Alzheimer’s disease (AD) is a devastating fatal neurological condition that we’ve all heard or read about or have first-hand experience through our family connection. It is characterized by memory loss and abnormal behavior.
Amyloid beta plaque
This article discusses the role of amyloid beta plaque and the possibility of preventing or slowing its development. Formation of this plaque is the first event in the pathology of Alzheimer’s eventually resulting in nerve cell death.1
What is Amyloid-Beta Plaque?
Amyloid-beta is produced throughout life in healthy brains. A specific enzyme “snips” very small strands of amyloid-beta (AB) from the amyloid-beta precursor protein (APP). In the healthy brain APP plays an essential role in nerve growth and nerve repair. In the healthy brain any excess AB is broken down, washed out of the brain, and eliminated from the body.
However when the enzyme snips longer strands, they are sticky and begin to tangle and accumulate in clumps of misfolded proteins in the spaces between nerve cells.2 It is unknown exactly why the responsible enzyme snips longer strands that do not readily dissolve, but interaction between APP and tau protein (linked with microtubule functioning in the brain), is likely part of the process.
The amyloid plaques first develop in the areas of the brain concerned with memory and other cognitive functions, the cerebral cortex, which is the outer layer of nerve tissue in the brain. as well as the hippocampus. The cerebral cortex controls “attention, perception, awareness, thought, memory, language, and consciousness.”3
Nutrients that may help prevent plaque deposits
Researchers have been investigating nutrients that may help break down these deposits of plaque or prevent their build-up.
Top brain nutrients that appear to have the widest range of brain benefits include: acetyl-L-carnitine, ashwagandha, apigenin, curcumin, DHA (or fish oil), gingko biloba, ginseng, grapeseed extract, green tea extract, lutein, N-acetyl-cysteine, resveratrol, olive leaf extract, phosphatidylserine, PQQ (pyrroloquinoline quinone), vinpocetine, vitamin E, and zeaxanthin.
Any nutrients that may help delay or prevent Alzheimer’s must directly or indirectly impact amyloid-beta plaque production. Therefore, they need to be able to:
- cross the blood brain barrier, and
- reduce development of beta-amyloid plaque or its precursors.
In addition, they must:
- support growth of new nerve cells (neurogenesis),
- support brain adaptability,
- provide antioxidant support,
- reduce inflammation, and
- reduce excessive apoptosis (nerve cell death).
Alpha Lipoic Acid – The alpha R form is the one most easily utilized by the body. Supplementation with alpha lipoic acid inhibits progress of tau protein toward fibrils of plaque, reduces cognitive decline, lipid peroxidation, inflammation, and tau-induced iron overload.4
Astaxanthin in addition to enhance learning and memory, astaxanthin reduces tau hyperphosphorylation, a precursor process to beta-amyloid plaque.5 particularly when supplemented with DHA.
Curcumin – has been found to inhibit amyloid beta plaque, inhibit formation of amyloid beta oligomers and fibrils, inhibit acetylcholinesterase, mediate insulin signaling, reduce tau hyperphosphorylation, and binding to copper.6
DHA, a component of omega-3 essential fatty acids, reduces amyloid beta build-up7 (especially in conjunction with astaxanthin), but also promotes brain-derived nerve factor,8 supports cognition,9 and enhances neurogenesis. It supports cell differentiation, maturation, neuron survival, and inflammation reduction.
Ginger Root increases neurogenesis, raises BDNF levels, enhances cognitive function, and helps in reducing amyloid beta plaque for those with Alzheimer’s.10
Gotu Kola (Centella asiatica) may reverse amyloid beta toxicity in the brain. 14 15 Some other benefits include rejuvenating nerve and brain cells and is believed to be capable of increasing intelligence, longevity, and memory.16 17
Melatonin stimulates non-amyloidogenic processing and inhibits beta amyloid precursor protein processing culminating in amyloid aggregates.18 Much research shows the benefits of melatonin for PD motor and nonmotor impairments, including insomnia, anxiety, depression, and cognitive impairment.19
Pyrroloquinoline Quinone (PQQ) indirectly reduces beta-amyloid plaque accumulation by increasing circulation, protecting the brain against neurotoxins, improving mitochondrial function, and supporting BDNF.20
Zeaxanthin inhibits amyloid beta aggregation, and, combined with lutein, reduces AD mortality.21
This information is from Michael Edson’s new book “Natural Brain Support: Preventing and Treating Alzheimer’s and Dementia and Other Related Diseases Naturally.” This book is also available as an e-book.
We’ve created several brain-supporting nutrient packages that contain many of these components.
Brain and Memory Support Package 1 contains nerve and brain support mushrooms, a range of antioxidants including essential fatty acids and astaxanthin, our whole food, organic, GMO free eye and brain formula with lutein, zeaxanthin, bilberry, organic tomato, broccoli, spinach and more, and a proprietary blend of catalase, saw almetto, alpha lipoic acid, d-ribose, phosphatidylersine, rhodiola, transresveratrol, horse tail, quercetin, PABA, nettle root, fisetin, CoQ10, barley rgass, PQQ, fo ti, and biotin.
- Glenner GG. (1983). Alzheimer’s disease. The commonest form of amyloidosis. Arch Pathol Lab Med. Jun; 107(6):281-2. ↩
- Amyloid beta. Wikipedia. Retrieved Mar 6 2021 from https://en.wikipedia.org/wiki/Amyloid_beta. ↩
- Cerebral cortex. Wikipedia. Retrieved Mar 6 2021 from https://en.wikipedia.org/wiki/Cerebral_cortex. ↩
- Hiller S, DeKroon R, Hamlett ED, Xu L, Osorio C, et al. (2016). Alpha-lipoic acid supplementation protects enzymes from dam-age by nitrosative and oxidative stress. Biochim Biophys Acta. Jan;1860(1 Pt A):36-45. ↩
- Che H, Li Q, Zhang T, Wang D, Yang L, et al. (2018). Effects of Astaxanthin and Docosahexaenoic-Acid Acylated Astaxanthin on Alzheimer’s Disease in APP/PS1 Double-Transgenic Mice. J Agric Food Chem. May 16;66(19):4948-4957. ↩
- Tang M, Taghibiglou C. (2017). The Mechanisms of Action of Curcumin in Alzheimer’s Disease. J Alzheimers Dis. 2017;58(4):1003-1016. ↩
- Grimm MOW, Michaelson DM, Hartmann T. (2017). Omega-3 fatty acids, lipids, and apoE lipidation in Alzheimer’s disease: a rationale for multi-nutrient dementia prevention. J Lipid Res. Nov;58(11):2083-2101. ↩
- Matsuoka Y, Nishi D, Tanima Y, Itakura M, Kojima A, et al. (2015). Serum pro-BDNF/BDNF as a treatment biomarker for re-spose to docosahexaenoic acid in traumatized people vulnerable to developing psychological distress: a randomized controlled trial. Transl Psychiatry. Jul 7;5:e596. ↩
- Weiser MJ, Butt CM, Mohajeri MH. (2016). Docosahexaenoic Acid and Cognition throughout the Lifespan. Nutrients. Feb 17;8(2):99 ↩
- Wightman EL. (2017). Potential benefits of phytochemicals against Alzheimer’s disease. Proc Nutr Soc. May;76(2):106-112. ↩
- Rege NN, Thatte UM, Dahanukar SA (1999). Adaptogenic properties of six rasayana herbs used in Ayurvedic medicine. Phytother Res. 1999;13:275–291. ↩
- Heo J.H., Lee S.T., Chu K., Oh M.J., Park H.J., Shim J.Y., Kim M. An open-label trial of Korean red ginseng as an adjuvant treat-ment for cognitive impairment in patients with Alzheimer’s disease. Eur J Neurol. 2008;15:865–868. ↩
- Heo J.H., Lee S.T., Oh M.J., Park H.J., Shim J.Y., Chu K., Kim M. Improvement of cognitive deficit in Alzheimer’s disease patients by long term treatment with Korean red ginseng. J Ginseng Res. 2011;35:457–461. ↩
- Balietti M, Giannubilo SR, Giorgetti B, Solazzi M, Turi A, et al. (2016). The effect of astaxanthin on the aging rat brain: gender-related differences in modulating inflammation. J Sci Food Agric. 2016;96:615–618. ↩
- Choi SK, Park YS, Choi DK, Chang HI. (2008). Effects of astaxanthin on the production of NO and the expression of COX-2 and iNOS in LPS-stimulated BV2 microglial cells. J Microbiol Biotechnol. Dec;18(12):1990-6. ↩
- Shinomol GK, Muralidhara, Bharath MM. (2011). Exploring the Role of “Brahmi” (Bacopa monnieri and Centella asiatica) in Brain Function and Therapy. Recent Pat Endocr Metab Immune Drug Discov. Jan; 5(1):33-49. ↩
- Cervenka F, Jahodár L. (2006). Plant metabolites as nootropics and cognitives. Ceska Slov Farm. Sep;55(5):219-29. ↩
- Singh B, Pandey S, Yadav SK, Verma R, Singh SP, et al. (2017). Role of ethanolic extract of Bacopa monnieri against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced mice model via inhibition of apoptotic pathways of dopaminergic neurons. Brain Res Bull. Oct;135:120-128. ↩
- Ishige K, Schubert D, Sagara Y. (2001). Flavonoids protect neuronal cells from oxidative stress by three distinct mechanisms. Free Radic Biol Med. Feb 15; 30(4):433-46. ↩
- Gong P, Deng F, Zhang W, Ji J, Liu J, et al. (2017). Tectorigenin attenuates the MPP+ -induced SH-SY5Y cell damage indicating a potential beneficial role in Parkinson’s disease by oxidative stress inhibition. ↩
- Hammond BR Jr, Miller LS, Bello MO, Lindbergh CA, Mewborn C, et al. (2017). Effects of Lutein/Zeaxanthin Supplementation on the Cognitive Function of Community Dwelling Older Adults: A Randomized, Double-Masked, Placebo-Controlled Trial. Front Aging Neurosci. 2017; 9: 254. ↩