The Real Cause of Alzheimer’s Disease Revealed

Alzheimer’s disease affects an estimated 5.4 million Americans and is the sixth leading cause of death in the U.S. Researchers have not even gotten close to creating effective long-term therapies for this disease. However, a recent breakthrough may open many new doors in the way of prevention, treatment and, hopefully, a cure.

For the past two decades, Alzheimer’s research has focused on what was considered the prime culprit in the development of the disease—amyloid-beta. This sticky protein fragment accumulates in the brain and forms plaques. These plaques disrupt cellular communication in the brain, triggering an inflammatory response that ultimately harms the cells.

But research out of the Mayo Clinic shows that another protein called tau may have an even more significant role in Alzheimer’s disease.1

In the first part of this study, researchers examined 3,618 postmortem brains. Of these, 1,375 had confirmed Alzheimer’s diagnoses. Because these patients died at different ages and stages of disease, researchers were given a “valuable timeline into disease progression.”

Evaluating the evolution of both amyloid and tau proteins in these brains, they discovered that the “severity of tau, but not amyloid, predicted age onset of cognitive decline, disease duration and mental deterioration.”

In the second part of the study, the researchers examined amyloid brain scans in participants while they were alive. They found that some of the scans showed visible amyloid, even though those people did not have Alzheimer’s or cognitive decline. This indicates that, while amyloid is present in brains afflicted with Alzheimer’s, it can be found in unaffected brains too.

Even so, you should not discount the potential harm these plaques can inflict. As the lead researcher stated, amyloid disturbs proper cellular communication, while tau causes the actual death of neurons.

Doctors use amyloid scanning pretty commonly, but tau imaging is still in its infancy. Researchers hope that by checking for both proteins in the brain, doctors will be able to more accurately diagnose Alzheimer’s, especially in the earlier stages.

Brain-Supportive Nutrients

While tau may very well be the future of Alzheimer’s research, you shouldn’t wait to protect your brain. Now is the time to start. Many nutrients have been scientifically proven to support healthy brain function. Some of the top picks include:

  • Curcumin. The medicinal compound found in the Indian spice turmeric, curcumin has potent antioxidant and anti-inflammatory properties. Research also shows that it has a great deal of promise in lessening Alzheimer’s risk and improving brain function. It actually interferes in the pathway that leads to the development of tau and amyloid plaques. Longvida® is a high-quality brand of curcumin specially formulated to enhance absorption.2-3
  • Phosphatidylserine (PS) is a phospholipid—an essential component in the membranes that surround each and every cell. PS is particularly abundant in brain and nerve cells. Your body makes the PS it needs to maintain proper cellular function. But therapeutic levels (achieved through supplementation) can improve memory, decrease age-related mental decline and treat Alzheimer’s.4-6
  • Omega-3 essential fatty acids have been shown time and again to provide countless benefits to the brain. According to a recent meta-analysis, omega-3s safeguard against mild cognitive impairment, dementia and the risk and progression of Alzheimer’s.7
  • Green tea. Exciting research shows that epigallocatechin gallate (EGCG), an antioxidant in green tea, can stop the accumulation of not only amyloid-beta but also tau!8

Remember, prevention is still the smartest path to take when it comes to Alzheimer’s and other dementias. And these nutrients can go a long way in helping you do just that.


  1. Mayo Clinic.
  2. Huang HC, et al. J Recept Signal Transduct Res. 2014 Feb;34(1):26-37.
  3. Rao PP, et al. Chem Biol Drug Des. 2015 Mar 16. [Epub ahead of print.]
  4. Kim HY, et al. Prog Lipid Res. 2014 Oct;56:1-18.
  5. Vakhapova V, et al. Dement Geriatr Cogn Disord. 2014;38(1-2):39-45.
  6. Lee B, et al. Prog Neuropsychopharmacol Biol Psychiatry. 2015 Jan 2;56:1-10.
  7. Waitzberg DL and Garla P. Nutr Hosp. 2014 Sep 1;30(3):467-77.
  8. Wobst HJ, et al. FEBS Lett. 2015 Jan 2;589(1):77-83.


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