You have to utilize the best available evidence today to avert Alzheimer’s disease a couple of decades ahead in your future. That is what the best authorities are saying today. The changes in the brain associated with early Alzheimer’s memory loss begin at least two decades prior to noticeable mental decline. Treatment when symptoms first begin to arise may be too late to reverse deleterious effects upon the brain.
Brain researchers now believe it would be more productive to develop a treatment that will be prescribed in the earliest stages of mental decline. [Molecular Neurodegeneration Oct 2013]
Beta amyloid plaque deposition in the brain may precede Alzheimer’s disease symptoms by 20 years. [Discovery Medicine May 2013]
The recent news headline racing across electronic news services says that an anti-Alzheimer’s vaccine received at age 40 could eradicate the brain plaques that interfere with brain cell signaling. [Telegraph UK June 3, 2014]
Professor James Nicoll, professor of neuropathology at Southamptom University (UK) says a vaccine can “kick-start” the immune system and eradicate plaque commonly found in the brains of Alzheimer’s subjects. The vaccine amazingly removed existing beta-amyloid plaque.
Professor Nicoll is quoted to say: ““But could we vaccinate before symptoms started? It could prevent the (plaque) accumulation in the first place.”
Vaccines fail miserably
But even Dr. Nicoll disclosed that while the idea of an anti-Alzheimer’s vaccine may seem promising, “he was dismayed to find it did not stop mental decline or early death.”
There is another sobering realization. Researchers won’t know if any vaccine works for decades following inoculation.
Dr. Nicoll did not disclose in his news interviews that the initial trials using a beta amyloid vaccine among Alzheimer’s disease subjects had to be halted due to side effects. [Acta Neuropathologica Sept 2010]
The vaccine works by provoking the immune system to create antibodies against beta amyloid plaque. The antibodies solubilize the plaque.
A post-mortem examination of human brains of vaccinated Alzheimer’s subjects reveals brain hemorrhages and an increase in the number of blood vessels in the affected areas. However, examination of two subjects who survived 4-5 years after vaccination revealed virtually complete absence of brain plaques. [Brain Dec 20080
Alzheimer’s disease was first described by German physician Alois Alzheimer’s in 1907. Immunotherapy for Alzheimer’s disease was first described by Schenk in 1999. [Neurodegenerative Diseases 2005] But 14 years of subsequent research has not produced a safe and effective vaccine.
Researchers doggedly pursue a vaccine
Researchers refuse to let go of the idea of an anti-Alzheimer’s vaccine. After more than a decade of failed research investigators continue to say it “remains one of the most promising emerging strategies for developing disease-modifying treatments for Alzheimer’s disease. [Journal Internal Medicine March 2014]
Unfathomably, researchers know that an aged immune system that has gone awry and is over-responsive and produces chronic brain inflammation is believed to be responsible for the onset and progression of this disease. [Nature Reviews Immunology Dec 2013] Yet vaccines provoke the very same immune response that causes the disease. The immune response needs to be normalized, not over-stimulated, to conquer this brain disease. Vaccines appear to be counterproductive by design.
A recent review of ongoing human clinical trials of Alzheimer’s vaccines asks: “Is there still any hope for amyloid-based immunotherapy for Alzheimer’s disease? [Current Opinion Psychiatry March 2014]
However a recent vaccine trial in rodents produced a striking reduction of beta amyloid brain plaque that even resulted in improved mental performance. [Journal Alzheimer’s Disease March 2014] So at least the laboratory animals have hope.
Is plaque eradication a cure?
About 19% of healthy senior adults have the same abnormalities as Alzheimer’s subjects. Some scientists believe up to 30% of Alzheimer’s cases are misdiagnosed. [Medical-Surgical Journal of the Society of Physicians and Naturalists Jan 2013]
Critics point to the fact that accumulation of beta amyloid plaque in the brain is not correlated with memory deficits. However, the accumulation of tau protein is. So strategies to remove tau protein may be more productive. [Nature Reviews Neurology Dec 2013]
Modern pharmacology appears to be headed in the wrong direction in its effort to make drugs or vaccines that address beta amyloid plaque.
One of the problems Alzheimer’s patients face is that due to impaired blood flow to the brain with advancing age the brain compensates and begins to generate new blood vessels, a process called angiogenesis. The eradication of beta amyloid plaque neutralizes the biological trigger that produces new blood vessels (angiogenesis). [Science Reports 2013]
Natural molecules like resveratrol have been shown to exert strong anti-angiogenic action and may serve to inhibit the development of abnormal blood vessels in the brain with advancing age. [Food Chemistry Toxicology Nov 2013] This has already been demonstrated in humans in the human eye. [Nutrients June 2013]
Alzheimer’s therapy without vaccines
So can the immune system be primed to work efficiently, but not over-react, to inhibit the formation of brain plaque without the need for problematic vaccines?
Researchers are pointing to natural molecules found in Mediterranean diets as brain-protective agents. [Molecular Neurobiology Oct 2013]
Resveratrol, known as a red wine molecule, has been shown in lab dish studies to suppress formation of inflammatory molecules in the brain. [Biochemical Biophysical Research Communications Sept 2012] Resveratrol works synergistically with vitamin D in this regard. [Molecular Nutrition Food Research March 2014]
There is a strong correlation between Alzheimer’s disease and lack of sunlight/low vitamin D blood levels. [Bone Dec 1998]
The Journal of Alzheimer’s Disease published a recent paper that pointed to vitamin D3 (the natural form of the vitamin, not synthetic D2) and it improved the ability of white blood cells known as phagocytes that limit beta amyloid formation. This test was performed in a lab dish with peripheral blood mononuclear cells obtained from Alzheimer’s disease patients. The study concluded that low intake levels of vitamin D and DHA-omega-3 oils promotes inflammation that compromises the ability of phagocytes to digest amyloid brain plaque. [Journal Alzheimer’s Disease Jan 2013]
Vitamin D activates the innate immune system, normalizing production and activity of white blood cells called neutrophils and macrophages. Brain clearance of beta amyloid plaque is facilitated by phagocytes the solubilize beta amyloid plaque. The ability of phagocytes to digest beta amyloid is defective among Alzheimer’s subjects, a function that is restored in lab dishes when vitamin D3 is added.
Combination of vitamin D3 with polyphenols such as curcumin from turmeric spice appears to be a way to recover a dysregulated innate immune system among Alzheimer’s subjects. [Journal Alzheimer’s Disease 2012]
There are alternatives to unproven vaccines. Researchers indicate there are two types of macrophage white blood cells, one that responds to vitamin D3 and polyphenols such as curcumin and a second type that responds to vitamin D3 only. Omega-3 oils also calm inflammation associated with this brain disease. [CNS Neurological Disorders Drug Targets April 2010]
Acetyl coenzyme-A enzyme and Alzheimer’s
Your liver builds cholesterol molecules by stringing together molecules of acetyl coenzyme A. Statin cholesterol-lowering drugs disrupt this process.
It turns out that acetyl coenzyme A is also used in energy metabolism: the cellular power plants (mitochondria) in your cells break down glucose, amino acids, and fatty acids into molecules of acetyl coenzyme A that are turned into adenosine triphosphate (ATP) the cellular energy component.
Researchers report that acetyl-coenzyme-A is a key factor for survival of brain cells.
Cholesterol-lowering statin drugs disrupt the cholesterol synthesis process.
Sugar (glucose) is utilized in the brain to produce pyruvate, a precursor for acetyl coenzyme-A. Brain cells require acetyl coenzyme-A to produce a brain chemical known as acetycholine that transmits signals from one brain cell to another.
Alzheimer’s is characterized by a decrease in acetyl coenzyme-A and a decline in acetycholine and mental function. One strategy to waylay Alzheimer’s disease is to preserve proper supply of acetyl coenzyme-A in the diseased brain. [Neurochemical Research Aug 2013] This suggests use of statin cholesterol-lowering drugs is counterproductive to Alzheimer’s disease prevention.
The sugar connection
Population-wise, there is an association between adult diabetes and mental decline. [Journal Alzheimer’s Disease May 23, 2014]
Another prevalent factor involved in Alzheimer’s disease appears to be a perturbed brain sugar metabolism. [Progressive Neurobiology Sept 2013]
The brain has a high demand for sugar. Reduced glucose metabolism is an invariant characteristic of Alzheimer’s disease. Diabetes predisposes to Alzheimer’s disease. It is known that vitamin B1-dependent processes in the brain strongly correlate with mental decline and vitamin B1 is critical for proper glucose metabolism.
Vitamin B1 (thiamin) deficiency exacerbates amyloid and tau protein plaque formation and impairs memory. B1 treatment with benfotiamine, a highly absorbable form of vitamin B1, diminishes plaque and reverses memory decline. Researchers recently concluded that: “the use of benfotiamine could provide a safe intervention to reverse biological and clinical processes of AD progression.” [Molecular Cell Neuroscience July 2013]
Human trials using oral thiamine have been shown to improve the mental function of patients with Alzheimer’s disease. [American Journal Alzheimer’s Disease Other Dementia Dec 2011]
Whereas other antioxidants such as vitamins C and E counter oxygen-derived free radicals that can damage living tissues, vitamin B1/thiamin inhibits free radicals derived from nitrogen gas. [Neurochemical Research Dec 2010]
In laboratory mice, it is benfotiamine, the fat-soluble form of vitamin B1, that works to correct mental decline, not the water-soluble thiamin. [Brain May 2010]
An important note, benfotiamine therapy may not work without sufficient magnesium. [Evidence Based Complementary Alternative Medicine June 2007]
B vitamin supplementation (800 micrograms folic acid, 20 mg vitamin B6, 500 micrograms vitamin B12 reduces by as much as 7-fold the progressive shrinkage of grey matter in the aging brain, particularly in regions involved in Alzheimer’s disease. [Proceedings National Academy Science June 2013]
Minerals for Alzheimer’s
Minerals play a role in mental decline. A study involving 1406 senior adults for 8 years revealed that high magnesium intake was associated with a 93% relative reduction in the risk for age-related mental decline. Iron consumption significantly increases the risk. [Frontiers Aging Neuroscience Feb 2014]
Other researchers report magnesium has a therapeutic application in Alzheimer’s disease. [Journal Alzheimer’s Disease 2010]
Researchers suggest at-risk or current Alzheimer’s subjects limit intake of iron-rich red meat, increase intake of magnesium, and increase intake of polyphenols such as resveratrol (wine, grapes), quercetin (red onion, red apple peel), curcumin (turmeric spice), catechin (tea), all which are mineral-controlling molecules. [Frontiers Human Neuroscience Oct 2013]
Administration of clioquinol, a copper-chelating (key-lay-ting) drug has been demonstrated to inhibit deposits of amyloid in Alzheimer’s brains but its use has produced toxic side effects. [Current Alzheimer’s Research June 2013]
Resveratrol is a copper-chelating natural molecule that does not exhibit toxicity in modest doses (below 300 mg). [Biochemical Pharmacology May 1997] Resveratrol has been shown to promote the efflux (exit) of beta amyloid plaque from the brain via its ability to chelate copper. [Journal Biological Chemistry Nov 2005]
Challenge to amyloid plaque theory of Alzheimer’s Disease
Recently researchers challenged the amyloid brain plaque theory of the origin of Alzheimer’s disease. Investigators point to fibrin-based blood clots in the brain that resist breakdown and promote inflammation. Iron-induced free radicals have now been identified as agents to promote fibrin-like clots that are “remarkably resistant to degradation.”
Similar insoluble deposits are present in Alzheimer’s disease brains. These clots can then impair delivery of oxygen to the brain. These fibrin-based clots can be degraded by magnesium and certain polyphenols such as resveratrol. [Frontiers Human Neuroscience Oct 2013]
There is a defect in the internal antioxidant defense system among Alzheimer’s subjects. Internally made enzymatic antioxidants catalase, superoxide dismutase and glutathione are significantly lower among Alzheimer’s patients. [Journal Trace Element Medicine Biology July 2010]
The internal antioxidant system is activated via Nrf2 gene transcription factor. [Neuropharmacology April 2014] There are over 60 natural molecules that have been identified as Nrf2 activators that may correct a flawed antioxidant system. [Pharmaceutical Research Nov 2011]
While the provision of omega-3 oils to Alzheimer’s subjects did not show differences in mental decline it is believed omega-3 oils should be provided years in advance of the disease-induced symptoms. [Advances Nutrition Nov 2013]
In laboratory mice, combinations of polyphenols (resveratrol, catechin, quercetin, curcumin, others) reduce total amyloid plaque content in the brain better than single polyphenols. [Frontiers Aging Neuroscience March 2014]
The argument will be that these natural agents are unproven, but so will the vaccines.
To date, all efforts to develop a disease-modifying treatment for Alzheimer’s disease (AD) have been unsuccessful. [Pharmacy & Therapeutics May 2014] Commercial interests (pharmaceutical and vaccine companies, physicians) control research and applied science while ignoring non-prescription remedies that often are far more cost effective. [Pharmacy & Therapeutics May 2014]
Drugs or vaccines may someday allay some of the symptoms of Alzheimer’s disease but they would not be appropriate if the symptomology is induced by overconsumption of alcohol or other factors involving a shortage of nutrients (e.g. magnesium, vitamin B1).
The fact that Medicare face a funding shortfall of trillions of dollars to meet the heath care needs of Americans suggests these economical non-prescription remedies need to be prioritized. But modern medicine keeps beating a drum for blockbuster drugs and vaccines.
A health regimen to prevent or reverse Alzheimer’s disease might include:
- Low red meat intake to prevent iron overload.
- Avoidance of copper supplements
- Avoidance of statin drugs that impair acetyl coenzyme-A
- High intake of green leafy vegetables and nuts for magnesium as well as magnesium dietary supplements.
- Sunshine and vitamin D3 supplements [Ortopedia, Traumatologia, Rehabilitacja July-Aug 2008]
- B vitamins (folic acid, vitamin B6 as pyridoxyl phosphate)
- Benfotiamine (fat soluble vitamin B1)
- DHA-rich omega-3 fish oil
- Nrf2 activators that correct defective internal antioxidant status (sulforaphane from broccoli sprouts, resveratrol from wine and grapes, curcumin from turmeric spice, quercetin from red apples and onions).
- Limitation of alcohol intake (depletes vitamin B1, magnesium)
- Smoking cessation
- Adherence to recommendations may delay onset of symptoms by 15-20 years. [Journal Alzheimer’s Disease 2014]