HOW PERCEPTA™ WORKS

Plaques and Tangles in the Normal Aging Brain

HOW PERCEPTA™ WORKS

Plaques and Tangles in the Normal Aging Brain

Your brain is an amazing thing, perhaps the most complex organ in the universe! Right now, your brain contains about 100 billion nerve cells all constantly connecting, firing and helping you get through the day. Starting in our early adulthood, however, our brains begin a slow, deliberate decline, as they begin to accumulate “plaques and tangles.”

Your brain is an amazing thing, perhaps the most complex organ in the universe! Right now, your brain contains about 100 billion nerve cells all constantly connecting, firing and helping you get through the day. Starting in our early adulthood, however, our brains begin a slow, deliberate decline, as they begin to accumulate “plaques and tangles.”

How Percepta™ works. 

Your brain is the most complex organ in the universe. It weighs only three pounds, or about 2% of your body’s weight. Yet it uses 20-30% of the calories you consume, 20% of the oxygen you breathe, and 25% of the blood flow in your body; it consist of 85% water. There are approximately 100 billion nerve cells (i.e. neurons) in your brain, and up to a quadrillion synapses1. Starting in your early adulthood, there is a slow but deliberate accumulation of two neurotoxic proteins in your brain as you age2.

Your brain is the most complex organ in the universe.

Beta-amyloid plaques form between nerve cells (i.e. neurons) and have been shown to kill surrounding nerve cells.

First is the brain accumulation of an insoluble (aggregated) specific protein known as the “beta-amyloid protein” (i.e. “Aβ” or “Abeta”). Beta-amyloid protein deposits in the form of “plaques” (that look like “meatballs” in the brain under a light microscope) have been shown to be instrumental in killing healthy neurons (i.e. nerve cells)3-5. The accumulation of “plaques” in the brain leads to a decline in hippocampus-dependent memory and cognition in the normal aging brain. Dr. Snow’s laboratories developed and patented methods to produce “plaques” in a test-tube: (identical to what is seen in the human brain) and used these methods to screen for and identify natural “plaque-reducing” nutraceutical ingredients6.

The second neurotoxic protein that accumulates in the aging brain is known as the “tau protein” and forms twisted paired helical filaments inside neurons (or nerve cells) called “tangles”7-8. Tangles accumulate inside neurons and cause neurons to die. “Tangles” look like dried spaghetti strands under a light microscope.

Dr. Snow’s research team was the sole supplier of the tau 4-repeat domain to Sigma Aldrich which was sold to researchers all over the world to make “tangles” in a test-tube or petri dish9. Thus, in the normal aging brain, you have the accumulation of both “plaques and tangles” that cause neurons to die; connections between nerve cells (called synapses) to disintegrate; and memory and cognition to progressively decline.

Neurofibrillary tangles consisting of tau protein form inside neurons and also cause neurons to die.

Compounds or agents able to disaggregate and reduce the accumulation of “plaques and tangles” have been shown to lead to memory improvement and a reduction in memory decline10-18. The only difference between a healthy brain and an aging brain is the number of “plaques and tangles” in the brain. The more “plaques and tangles” you accumulate as you normally age, the worse your memory, focus, concentration and cognition will be.

Percepta™ is postulated to be the world’s first oral nootropic to target the real reason we lose memory as we age: The accumulation of brain “plaques and tangles.”*

References:

  1. Chopra, Deepak, and Tanzi, Rudolph. Super Brain: Unleashing the Explosive Power of Your Mind to Maximize, Health, Happiness and Spiritual Well-Being. Three Rivers Press, New York, 2012.
  2. Baker-Nigh, A., et al. Neuronal amyloid-β accumulation within cholinergic basal forebrain in ageing and Alzheimer’s disease. Brain 138:1722-1737, 2015.
  3. Rodrique, K.M., Kennedy, K.M., & Park, D.C. Beta-amyloid deposition and the aging brain.Neuropsychology Rev. 19:436-450, 2009.
  4. Rodrique, K.M., et al. β-amyloid burden in healthy aging. Regional distribution and cognitive consequences. Neurology 78:387-395, 2012.
  5. Wolk, D.A., and Klunk, W.E. Update on amyloid imaging: from healthy aging to Alzheimer’sdisease. Curr. Neurol. Neurosc. Rep. 9:345-352, 2009.
  6. Catillo, G.M., and Snow, A.D. US Patent #7148001 B2. In vitro formation of congophilic maltese-cross amyloid plaques to identify anti-plaque therapeutics for the treatment of Alzheimer’s and prion diseases. Issued: Dec 12, 2006.
  7. Jin, M. et al. Soluble amyloid beta-protein dimers isolated from Alzheimer cortex directly induce tau hyperphosphorylation and neurite degeneration. Proc. Natl. Acad. Sci. USA 108:5819-5824, 2011.
  8. Scholl, M. et al. PET imaging of tau deposition in the aging human brain. Neuron 89:971-982, 2016.
  9. See www.sigmaaldrich.com and look up tau 4-repeat domain human.
  10. Schenk et al. Immunization with amyloid-β attenuates Alzheimer’s-disease-like pathology in PDAPP mouse. Nature 400:173-177, 1999.
  11. Bard, F. et al. Peripherally administered antibodies against amyloid beta-peptide enters the central nervous system and reduce pathology in a mouse model of Alzheimer’s disease. Nature Medicine 6:916-919, 2000.
  12. Janus, C. et al. Aβ peptide immunization reduces behavioral impairment and plaques in a model of Alzheimer’s disease. Nature 408:979-982, 2000.
  13. Morgan, D., et al. Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer’s disease. Nature 49:982-985, 2000.
  14. Hock C., et al. Antibodies against β-amyloid slow cognitive decline in Alzheimer’s disease. Neuron 38:547-554, 2003.
  15. Walsh, D.M. and Selkoe, D.J. Deciphering the molecular basis of memory failure in Alzheimer’s disease. Neuron 44:181-193, 2004.
  16. Wang, A., Das, P., Switzer, R.C., Golde, T.E. and Jankowsky, J.L. Robust amyloid clearance in a mouse model of Alzheimer’s disease provides novel insights into the mechanism of amyloid-beta immunotherapy. J. Neuroscience 31:4124-4136, 2011.
  17. Bohrmann B., et al. Gatenerumab: a novel human anti-Aβ antibody demonstrates sustained cerebral amyloid-β binding and elicits cell mediated removal of human amyloid-β. J. Alzheimer’s Dis. 28:49-69, 2012.
  18. Ostrowitzki et al. Mechanism of amyloid removal in patients with Alzheimer’s disease treated with gatenerumab. Arch. Neurology 69:198-207, 2012.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to treat, diagnose, cure or prevent any disease.