of brain networks involved in AD has “great potential” for characterizing pathophysiologic changes during the preclinical phase of AD.

They note that rs-fcMRI abnormalities have been “consistently” observed in the DMN in patients with symptomatic AD. More recent rs-fcMRI investigations have detected DMN changes in asymptomatic individuals.

For their latest study, Dr. Ances and colleagues examined changes in the DMN in relation to CSF Aβ42 and ptau in a cross-sectional longitudinal cohort of 207 older adults with normal cognition (Clinical Dementia Rating, 0).

They found that decreased CSF Aβ42 and increased CSF ptau were each independently associated with reduced DMN integrity, with the most prominent decreases in functional connectivity observed in the posterior cingulate cortex (PCC) and medial temporal lobe (MTL).

These are “2 key hubs that are often affected by AD” and are associated with memory, Dr. Ances said. Memory impairment in the early phases of AD may be attributable to the “convergent effects of both amyloid and tau pathology,” the researchers note in their paper.

They also note that the effects of CSF Aβ42 and ptau on DMN functional connectivity were not due to age or structural atrophy in the PCC and MTL.

Caveats “Substantial”

In an accompanying editorial in JAMA Neurology, William Jagust, MD, from the Helen Wills Neuroscience Institute and School of Public Health at University of California, Berkeley, agrees that this technique has potential but that more study is needed.

“From a clinical perspective,” he writes, “the results suggest that a relatively simple magnetic resonance imaging measure might be a reasonable biomarker for early AD. The caveats, however, are substantial.”

For example, he notes that “technical factors in assessing resting state networks are crucial: small amounts of head motion can produce artifacts that are difficult to detect, there are multiple approaches to data analysis, and reliability over time and across centers has not been extensively established.”

Dr. Jagust also says validating this approach as a biomarker requires much stronger links to disease phenotypes that include the progression to AD dementia. “Nevertheless, the appeal of this technique is that it can be performed on available clinical instruments, requires no particular cognitive task, and can be obtained in a few minutes,” Dr. Jagust writes.

Targeting the PCC and the MTL “could be a simple and widely applicable data-analytic approach to track early disease if the difficult technical issues, predictive value, sensitivity, and specificity can be worked out,” he concludes.

Source: medscape.com

 

 

Vitamins Offer Hope for Alzheimer’s.

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Story at-a-glance

  • Alzheimer’s disease is currently at epidemic proportions, with 5.4 million Americans—including one in eight people aged 65 and over—living with it. There is no known cure, and few truly effective treatments
  • Research suggests the best hope is in prevention focusing on diet, exercise and staying mentally active.
  • Two recent studies show that compounds in cinnamon, and vitamins B12, B6, and folate may delay the onset and/or slow progression of the disease
  • Vitamin treatment consisting of 0.8 mg folic acid, 20 mg vitamin B6 and 0.5 mg vitamin B12 slowed shrinkage of the whole brain volume over the course of two years
  • The vitamin treatment also reduced, by as much as seven-fold, the cerebral atrophy in certain brain regions that are particularly vulnerable to damage associated with Alzheimer’s disease
  • Research suggests that being exposed to general anesthesia can increase the risk of dementia in the elderly by as much as 35 percent.
  • cinnamon

In the United States, Alzheimer’s disease is currently at epidemic proportions, with 5.4 million Americans—including one in eight people aged 65 and over—living with the disease, according to the Alzheimer’s Association’s 2011 Alzheimer’s Disease Facts and Figures1.

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, rivaling the current prevalence of obesity and diabetes.

There is still no known cure for this devastating disease, and very few treatments.Alzheimer’s drugs are often of little to no benefit at all, which underscores the importance of prevention throughout your lifetime.

Research repeatedly suggests the best hope for patients lies in prevention through optimal diet, exercise and staying socially and mentally active. As recently reported by Forbes2:

“[A] new study in Science suggested that last year’s ‘breakthrough’ pharmaceutical, bexarotene (Targretin) – a cancer drug that had initially received wide publicity for helping break up the plaques in Alzheimer’s – doesn’t seem to do this very well at all, and can have significant adverse side effects for the patient.

‘Something happened in that initial report – either something technically or otherwise, which we can’t put our hands on at this point in time,” study author Sangram Sisodia told US News & World Report. ‘Something is seriously wrong.’

While memory loss is common among Westerners, it is NOT a “normal” part of aging. Research has shown that even mild “senior moments” are caused by the same brain lesions associated with Alzheimer’s disease and other forms of dementia. These cognitive changes are by no means inevitable!

People who experience very little decline in their cognitive function up until their deaths have been found (post-mortem) to be free of brain lesions, showing that it’sentirely possible to prevent the damage from occurring in the first place. At the end of this article, I share my best tips for maintaining healthy brain function well into old age.

In recent years, researchers studying natural compounds have offered new hope. For example, two recent studies suggest that compounds in cinnamon, as well as vitamins B12, B6, and folate may delay the onset and/or slow progression of the disease.

The Promise of Cinnamon and Vitamins in the Fight Against Alzheimer’s Disease

The first study in question, published in the Journal of Alzheimer’s Disease3,found that cinnamaldehyde and epicatechin, two compounds found in cinnamon, have an inhibitory effect on the aggregation of a particular protein called tau. Tau plays a large role in the structure and function of neurons.

But while a normal part of cell structures, this protein can begin to accumulate, forming “neurofibrillary tangles” that are a hallmark of Alzheimer’s disease. Both compounds were found to protect tau from oxidative damage that can lead to dysfunction.

Donald Graves, adjunct professor in UCSB‘s Department of Molecular, Cellular, and Developmental Biology and co-author of the study explained the protective process to Medical News Today4:

“‘Take, for example, sunburn, a form of oxidative damage. If you wore a hat, you could protect your face and head from the oxidation. In a sense this cinnamaldehyde is like a cap. While it can protect the tau protein by binding to its vulnerable cysteine residues, it can also come off,’ Graves added, which can ensure the proper functioning of the protein.”

It’s interesting to note that there’s a high correlation between type 2 diabetes and Alzheimer’s disease. Some even believe Alzheimer’s may be a form of brain diabetes. Insulin and insulin receptors in your brain are crucial for learning and memory, and it’s known that these components are lower in people with Alzheimer’s disease.

In addition to the above findings, cinnamon has also been found to have beneficial effects on blood glucose management in type 2 diabetics. This is one of the reasons I include cinnamon in my healthy coconut candy recipe.

B Vitamins Again Show Promise in Alzheimer’s Prevention

The other study, published in Proceedings of the National Academy of Sciences5, found that vitamins B6, B12, and folic acid may help slow the progression of the disease, confirming and supporting previous studies. As reported in the featured article6:

“The fact that B-family vitamins may play a significant role in dementia, or more specifically in warding it off has been consistently illustrated. What is news from the current study, however, is that high-dose B-vitamin treatment in people at risk for the disease ‘slowed shrinkage of whole brain volume,’ and especially reduced shrinkage in areas known to be affected in Alzheimer’s disease.”

The 156 study participants, all of whom were over the age of 70, were diagnosed with mild cognitive impairment. This, along with midlife hypertension, midlife obesity and diabetes, is a known risk factor for Alzheimer’s. One group of participants received a placebo while the other received high-dose B-vitamin treatment consisting of:

  • 0.8 mg folic acid
  • 20 mg vitamin B6
  • 0.5 mg vitamin B12

It is important to note that vitamin B12 comes in many forms and it is typically injected because it is not absorbed well by most people, especially in the elderly who need it most. This is due to it being one of the largest vitamins known. The most common form is cyanocobalamin but a better from would be methylcobalamin. A better alternative to B12 injections would also be sublingual sprays, which are absorbed very similarly to the injections.

The treatment effectively slowed shrinkage of the whole brain volume over the course of two years. It also reduced, by as much as seven-fold, the cerebral atrophy in certain brain regions that are particularly vulnerable to damage associated with Alzheimer’s disease. Another major boon: The supplements cost less than 50 cents a day and are readily available in pharmacies and health-food stores. In the placebo group, higher homocysteine levels at baseline were associated with faster atrophy in these same regions. According to the researchers7:

“We… show that the beneficial effect of B vitamins is confined to participants with high homocysteine… and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in gray matter atrophy, thereby slowing cognitive decline.

Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline.”

Dr. A. David Smith, professor emeritus of pharmacology at Oxford University, founding director of the Oxford Project to Investigate Memory and Ageing, and senior author of the study told Bloomberg News8 that this B-vitamin treatment is “the first and only disease-modifying treatment that’s worked. We have proved the concept that you can modify the disease.” This shouldn’t come as a surprise to anyone who understands that without proper nutrition and exercise, your brain will be increasingly vulnerable to damage with age…

Vitamin B Cocktail Already Used for Dementia Prevention in Sweden

Three years ago, the same group of researchers showed that the atrophy rate in patients’ whole brains was reduced by about 30 percent in those taking the vitamin cocktail9. The atrophy rate was even higher—53 percent—in those who had elevated homocysteine levels, a benefit that was reconfirmed in the featured study. According to Bloomberg10:

“The studies, known as Vitacog, were funded by seven charities and government agencies and vitamin maker Meda AB of Solna, Sweden. Smith is an inventor on three patents held by Oxford University for B vitamin formulations to treat Alzheimer’s disease… Vitamin B12 is found in liver, fish and milk and folic acid in fruit and vegetables. Deficiency of folate and B vitamins is already linked to dementia…

Doctors in Sweden began measuring homocysteine in people who report declining memory about two years ago, said [Johan] Lokk [professor and head physician in the geriatric department at Karolinska University Hospital in Sweden, who wasn’t involved in the study]...

Swedish patients with high homocysteine are given folic acid and B vitamins, even if they aren’t deficient. ‘We think the increased homocysteine level could be deleterious to the brain,’ Lokk said. ‘We wanted to be on the offensive in diagnosing and treating patients. In our opinion, it is harmless and cheap.’”

General Anesthesia Could Increase Risk of Dementia in Elderly by 35 Percent

Related research suggests that being exposed to general anesthesia can increase the risk of dementia in the elderly by as much as 35 percent. The research was presented at the annual congress of the European Society of Anesthesiology (ESA). As reported by Medical News Today11:

“Postoperative cognitive dysfunction, or POCD, could be associated with dementia several years later. POCD is a common complication in elderly patients after major surgery. It has been proposed that there is an association between POCD and the development of dementia due to a common pathological mechanism through the amyloid β peptide. Several experimental studies suggest that some anesthetics could promote inflammation of neural tissues leading to POCD and/or Alzheimer’s disease (AD) precursors including β-amyloid plaques and neurofibrillary tangles.”

Participants aged 65 and over were followed for a total of 10 years. Participants exposed to at least one general anesthetic over the follow-up had a 35 percent increased risk of developing a dementia compared to those who were not exposed to anesthesia. According to lead researcher Dr. Francois Sztark12:

“These results are in favor of an increased risk for dementia several years after general anesthesia. Recognition of POCD is essential in the perioperative management of elderly patients. A long-term follow-up of these patients should be planned.”

Tips for Avoiding Alzheimer’s Disease

The beauty of following my revised Nutrition Plan is that it helps treat and prevent all chronic degenerative diseases, from the common ones like heart disease, diabetes, obesity and Alzheimer’s to the ones you have never heard of or can’t even pronounce. So please read the Plan as soon as you can. It is divided into three helpful sections, Beginner, Intermediate and Advanced to help you start at the right level.

The plan is the first step in addressing Alzheimer’s disease, which is currently at epidemic proportions, with 5.4 million Americans – including one in eight people aged 65 and over – living with the disease.

Remember, while memory loss is indeed common among Westerners, it is NOT a “normal” part of aging, and cognitive changes are by no means inevitable. People who experience very little decline in their cognitive function up until their deaths have been found (post-mortem) to be free of brain lesions, showing that it’s entirely possible to prevent the damage from occurring in the first place… and one of the best ways to do this is by leading a healthy lifestyle.

  • Sugar and Fructose. Ideally, you’ll want to keep your sugar levels to a minimum and your total fructose below 25 grams per day, or as low as 15 grams per day if you have insulin resistance or any related disorders.
  • Improve magnesium levels. There is some exciting preliminary research strongly suggesting a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Unfortunately, most magnesium supplements do not pass the blood brain levels, but a new one, magnesium threonate, appears to and holds some promise for the future for treating this condition and may be superior to other forms.
  • Optimize your vitamin D levels with safe sun exposure. Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed. Researchers believe that optimal vitamin D levels may enhance the amount of important chemicals in your brain and protect brain cells by increasing the effectiveness of the glial cells in nursing damaged neurons back to health.

Vitamin D may also exert some of its beneficial effects on Alzheimer’s through its anti-inflammatory and immune-boosting properties. Sufficient vitamin D is imperative for proper functioning of your immune system to combat inflammation that is also associated with Alzheimer’s.

  • Keep your fasting insulin levels below 3. This is indirectly related to fructose, as it will clearly lead to insulin resistance. However other sugars (sucrose is 50 percent fructose by weight), grains and lack of exercise are also important factors. Lowering insulin will also help lower leptin levels which is another factor for Alzheimer’s.
  • Vitamin B12: In addition to the research presented above, a small Finnish study published in the journal Neurology13 also found that 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, the risk of developing Alzheimer’s was reduced by two percent. Remember sublingual methylcobalamin may be your best bet here.
  • Eat a nutritious diet, rich in folate, such as the one described in my nutrition plan. Vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day. Avoid supplements with folic acid, which is the inferior synthetic version of folate.
  • 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 are now severely contaminated with mercury.) High intake of the omega-3 fats EPA and DHA help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression, and lowering your risk of developing the disorder.
  • Avoid and eliminate mercury from your body. Dental amalgam fillings, which are 50 percent mercury by weight, are one of the major sources of heavy metal toxicity. However you should be healthy prior to having them removed. Once you have adjusted to following the diet described in my 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, vaccine adjuvants, etc.
  • Exercise regularly. It’s been suggested that exercise can trigger a change in the way the amyloid precursor protein is metabolized14, thus, slowing down the onset and progression of Alzheimer’s. Exercise also increases levels of the protein PGC-1alpha. Research has also shown that people with Alzheimer’s have less PGC-1alpha in their brains11 and cells that contain more of the protein produce less of the toxic amyloid protein associated with Alzheimer’s. I would strongly recommend reviewing the Peak Fitness Technique for my specific recommendations.
  • Avoid flu vaccinations as most contain both mercury and aluminum, well-known neurotoxic and immunotoxic agents.
  • Eat blueberries. Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against Alzheimer’s and other neurological diseases. Like any fruit though, avoid excesses here.
  • 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 and statin drugs. Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of coenzyme Q10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.

Other Natural Treatments for Your Anti-Alzheimer’s Arsenal

Finally, there are a few other nutritional recommendations worth noting for their specific benefits in preventing and treating dementia. So, although your fundamental strategy for preventing dementia should involve a comprehensive lifestyle approach, you may want to consider adding a few of these natural dietary agents to your anti-Alzheimer’s arsenal. These four natural foods/supplements have good science behind them, in terms of preventing age-related cognitive changes:

  1. Coconut Oil: The primary fuel your brain needs for energy is glucose. However, your brain is able to run on more than a single type of fuel, one being ketones (ketone bodies), or ketoacids. Ketones are what your body produces when it convertsfat (as opposed to glucose) into energy.

The medium-chain triglycerides (MCT) found in coconut oil are GREAT source of ketone bodies, because coconut oil is about 66 percent MCTs. In fact, ketones appear to be the preferred source of brain food in patients affected by diabetes or Alzheimer’s.

  1. Astaxanthin is a natural pigment with unique properties and many clinical benefits, including some of the most potent antioxidant activity currently known. As a fat-soluble nutrient, astaxanthin readily crosses your blood-brain barrier. One study15 found it may help prevent neurodegeneration associated with oxidative stress, as well as make a potent natural “brain food.”

The molecules of astaxanthin neutralize free radicals and other oxidants without being destroyed or becoming pro-oxidants themselves in the process. It’s is a unique molecule whose shape allows it to precisely fit into a cell membrane and span its entire width. In this position, astaxanthin can intercept potentially damaging molecules before they can damage your cells.

You can get some astaxanthin by taking krill oil, which is a fantastic omega-3 fat supplement. But you can boost your astaxanthin even MORE by adding a pure astaxanthin supplement to your nutritional regimen. For optimal absorption, make sure to take krill oil and/or astaxanthin with a fat-containing meal, since both are fat-soluble.

  1. Gingko biloba: Many scientific studies have found that Gingko biloba has positive effects for dementia. Gingko, which is derived from a tree native to Asia, has long been used medicinally in China and other countries. A 1997 study from JAMAshowed clear evidence that Gingko improves cognitive performance and social functioning for those suffering from dementia.

Research since then has been equally promising. One study in 2006 found Gingko as effective as the dementia drug Aricept (donepezil) for treating mild to moderate Alzheimer’s type dementia. A 2010 meta-analysis found Gingko biloba to be effective for a variety of types of dementia.

  1. Alpha lipoic acid (ALA): ALA can stabilize cognitive functions among Alzheimer’s patients and may slow the progression of the disease.

Source: mercola.com