Beta-amyloid plaques

Beta-amyloid and Tau: What Do These Proteins Have to do With Alzheimer’s?

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Alzheimer’s disease is a neurodegenerative disorder that has been analyzed for decades. Researchers say it is caused by the accumulation of beta-amyloid and tau proteins in the brain.

Brain-Scan Alzheimer's

Two common proteins begin to spread through the brains of those with Alzheimer’s. Despite decades of study, scientists still don’t understand why they become so dangerous.

If you look at the brain of an Alzheimer’s patient, you’ll see clear and undeniable damage.

Clusters of dead nerve cells. Hard plaques cemented between cells and thick tangles of proteins twisted up inside the cells themselves. 

These are the hallmarks of Alzheimer’s, and they drive the disease’s infamous symptoms, like memory loss, behavioral issues and problems thinking.

What Causes Alzheimer’s Disease?

The majority of the damage comes from two specific proteins, beta-amyloid and tau. These protein-rich plaques and tangles degrade the brain beyond repair.

With brain imaging and other techniques, researchers have been digging into the roots of the proteins associated with Alzheimer’s disease for decades. We now have a good idea of how they form, but it’s the why that’s missing.

But with brain imaging and early detection, researchers are now able to study these proteins long-term, watching them accumulate as the disease progresses. Many think that if we can watch them build up, we can find a way to break them back down — ultimately curing Alzheimer’s. That’s easier said than done, of course, because both tau and beta-amyloid proteins wreak havoc in their own, separate ways.

What Are Beta-Amyloid Plaques?

While amyloid precursor proteins (APP) — beta-amyloid’s parent protein — are best known for their contribution to Alzheimer’s disease, they might not deserve such a bad rap. APP is abundant in the brain and is found in synapses, tiny bridges that allow neurons to pass chemical and electrical signals to one another.

While the main function of APP is unknown, some scientists think they help guide neurons through the brain during early development or help cells attach to one another. But whatever use our bodies have for APP, it can turn into a deadly problem under the right conditions.

“APP is produced in the brain and is normally metabolized by an enzyme called alpha secretase, which cuts it in half and flushes it out with no problems,” says Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center. “But in people who develop Alzheimer’s disease, instead of being cut by alpha secretase, APP is cut by two other enzymes — beta secretase and gamma secretase.”

Beta-Amyloid Proteins in the Brain

When this happens, for reasons Petersen and other researchers aren’t exactly sure of, APP is chopped into strands of amino acids that the brain can’t metabolize, called beta-amyloid proteins.

Unable to break down, these proteins start sticking together, ultimately forming hard plaque deposits in the synapses between cells. Beginning in the hippocampus, these dense clusters block communication between neurons and kick-start cell death, triggering a loss of memory. And things only get worse from there.

Once beta-amyloid plaques begin to form, it seems to open the door to the accumulation of Alzheimer’s other hallmark protein: tau. Researchers aren’t sure why this is, but they do know that it’s a key turning point in neurodegeneration.

What Is Tau Protein?

Unlike beta-amyloid, researchers have a good understanding of tau and how it functions in the brain. 

“Tau is a normal protein that exists in every cell in the body,” said Juan Troncoso, director of the Brain Resource Center at the Johns Hopkins University School of Medicine.

Our cells’ overall structures are supported by microtubules, hollow tubes that give cells their shape. Along with another protein called tubulin, tau binds to these microtubules to keep them strong and stabilized.

Tau Proteins and Alzheimer’s

But for reasons unknown, tau proteins in Alzheimer’s patients go through a process called hyperphosphorylation. Here, the addition of phosphate molecules causes tau proteins to break down and lose their shape.

Too weak to support microtubules, they begin detaching and sticking to each other instead. The degenerate tau proteins tangle together inside of neurons, growing large enough to block the chemical and electrical signals that travel toward the synapses and onto neighboring cells. 

“That leads to the death of that neuron, and maybe the one next to it, and the one next to that one,” adds Petersen. “And if those neurons are in the memory part of the brain, then the person becomes forgetful.”

Unfortunately, becoming forgetful is only the beginning. As plaques and tangles spread from the hippocampus to the cerebral cortex, behavior, reasoning and language start to fade, too. This degradation continues until patients can no longer perform basic bodily functions, like eating and swallowing. The result is ultimately death.

Alzheimer’s Treatments

As of now, treatments for Alzheimer’s are limited. There are a handful of drugs and lifestyle adjustments that can ease symptoms, and studies on fasting diets are starting to show early promise. But researchers are confident that tau and beta-amyloid proteins hold the key to untangling Alzheimer’s.

“Because they’re so prominent in microscopic examinations of the brain, they have become targets for potential therapies,” said Troncoso, who has spent decades studying the disease. “If you can remove or prevent the accumulation of beta-amyloid with a vaccine or an antibody, then you may prevent or slow down the development of the disease.”

Targeting Gut Bacteria May Be The Key To Preventing Alzheimer’s

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Diet could be a powerful mode of prevention.

A new study suggests that a gut-healthy diet may play a powerful role in preventing one of the most feared diseasesin America.

Mounting research continues to show the links between the health of the gut and that of the brain. Now, a new study from Lund University in Sweden finds that unhealthy intestinal flora can accelerate the development of Alzheimer’s disease.

 The report, published Feb. 8 in the journal Scientific Reports, demonstrates that mice with Alzheimer’s have a different gut bacterial profile than those that do not have the disease.

The gut microbiome is highly responsive to dietary and lifestyle factors. This suggests that a gut-healthy diet may play a powerful role in preventing one of the most feared diseases in America.

 “Alzheimer’s is a preventable disease and in the near future we will likely be able to give advice on what to eat to prevent it,” study author Dr. Frida Fak Hållenius, associate professor at the university’s Food for Health Science Centre, told The Huffington Post. “Take care of your gut bacteria, by eating lots of whole-grains, fruits and vegetables.”
In the new study, Hållenius and her colleagues revealed a direct causal association between gut bacteria and signs of Alzheimer’s in mice. When a group of bacteria-free mice were colonized with the bacteria of rodents with Alzheimer’s, they developed brain plaques indicative of Alzheimer’s. When the bacteria-free mice were colonized with the bacteria of the healthy rodents, however, they developed significantly fewer brain plaques.

Beta-amyloid plaques between nerve cells in the brain are a central marker of the disease. These sticky protein clumps accumulate between the brain’s neurons, disrupting signals and contributing to the gradual killing off of nerve cells.

“We don’t yet know how bacteria can affect brain pathology, we are currently investigating this,” Hållenius said. “We think that bacteria may affect regulatory T-cells in the gut, which can control inflammatory processes both locally in the gut and systemically ― including the brain.”

The contributions of microbes to multiple aspects of human physiology and neurobiology in health and disease have up until now not been fully appreciated.

The gut microbiome is intimately connected with the immune system, since many of the body’s immune cells are found in this area of the stomach, Hållenius added.

Anything that happens in the digestive tract can affect the immune system, she explained. “By changing the gut microbiota composition, you affect the immune system of the host to a large extent.”

The findings suggest that Alzheimer’s may be more more preventable than health experts previously thought. The composition of bacteria in the gut is determined by a mix of genetics and lifestyle factors. Diet, exercise, stress and toxin exposure all play a huge role in the gut’s bacterial makeup.

Now, the researchers can begin investigating ways to prevent the disease and delay its onset by targeting gut bacteria early on. And in the meantime, anyone can adopt a plant-based, whole foods diet and probiotic supplementation as a way to improve the health of their microbiome.

“The diet shapes the microbial community in the gut to a large extent, so dietary strategies will be important in prevention of Alzheimer’s,” Hållenius said. “We are currently working on food design that will modulate the gut microbiota towards a healthier state.”

The study is far from the first to show a connection between gut bacteria and Alzheimer’s. In a 2014 paper published in the journal Frontiers in Cellular Neuroscience, researchers listed 10 different ways that the microbiome may contribute to the development of Alzheimer’s disease, including fungal and bacterial infections in the intestinal tract and increased permeability of the blood-brain barrier.

“The contributions of microbes to multiple aspects of human physiology and neurobiology in health and disease have up until now not been fully appreciated,” that study’s authors wrote.

Alzheimer’s Disease May Result From Past Brain Infections

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It’s often stated as fact that Alzheimer’s disease is the result of a buildup of beta-amyloid plaques in your brain. Such plaques may increase in your brain as you age, but tend to be far more abundant in people with Alzheimer’s disease.

Memory Loss

Story at-a-glance

  • Beta-amyloid plaques associated with Alzheimer’s disease may not be intrinsically abnormal, and instead, may act as a natural antibiotic that protects your brain from infection
  • Researchers believe beta-amyloid traps infectious agents in your brain and imprisons them in a beta-amyloid “cage,” where they ultimately die
  • The “cages” left behind form the plaque buildup seen in Alzheimer’s
  • Alzheimer’s disease then, might be a byproduct of your brain’s attempts to fight off infections

Some people have a genetic mutation known to increase the production of beta-amyloid, but in most people the cause behind such buildup is unknown.

Provocative new research suggests that beta-amyloid buildup may not be intrinsically abnormal, and instead, may act as a natural antibiotic that protects your brain from infection. Alzheimer’s disease, then, might be a byproduct of your brain’s attempts to fight off infections.

Alzheimer’s Disease as a Byproduct of Infectious Disease

Harvard researchers have suggested that beta-amyloid proteins are antimicrobial peptides (part of your innate immune response) and have a beneficial role to play in your brain.

If viruses or bacteria cross your blood-brain barrier, the beta-amyloid traps the foreign invader and essentially imprisons it in a sticky beta-amyloid “cage,” where it ultimately dies.

The “cages” left behind form the plaque buildup seen in Alzheimer’s, the researchers suggest. The theory already has some strong scientific backing. So far, the researchers have infected brain cells in petri dishes with bacteria and found beta-amyloid was produced in response.

The experiment was repeated in yeast, roundworms, fruit flies and mice. In the latter case, salmonella infection in the brain led to the development of plaques in the brain’s hippocampus “overnight.”

And according to study author Rudolph E. Tanzi, Ph.D., of Harvard Medical School and Massachusetts General Hospital, “each plaque had a single bacterium at its center.”1 Mice that didn’t produce beta-amyloid were at greater risk of dying from the infection and did not have any plaques in their brains.

Beta-Amyloid May Be Both Protective and Damaging

It could be that a little bit of beta-amyloid is protective, while larger amounts lead to damage. You may develop more beta-amyloid plaques as you get older because your blood-brain barrier tends to become “leaky” with age, allowing the opportunity for more pathogens to enter your brain.

Separate research by Dr. Berislav Zlokovic, the director of the Zilkha Neurogenetic Institute at the University of Southern California, has shown that the leakiest area of the blood-brain barrier is near the hippocampus, where plaques typically form in Alzheimer’s disease.2

Even brain infections that caused no symptoms could potentially lead to the buildup of plaques, which may explain why some people with no known history of brain infections go on to develop Alzheimer’s.

It’s also likely that people have varying abilities to clear the plaques from their brains after infection. Part of this may be genetically based and there are likely other factors involved as well.

Alzheimer’s Previously Linked to Herpes Virus

Many are not aware that Alzheimer’s disease has been linked to viral infections in the past. In 1991, Ruth Itzhaki, Ph.D., professor emeritus of molecular neurobiology at Britain’s University of Manchester, and colleagues first linked the disease to herpes simplex virus 1 (HSV-1), which is the type that causes cold sores.

More than 100 studies have been published since supporting the link, but the scientific community has been slow to accept it as a possibility. Itzhaki told Newsweek:3

“There’s great hostility to the microbial concept amongst certain influential people in the field, and they are the ones who usually determine whether or not one’s research grant application is successful …

The irony is that they never provide scientific objections to the concepts — they just belittle them, so there’s nothing to rebut!”

Earlier this year, Itzhaki and colleagues penned an editorial, published in the Journal of Alzheimer’s Disease, that called for increased attention into the role infectious agents play in the progression of Alzheimer’s disease, cognitive impairment and other forms of dementia.4 The researchers explained:5

” … [W]e propose that infectious agents, including HSV-1, Chlamydia pneumonia, and spirochetes, reach the CNS [central nervous system] and remain there in latent form.

These agents can undergo reactivation in the brain during aging, as the immune system declines, and during different types of stress (which similarly reactivate HSV-1 in the periphery).

The consequent neuronal damage — caused by direct viral action and by virus-induced inflammation — occurs recurrently, leading to (or acting as a cofactor for) progressive synaptic dysfunction, neuronal loss, and ultimately AD [Alzheimer’s disease].

Such damage includes the induction of Aβ [amyloid beta] which, initially, appears to be only a defense mechanism.”

Infectious Prion-Like Protein Also Linked to Alzheimer’s

The accumulating research that suggests Alzheimer’s disease may have an infectious component is becoming too plentiful to ignore. In addition to viruses, bacteria and fungus, an infectious protein called TDP-43 has also been linked to the disease.

TDP-43 behaves like infectious proteins known as prions, which are responsible for the brain destruction that occurs in Mad Cow and Chronic Wasting Diseases — two types of bovine spongiform encephalopathy.

According to research published in 2011, TDP-43 pathology is detected in 25 to 50 percent of Alzheimer’s patients, particularly in those with hippocampal sclerosis, characterized by selective loss of neurons in the hippocampus, which is associated with memory loss.6

Research presented at the 2014 Alzheimer’s Association International Conference (AAIC) also revealed Alzheimer’s patients with TDP-43 were 10 times more likely to have been cognitively impaired at death than those without.7

The common denominator between Mad Cow and Chronic Wasting Diseases (the latter of which affects deer and elk) is forcing natural herbivores to eat animal parts and byproducts, such as blood and bone meal.

This is common practice in concentrated animal feeding operations (CAFOs). The evidence also suggests humans may be infected with TDP-43 via contaminated meats.

The most infectious parts of a cow carrying these prions are the brain and spinal cord, which may be found in hot dogs, bologna, and products containing either gelatin or ground meat.8 The human version of Mad Cow disease is known as variant Creutzfeldt-Jakob disease (vCJD).

Symptoms of vCJD are similar to Alzheimer’s and include staggering, memory loss, impaired vision, and dementia,9 and there’s no known cure. An intriguing suggestion is that Alzheimer’s is a slower moving version of Mad Cow disease, acquired by eating contaminated CAFO meats.

Vitamin D Linked to a Lower Risk of Alzheimer’s

A wide variety of brain tissue contains vitamin D receptors, and when they’re activated by vitamin D, it facilitates nerve growth in your brain.

Researchers also believe that optimal vitamin D levels boost levels of important brain chemicals and protect brain cells by increasing the effectiveness of glial cells in nursing damaged neurons back to health.

Vitamin D may also exert some of its beneficial effects on your brain through its anti-inflammatory and immune-boosting properties. It also helps produce 200 to 300 different antimicrobial peptides in your body, which kill bacteria, viruses and fungi and could be important if Alzheimer’s does turn out to be infectious in nature.

Seniors with severe vitamin D deficiency may raise their risk for dementia by 125 percent, and vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer’s disease.10 Sufficient vitamin D (50 to 70 nanograms/milliliter) is imperative for overall health, and likely, for brain health as well.

Lifestyle Strategies to Prevent Alzheimer’s Disease

There are an estimated 5.4 million Americans living with Alzheimer’s disease, and rates are expected to increase rapidly. By 2050, the number of people age 65 and older with Alzheimer’s may reach nearly 14 million, “barring the development of … breakthroughs to prevent or cure the disease,” the Alzheimer’s Association reported.11

For now, the underlying causes and cures for Alzheimer’s are unknown, but there are some lifestyle strategies that may boost your immune system health and significantly lower your risk. Diet is part and parcel of a successful prevention plan, and my optimized nutrition plan can set you on the right path in this regard. In terms of your diet and other lifestyle factors, the following suggestions may be among the most important for Alzheimer’s prevention:

Replace processed foods with real foods

The vast majority of processed foods contain genetically engineered (GE) grains, which are heavily contaminated withglyphosate — an herbicide ingredient thought to be worse than DDT (DDT has already been linked to the development of Alzheimer’s).

Eating real food will also limit your exposure to trans fats. As a general rule, to avoid trans fats you need to avoid any and all foods containing or cooked in partially hydrogenated vegetable oil, so be sure to check the list of ingredients.
Avoid sugar and refined fructose

Alzheimer’s appears to be intricately linked to insulin resistance. 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/leptin resistance or any related disorders.
Optimize omega-6:3 ratio, ideally should be 1:1 to 5:1

Healthy fats that your brain needs for optimal function include organically raised grass-fed meats, coconut oil, olives and olive oil, avocado, nuts, organic pastured egg yolks, and butter made from raw grass-fed milk.

High intake of the omega-3 fats EPA and DHA are also helpful for preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression and lowering your risk of developing the disorder. It is imperative to also reduce industrial omega-6 oils, like soy, corn, sunflower, and safflower oils.
Avoid gluten and casein (primarily wheat and pasteurized dairy, but don’t avoid raw dairy, such as whole milk, and organic butter)

Research shows that your blood-brain barrier is negatively affected by gluten. Gluten also makes your gut more permeable, which allows proteins to get into your bloodstream, where they don’t belong. That then sensitizes your immune system and promotes inflammation and autoimmunity, both of which may play a role in the development of Alzheimer’s.

Cream is perhaps the most important part of raw milk because the cream is where all the energy is that’s needed to digest the milk protein casein. That’s why it’s important to consume full-fat, raw dairy products instead of non-fat or skim dairy products. The cream is also responsible for regulating the sugar absorption into your blood. It decreases the likelihood of insulin spikes.
Opt for organic, grass-fed, and finished meat

The vast majority of all store-bought meats and meats served in restaurants come from CAFOs unless otherwise labeled as organic or grass-fed.
Optimize your gut flora

Regularly eat fermented foods or take a high potency and high-quality probiotic supplement.
Reduce your overall calorie consumption and/or intermittently fast

Ketones are mobilized when you replace carbs with coconut oil and other sources of healthy fats. Intermittent fasting is a powerful tool to jumpstart your body into remembering how to burn fat and repair the insulin/leptin resistance that is also a primary contributing factor for Alzheimer’s.
Improve your magnesium levels

Preliminary research strongly suggests a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Unfortunately most magnesium supplements do not pass the blood-brain barrier. Magnesium threonate appears to, however, and holds some promise for the future for treating this condition and may be superior to other forms.
Get plenty of folate

Vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day. Avoid folic acid supplements, which are the inferior synthetic version of folate.
Exercise regularly

It’s been suggested that exercise can trigger a change in the way amyloid precursor protein is metabolized, thus slowing down the onset and progression of Alzheimer’s. Exercise also increases levels of the protein PGC-1alpha. Research has shown that people with Alzheimer’s have less PGC-1alpha in their brains and cells that contain more of the protein produce less of the toxic amyloid protein associated with Alzheimer’s.
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 and eliminate aluminum from your body

Sources of aluminum include antiperspirants, non-stick cookware, vaccine adjuvants, etc. For tips on how to detox aluminum, please see my article, “First Case Study to Show Direct Link Between Alzheimer’s and Aluminum Toxicity.”
Avoid flu vaccinations

Many contain both mercury and aluminum, well-known neurotoxic and immunotoxic agents.
Avoid anticholinergics 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.
Challenge your mind daily

Mental stimulation, especially learning something new, such as how to play an instrument or speak 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.