Nattokinase and beta-amyloid plaques

November 27, 2012 at 3:02 PM

Many families that have purchased Neprinol for their mother or father’s arthritis have seen not only an improvement in their arthritis symptoms, but have also noticed that their memory has improved and nearly returned to normal. While they might call this improvement a miracle, it is not due to luck or divine intervention. It all comes down to Neprinol’s ability to dissolve the protein fibrin.

 

Fibrin is a protein that is naturally found in blood and is responsible for forming blood clots and scar tissue. Usually our bodies keep fibrin levels in check with enzymes that break down any excess fibrin. However, with age our bodies make fewer enzymes, allowing fibrin to build up. That can lead or contribute to many serious diseases, including Alzheimer’s.

 

The Role of Fibrin in Alzheimer’s

One of the causes of Alzheimer’s disease is the buildup of hard plaques between brain cells. These plaques are made up of a protein called beta-amyloid, which is a small fragment of a naturally produced brain protein called amyloid precursor protein. Beta-amyloid is usually broken down and eliminated, but this doesn’t occur as efficiently as we get older1. However, just having a lot of beta-amyloid doesn’t automatically lead to plaque development.

 

Around the brain is a barrier that stops anything harmful in the blood from entering the brain - called the blood-brain barrier. Studies have shown that age-related damage to the blood-brain barrier allows fibrin and other proteins to leak into the brain2. Once inside the brain, the fibrin joins with any beta-amyloid that is there to form clots. These clots obstruct blood flow and contribute to inflammation, damaging the brain and leading to the memory loss and other problems associated with Alzheimer’s2-4.

 

Researchers have been studying fibrin as a potential way to treat Alzheimer’s. Scientists from Rockefeller University found that they could reduce inflammation and blood vessel damage in the brains of Alzheimer’s mice by decreasing the amount of fibrin in their blood with a natural enzyme2,5. A later study showed that breaking up fibrin reduced the amount of amyloid deposits found in the brain blood vessels of Alzheimer’s mice and also improved their memories4.

 

Neprinol

Neprinol is a combination of nattokinase, an enzyme extracted from a popular Japanese fermented soybean food, and serrapeptase, an enzyme from silkworms, as well as several other enzymes. When these enzymes are introduced into the bloodstream, they work throughout the entire body, to break down fibrin and other proteins, like beta-amyloid. In one study, nattokinase was shown to effectively degrade beta-amyloid protein6. This is evidence that nattokinase is useful in improving the symptoms of Alzheimer’s disease due to its ability to help remove the beta-amyloid plaques in the brain. Also, by clearing any other “garbage” from the blood, Neprinol greatly reduces the amount of stress on the immune system. When the blood is clean the immune system becomes less aggravated and inflammation levels drop. This also has a positive effect on Alzheimer’s since the disease is partly due to inflammation in the brain7, 8.

 

Despite the proof that decreasing fibrin and inflammation can reduce the symptoms of Alzheimer’s, Neprinol and other enzyme supplements have not yet been rigorously tested in humans for this purpose. Still, Neprinol customers report that it helps in their relatives with Alzheimer’s and the studies exist to explain how it works. With few supplements available that help with Alzheimer’s, Neprinol is a great option.

 

References:

  1. Vinters HV, Wang ZZ, Secor DL. Brain parenchymal and microvascular amyloid in Alzheimer’s disease. Brain Pathol. 1996;6(2):179-195.
  2. Paul J, Strickland S, Melchor JP. Fibrin deposition accelerates neurovascular damage and neuroinflammation in mouse models of Alzheimer’s disease. J Exp Med. 2007; 204(8):1999-2008.
  3. Merkle DL, Cheng CH, Castellino FJ, Chibber BA. Modulation of fibrin assembly and polymerization by the beta-amyloid of Alzheimer’s disease. Blood Coagul Fibrinolysis. 1996;7(6):650-658.
  4. Cortes-Canteli M, Paul J, Norris EH, et al. Fibrinogen and beta-amyloid association alters thrombosis and fibrinolysis: a possible contributing factor to Alzheimer’s disease. Neuron. 2010;66(5):695-709.
  5. Deane R, Zlokovic BV. Role of the blood-brain barrier in the pathogenesis of Alzheimer’s disease. Curr Alzheimer Res. 2007;4(2):191-197.
  6. Hsu RL, Lee KT, Wang JH, Lee LY, Chen RP. Amyloid-degrading ability of nattokinase from Bacillus subtilis natto. J Agric Food Chem. 2009;57(2):503-508.
  7. Tuppo EE, Arias HR. The role of inflammation in Alzheimer’s. Int J Biochem Cell Bio. 2005;37:289-305.
  8. Zotova E, Nicoll JAR, Kalaria R, Holmes C, Boche D. Inflammation and Alzheimer’s disease: relevance to pathogenesis and therapy. Alzheimers Res Ther. 2010;2:1.


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