Smart Publications

Clarifying the Complex World of Nutrition Science

  • Email this article
  • Print this article
  • A
  • A
  • A

Clear Your Brain of the Toxic Gunk that Causes Alzheimer’s Disease!

Many of us have heard friends complain—in jest—that they think they’re getting Alzheimer’s disease. Or maybe you’ve made that comment yourself after forgetting an appointment or locking your keys in the car. But it’s nothing to joke about, and actually, unless you’re a caregiver and/or have someone close to you with the disease, most people have no idea that Alzheimer’s disease entails a lot more than forgetfulness. Alzheimer’s disease literally kills the brain, wiping out the ability to use language, add a simple column of numbers, read the newspaper, control thoughts, and eventually recognize close friends and family.

Normal Neuron Alzheimer's Neurons
Normal Brain Neurons
Alzheimer's Neurons with Amyloid Plaques and Neurofibrillary Tangles

Initially, the only symptom of Alzheimer’s may be mild forgetfulness, like forgetting what you went into a room for, what you ate for lunch, or where you put your hat. In later stages, behavioral and personality changes such as aggressive acts or aimless wandering may accompany the cognitive decline. Eventually, patients are bedridden and require total care.

-Sponsored Ads-

Advanced Prostate Formula

Save 25% to 50% on ProstaE8
Prostate Protection Formula

Whether you know someone with Alzheimer’s or not, please keep on reading this report . . . because:

1) We want to tell you about nine nutraceuticals that have been shown to clear amyloid—the toxic gunk that causes Alzheimer’s—out of your brain.

2) These herbs and nutrients can help prevent Alzheimer’s disease from grabbing hold of your brain.

3) These nutraceuticals produce a cognitive-enhancing effect that can support your memory NOW.

4) Sooner or later, you will know someone with Alzheimer’s disease.

5) 14 million Baby Boomers are predicted to succumb to this disease in the
next decade.

After years of research, most scientists now believe that amyloid plaques and neurofibrillary tangles—within the brain—are the hallmarks of Alzheimer’s disease, and that they contribute to the degradation of the neurons in the brain and the subsequent symptoms of the disease.

What is amyloid protein?

Amyloid is a microscopic protein fragment of a larger protein called amyloid precursor or protein (APP) that is normally found throughout the body. In Alzheimer’s disease, this protein is processed improperly,
creating a substance called beta-amyloid, which is toxic to brain cells. In a healthy brain, these protein fragments would be broken down and eliminated. But in Alzheimer’s disease the fragments accumulate to form insoluble plaques.

What are neurofibrillary tangles?

These bundles of twisted filaments are the other structural indicator of Alzheimer’s disease. Neurofibrillary tangles are made up of tau protein. In healthy neurons, tau forms part of a structure called a microtubule, which helps transport nutrients and other important substances from one part of the nerve cell to another. In Alzheimer’s disease, however, the tau protein is abnormal and the microtubule structures collapse, which leads to the death of brain cells.

How do you know it’s Alzheimer’s?*
*Alzheimer’s disease is more than forgetting where you put the car keys, or walking into a room and wondering what you went in there for.

Here’s a guideline to help you access your concerns.
Does the person you are concerned about:

  1. Repeat things or ask the same questions over and over?
  2. Seem more forgetful, or have trouble with short term memory?
  3. Need reminders to do things like chores, grocery shop, eat, take
  4. nutritional supplements, etc.?
  5. Forget appointments, family occasions, or holidays?
  6. Feel “blue,” or cry more often than in the past?
  7. Have trouble doing calculations, managing finances, or balancing the checkbook?
  8. Show a loss of interest in activities such as hobbies, reading, attending religious services, or other social activities?
  9. Need help preparing a meal, dressing, bathing, or using the bathroom?
  10. Become irritable, agitated, suspicious, or hear or believe things that are not real?
  11. Get lost while driving or drive unsafely?
  12. Have trouble finding the right words, finishing sentences, or naming people or things?

*Adapted from Mundt JC, Freed DM, Griest JH. Lay person-based screening for early detection of Alzheimer’s disease: development and validation of an instrument. J Gerontol Psychol Sci Sco. 2000, 55B: 163-170.

Page 1 of 3 pages  1 2 3 >

Editor's Note:

The natural health solutions described in these article are available through many on-line retailers including those listed below. By clicking these links you help support the important alternative health research we provide.

Visit NutriStand – The Nutrition Newsstand from the Supplement Man for Science-Based Nutritional Supplements!

Visit International Antiaging-Systems for hard to find therapies. They specialize in Tomorrow's Treatments Today™.

Visit – a great way to find competitive deals on supplements offered by many different manufacturers.

Visit VitaE8 - The Ultimate Vitamin E – to learn more about the importance of full-spectrum vitamin E supplements.

These articles are not intended to diagnose, treat, cure, or prevent any disease. Always consult with a physician before embarking on a dietary supplement program.


  1. Adapted from a fact sheet published by the Alzheimer’s Association, Experimental Alzheimer drugs targeting beta-amyloid and the “amyloid hypothesis.” ©2005 Alzheimer’s Association. All rights reserved. This is an official publication of the Alzheimer’s Association but may be distributed by unaffiliated organizations and individuals. Such distribution does not constitute an endorsement of these parties or their activities by the Alzheimer’s Association.

  2. Scientists: New brain research needed. Experts fear worldwide epidemic of Alzheimer’s disease, Associated Press.

  3. Paris D, et al. AB vasoactivity: an inflammatory reaction. Ann NY Acad Sci 2000, Apr; 903: 97-109.

  4. Picoulin, Kathryn, Reversing Alzheimer’s Naturally. 2002, Auburn Hill Publishing Co., Ca.

  5. Paris D, Townsend KP, Obregon DF, Humphrey J, Mullan M. Pro-inflammatory effect of freshly solubilized beta-amyloid peptides in the brain. Prostaglandins Other Lipid Mediat. 2002 Sep;70(1-2):1-12.

  6. Adapted from a fact sheet published by the Alzheimer’s Association, Experimental Alzheimer drugs targeting beta-amyloid and the “amyloid hypothesis.” ©2005 Alzheimer’s Association. All rights reserved. This is an official publication of the Alzheimer’s Association but may be distributed by unaffiliated organizations and individuals. Such distribution does not constitute an endorsement of these parties or their activities by the Alzheimer’s Association.

  7. “Neurofibrillary tangles” 

  8. Higgins, Guy A. a; Jacobsen, Heimut Transgenic mouse models of Alzheimer’s disease: phenotype and application. Behavioural Pharmacology. 14(5-6):419-438, September 2003. 

  9. Rockenstein EM, McConlogue L, Tan H, Power M, Masliah E, Mucke L. Levels and alternative splicing of amyloid beta protein precursor (APP) transcripts in brains of APP transgenic mice and humans with Alzheimer’s disease. J Biol Chem. 1995 Nov 24;270(47):28257-67.

  10. Hsaio, K., P. Chapman, S. Nilsen, C. Eckman, Y. Harigaya, S. Younkin, F. Yang, & G. Cole: Correlative memory deficits, beta-amyloid elevation, and amyloid plaques in transgenic mice. Science 274, 99-103 (1996)

  11. Schupf, N. Genetic and host factors for dementia in Down’s syndrome. The British Journal of Psychiatry (2002) 180: 405-410.

  12. Deb S, Braganza J, Norton N, Williams H, Kehoe PG, Williams J, Owen MJ. APOE epsilon 4 influences the manifestation of Alzheimer’s disease in adults with Down’s syndrome. Br J Psychiatry. 2000 Nov;177:469-70.

  13. Xiao XQ, Yang JW, Tang XC. Huperzine A protects rat pheochromocytoma cells against hydrogen peroxide-induced injury. Neurosci Lett. 1999 Nov 12; 275(2): 73-6.

  14. Ye JW, Cai JX, Wang LM, Tang XC. Improving effects of huperzine A on spatial working memory in aged monkeys and young adult monkeys with experimental cognitive impairment. J Pharmacol Exp Ther. 1999 Feb; 288(2): 814-9.

  15. Iuvone T, De Filippis D, Esposito G, D’Amico A, Izzo AA. The spice sage and its active ingredient rosmarinic acid protect PC12 cells from amyloid-{beta} peptide-induced neurotoxicity. J Pharmacol Exp Ther. 2006 Feb 22; [Epub ahead of print].

  16. Pereira P, Tysca D, Oliveira P, da Silva Brum LF, Picada JN, Ardenghi P. Neurobehavioral and genotoxic aspects of rosmarinic acid. Pharmacol Res. 2005 Sept; 52(3):199-203.

  17. Bate, Clive, Salmona Mario, WIlliams, AlunGinkgolide B inhibits the neurotoxicity of prions or amyloid-β1-42. Journal of Neuroinflammation 2004, 1:4 doi:10.1186/1742-2094-1-4. 

  18. Yao Z, Drieu K, Papadopoulos V. The Ginkgo biloba extract EGb 761 rescues the PC12 neuronal cells from beta-amyloid-induced cell death by inhibiting the formation of beta-amyloid-derived diffusible neurotoxic ligands. Brain Res. 2001 Jan 19;889(1-2):181-90.

  19. Luo Y, Smith JV, Paramasivam V, Burdick, A, Curry, KJ. Buford JP, Khan I, Netzer WJ, XU H, Butko P. Inhibition of amyloid-beta aggregation and caspase-3activation by the Ginkgo biloba extract EGb761. Proc Natl Acad Sci USA 2002 Sept 17;99(19):12197-202.

  20. Rudakewich M, Ba F, Benishin CG. Neurotrophic and neuroprotective actions of ginsenosides Rb(1) and Rg(1). Planta Med. 2001 Aug;67(6):533-7. 

  21. Lee TF, Shiao YJ, Chen CF, Wang LC. Effect of ginseng saponins on beta-amyloid-suppressed acetylcholine release from rat hippocampal slices. Planta Med.

  22. Wang LC, Wang B, Ng SY, Lee TF. Effects of ginseng saponins on beta-amyloid-induced amnesia in rats. J Ethnopharmacol. 2006 Jan 3;103(1):103-8. Epub 2005 Sep 8. 

  23. Tohda C, Matsumoto N, Zou K, Meselhy MR, Komatsu K. Abeta(25-35)-induced memory impairment, axonal atrophy, and synaptic loss are ameliorated by M1, A metabolite of protopanaxadiol-type saponins. Neuropsychopharmacology. 2004 May;29(5):860-8.

  24. Chihiro Tohdaa, Tomoharu Kuboyamaa,b, Katsuko Komatsua,b Search for Natural Products Related to Regeneration of the Neuronal Network. Neurosignals 2005;14:34-45 (DOI: 10.1159/000085384).

  25. Joo SS, Won TJ, and Lee DI, Reciprocal activity of ginsenosides in the production of proinflammatory repertoire, and their potential roles in neuroprotection in vivo, Planta Medica 2005; 71(5): 476-481.

  26. Joo SS, Lee do I. Potential effects of microglial activation induced by ginsenoside Rg3 in rat primary culture: enhancement of type A Macrophage Scavenger Receptor expression. Arch Pharm Res. 2005 Oct;28(10):1164-9. 

  27. Liu JX, Cong WH, Xu L, Wang JN. Effect of combination of extracts of ginseng and ginkgo biloba on acetylcholine in amyloid beta-protein-treated rats determined by an improved HPLC. Acta Pharmacol Sin. 2004 Sep;25(9):1118-23.

  28. Kidd PM. A review of nutrients and botanicals in the integrative management of cognitive dysfunction. Altern Med Rev. 1999 Jun;4(3):144-61.

  29. Pereira C, Agostinho P, Oliveira CR. Vinpocetine attenuates the metabolic dysfunction induced by amyloid beta-peptides in PC12 cells. Free Radic Res. 2000 Nov;33(5):497-506.

  30. Wang R, Tang XC. Neuroprotective effects of huperzine A. A natural cholinesterase inhibitor for the treatment of Alzheimer’s disease. Neurosignals. 2005;14(1-2):71-82. 

  31. Gao X, Tang XC. Huperzine a attenuates mitochondrial dysfunction in beta-amyloid-treated PC12 cells by reducing oxygen free radicals accumulation and improving mitochondrial energy metabolism. J Neurosci Res. 2006 May 1;83(6):1048-57.

  32. BBC News, “Curry May Slow Alzheimer’s.” Wednesday, 21 November, 2001.

  33. Yang F, Lim GP, Begum AN, Ubeda OJ, Simmons MR, Ambegaokar SS, Chen PP, Kayed R, Glabe CG, Frautschy SA, Cole GM. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J Biol Chem. 2005 Feb 18;280(7):5892-901. 
    Epub 2004 Dec 7.

  34. Brain Research Institute, UCLA, press release, “Curry Spice May Fight Alzheimer’s Disease.” News release, UCLA.

  35. Sun QQ, Xu SS, Pan JL, Guo HM, Cao WQ. Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students. Zhongguo Yao Li Xue Bao. Acta Pharmacol Sin 1999 Jul; 20(7): 601-3.

  36. Ono K, Hasegawa K, Naiki H, Yamada M. Preformed beta-amyloid fibrils are destabilized by coenzyme Q10 in vitro. Biochem Biophys Res Commun. 2005 Apr 29;330(1):111-6.

  37. Ono K, Yoshiike Y, Takashima A, Hasegawa K, Naiki H, Yamada M. Potent anti-amyloidogenic and fibril-destabilizing effects of polyphenols in vitro: implications for the prevention and therapeutics of Alzheimer’s disease. J Neurochem. 2003 Oct;87(1):172-81. 

  38. Ono K, Hirohata M, Yamada M. Ferulic acid destabilizes preformed beta-amyloid fibrils in vitro. Biochem Biophys Res Commun. 2005 Oct 21;336(2):444-9.

  39. Lee KH, Shin BH, Shin KJ, Kim DJ, Yu J. A hybrid molecule that prohibits amyloid fibrils and alleviates neuronal toxicity induced by beta-amyloid (1-42). Biochem Biophys Res Commun. 2005 Mar 25;328(4):816-23.

  40. Mohmmad Abdul H, Butterfield DA. Protection against amyloid beta-peptide (1-42)-induced loss of phospholipid asymmetry in synaptosomal membranes by tricyclodecan-9-xanthogenate (D609) and ferulic acid ethyl ester: implications for Alzheimer’s disease. Biochim Biophys Acta. 2005 Jun 30;1741(1-2):140-8. Epub 2004 Dec 25.

  41. Cho JY, Kim HS, Kim DH, Yan JJ, Suh HW, Song DK. Inhibitory effects of long-term administration of ferulic acid on astrocyte activation induced by intracerebroventricular injection of beta-amyloid peptide (1-42) in mice. Prog Neuropsychopharmacol Biol Psychiatry. 2005 Jul;29(6):901-7.

  42. Yan JJ, Cho JY, Kim HS, Kim KL, Jung JS, Huh SO, Suh HW, Kim YH, Song DK. Protection against beta-amyloid peptide toxicity in vivo with long-term administration of ferulic acid. Br J Pharmacol. 2001 May;133(1):89-96.

  43. Bhattacharya A, Ghosal S, Bhattacharya SK. Anti-oxidant effect of Withania somnifera glycowithanolides in chronic footshock stress-induced perturbations of oxidative free radical scavenging enzymes and lipid peroxidation in rat frontal cortex and striatum. J Ethnopharmacol. 2001 Jan;74(1):1-6.

  44. Schliebs R, Liebmann A, Bhattacharya SK, Kumar A, Ghosal S, Bigl V. Systemic administration of defined extracts from Withania somnifera (Indian Ginseng) and Shilajit differentially affects cholinergic but not glutamatergic and GABAergic markers in rat brain. Neurochem Int. 1997 Feb;30(2):181-90.

  45. Kuboyama T, Tohda C, Zhao J, Nakamura N, Hattori M, Komatsu K. Axon- or dendrite-predominant outgrowth induced by constituents from Ashwagandha. Neuroreport. 2002 Oct 7;13(14):1715-20.

  46. Tohda C, Kuboyama T, Komatsu K. Dendrite extension by methanol extract of Ashwagandha (roots of Withania somnifera) in SK-N-SH cells. Neuroreport. 2000 Jun 26;11(9):1981-5.

  47. Kuboyama T, Tohda C, Komatsu K. Withanoside IV and its active metabolite, sominone, attenuate Abeta(25-35)-induced neurodegeneration. Eur J Neurosci. 2006 Mar;23(6):1417-26. 

  48. Tohda C, Kuboyama T, Komatsu K. Search for natural products related to regeneration of the neuronal network. Neurosignals. 2005;14(1-2):34-45. 

  49. Baycrest study uses advanced PET scanning technique to detect brain deposits associated with Alzheimer’s. Journal of Geriatric Psychiatry (AJGP). Nov.-Dec. 2004.

  50. Wegiel J, Wisniewski HM, Dziewiatkowski J, Popovitch ER, Tarnawski M. Differential susceptibility to neurofibrillary pathology among patients with Down syndrome. Dementia. 1996 May-Jun;7(3):135-41. 

  51. Memory loss and the brain.


  53. Cognitive Impairment Common in Seniors: Increases with Age, 
    Lack of Education. April 5, 2006.

Related Articles


Keep me updated

Carsolic Acid is found in Rosemary and Sage .............................................................................................................................  Neurosci Res. 2014 Feb;79:83-93. doi: 10.1016/j.neures.2013.11.004. Epub 2013 Dec 1.
Carnosic acid suppresses the production of amyloid-β 1-42 and 1-43 by inducing an α-secretase TACE/ADAM17 in U373MG human astrocytoma cells.
Yoshida H1, Meng P2, Matsumiya T2, Tanji K3, Hayakari R2, Xing F2, Wang L2, Tsuruga K4, Tanaka H5, Mimura J6, Kosaka K7, Itoh K6, Takahashi I8, Imaizumi T2.
Author information
Amyloid beta (Aβ) peptides are key molecules in the pathogenesis of Alzheimer’s disease (AD). The sequential cleavage of amyloid precursor protein (APP) by the β- and γ-secretases generates Aβ peptides; however, the alternate cleavage of APP by the α- and γ-secretases decreases Aβ production. We previously reported that carnosic acid (CA), a phenolic diterpene compound found in the labiate herbs rosemary and sage, suppresses Aβ (1-40 and 1-42) production by activating α-secretase in cultured SH-SY5Y human neuroblastoma cells (Neurosci. Res. 2013; 75: 94-102). Here, we investigated the effect of CA on the production of Aβ peptides (1-40, 1-42 and 1-43) in U373MG human astrocytoma cells. The treatment of cells with CA suppressed Aβ40/42/43 release (55-71% decrease at 50μM). CA treatment enhanced the mRNA expressions of an α-secretase TACE (tumor necrosis factor-α-converting enzyme, also called a disintegrin and metalloproteinase-17, ADAM17); however, the β-secretase BACE1 (β-site APP-cleaving enzyme-1) was not increased by CA. Knockdown of TACE by siRNA reduced soluble-APPα release enhanced by CA and partially recovered the CA-suppressed Aβ40/42/43 release. These results suggest that CA reduces Aβ production, at least partially, by activating TACE in human astroglial cells. The use of CA may have a potential in the prevention of Aβ-mediated diseases.
Copyright © 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
ADAM17; Alzheimer’s disease; Astrocytes; Aβ; Carnosic acid; TACE
PMID: 24295810

Now a person can study and get a professional with clear mind with the help of online life experience degree programs. These programs are very helpful in business world and a person is capable to apply new skills.

Leave a Comment

Commenting is not available in this channel entry.