Recently at an Alzheimer’s support group meeting the subject of inflammation and it’s role in Alzheimer’s Disease came up. I referred the group to an answer provided by Dr. Don Colbert about a year ago. Dr Colbert is a blender of alternative and traditional approachs to medical problems, a pretty smart guy.
The doctor was asked:
How can simple inflammation cause such a devastating disease?
Dr. Colbert’s answer with (references below provided by the doctor in his forum):
" Plaques and tangles are indeed the hallmarks of Alzheimer’s disease. But researchers looking at the brain damage caused by Alzheimer’s have always noted the presence of inflammation wherever plaques and tangles form.10 In the past, this inflammation was thought to be simply a consequence of Alzheimer’s disease. Now scientists believe the inflammation itself starts a chain reaction ultimately contributing to the developement of Alzheimer’s disease.11 When cells in the brain are disrupted by inflammation, amyloid, a protein normally found in the brain, begins to act chaotically. This chaos results in the creation of beta amyloid, protein that is toxic to cells in the brain. Sticky deposits of beta-amyloid build up and collect around the cells, making dense clumps or plaques. Because the brain can’t break the plaques down or get rid of them, they stay right where they are and slowly accumulate.10,12,13 The consequence of these abnormalities of protein in the brain is more than the cell death they cause. They also act as roadblocks, interfering with electrochemcial messengers being shot from cell to cell. Therefore, the remaining healthy cells’ activity is diminished as well. Research of identical twins has repeatedly shown that if one twin has Alzheimer’s disease, the other has a 60% chance of developing the disease, too. Scientists from the Karolinska Institute in Stockholm, Sweden, looked at information from 20,000 twins collected in the 1960s and found 109 pairs of siblings where only one twin had been diagnosed with Alzheimer’s. When the Swedish researchers analyzed data about the twins’ health, they found the twin with Alzheimer’s disease almost always had chronic gum disease. While bleeding gums are definitely not the cause of Alzheimer’s disease, the inflammation that plays a large part of chronic gum disease may signal an inflammatory process stuck in overdrive.16 In fact, the inflammatory process might occur years before the onset of Alzheimer’s, and be the result of any number of infections people can contract. That’s why current research is searching for ways to protect brain cells from inflammation. And why some countries have low rates of Alzheimer’s disease, like India."
Tangles result when long protein fibers that act like scaffolding for brain cells begin to twist and tangle. The cell is damaged and eventually dies. But the tangled proteins remain in the brain even after the dead neuron has been cleared away.10,14 And inflammation might be the culprit causing the long protein fibers to start tangling.15
1. Jha S, Patel R. Some observations on the spectrum of dementia. Neurol India. 2004;52:21 3-4.
2. Vas CJ, Pinto C, Panikker D, et al. Prevalence of dementia in an urban Indian population. Int Psychogeriatr 2001 ;1 3:439-50.
3. The Alzheimer’s Disease Fact Sheet. Alzheimer’s Disease Education & Referral Center. A service of the National Institute of Aging. Accessed on September 8, 2005.
4. Chandra V, Pandav R, Dodge HH, et al. Incidence of Alzheimer’s disease in a rural community in India: the Indo-US study. Neurology. 2001 ;57:985-9.
5. Ringman JM, Frautschy SA, Cole GM, Masterman DL, Cummings JL. A potential role of the curry spice curcumin in Alzheimer’s disease. Curr Alzheimer Res. 2005;2:131-6.
6. Curcuma longa (turmeric). Monograph. Altern Med Rev. 2001 ;6 Suppl:S62-6.
7. Sharma RA, Gescher AJ, Steward WP. Curcumin: The story so far. Eur J Cancer. 2005;41 :1955-68.
8. Weber WM, Hunsaker LA, Abcouwer SF, Deck LM, Vander Jagt DL. Anti-oxidant activities of curcumin and related enones. B!oorg Med Chem. 2005;1 3:3811-20.
9. Karunagaran D, Rashmi R, Kumar TR. Induction of apoptosis by curcumin and its implications for cancer therapy. Curr Cancer Drug Targets. 2005;5:1 17-
10. Curtis SM, Porth CM. Alzheimer’s disease. In: Porth CM. Pathophys!ology: Concepts of Altered Health States. 5th ed. Philadelphia, Pa: Lippincott; 2002: 914- 917.
11. Fryer JD, Holtzman DM. The bad seed in Alzheimer’s disease. Neuron. 2005;47:167-8.
12. Kranenburg O, Bouma B, Gent YY, et al. Beta-amyloid (Abeta) causes detachment of N1E¬115 neuroblastoma cells by acting as a scaffold for cell-associated plasminogen activation. Mol Cell Neurosc!. 2005;28:496-508.
13. Morgan C, Colombres M, Nunez MT, Inestrosa NC. Structure and function of amyloid in Alzheimer’s disease. Prog Neurob!ol. 2004;74:323-49.
14. Liazoghli D, Perreault S, Micheva KD, Desjardins M, Leclerc N. Fragmentation of the Golgi apparatus induced by the overexpression of wild-type and mutant human tau forms in neurons. Am J Pathol. 2005;166:1499-514.
15. Minghetti L. Role of inflammation in neurodegenerative diseases. Curr Op!n Neurol. 2005;18:315-21.
16. Andel R, Crowe M, Pedersen NL, Mortimer J, Crimmins E, Johansson B, Gatz M. Complexity of work and risk of Alzheimer’s disease: a population-based study of Swedish twins. J Gerontol B Psychol Sc! Soc Sc!. 2005;60:P251 -8.
17. Heady JA, Kennaway EL. The increase in deaths attributed to cancer of the lung. Br J Cancer. 1949;3:31 1-20.
18. Park SY, Kim DS. Discovery of natural products from Curcuma longa that protect cells from beta-amyloid insult: a drug discovery effort against Alzheimer’s disease. J Nat Prod. 2002;65:1227-31.
19. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J B!ol Chem. 2005;280:5892-901.
20. Ono K, Hirohata M, Yamada M. Ferulic acid destabilizes preformed beta-amyloid fibrils in vitro. B!ochem B!ophys Res Commun. 2005;336:444-449.
21. Ono K, Hasegawa K, Naiki H, Yamada M. Curcumin has potent anti-amyloidogenic effects for Alzheimer’s beta-amyloid fibrils in vitro. J Neurosc! Res. 2004;75:742-50.
22. Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sc!. 2004;1030:434-41.
23. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J B!ol Chem. 2005;280:5892-901.
24. Giri RK, Rajagopal V, Kalra VK. Curcumin, the active constituent of turmeric, inhibits amyloid peptide-induced cytochemokine gene expression and CCR5-mediated chemotaxis of THP-1 monocytes by modulating early growth response-1 transcription factor. J Neurochem. 2004;91 :1199-210.
25. Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosc!. 2001 ;21 :8370-7.
26. Cole GM, Morihara T, Lim GP, Yang F, Begum A, Frautschy SA. NSAID and Antioxidant Prevention of Alzheimer’s Disease: Lessons from In Vitro and Animal Models. Ann N Y Acad Sc!. 2004;1 035:68-84.
27. The Univerity of California at Los Angeles (UCLA) Alzheimer’s Disease Research Center (ADRC) Current studies: Mild to Moderate Alzheimer’s Disease and Curcumin. Information available at the ADRC Website: http://www.npistat.com/adrc/Treatment. asp.
28. Pasinetti GM. From epidemiology to therapeutic trials with anti-inflammatory drugs in Alzheimer’s disease: the role of NSAIDs and cyclooxygenase in betaamyloidosis and clinical dementia. J Alzhe!mers D!s. 2002;4:435-45.
29. What You Need to Know About Nonsteroidal Anti-Inflammatory Medications (NSAIDs). The Cleveland Clinic Health Information Center. Accessed on September 8, 2005. Available at: http://www.clevelandclinic.org/health/h ealthinfo/ docs/0700/071 4.asp?index=490 1.
Mail this post
Apparently Curcumin is great to use on meat to get the germs out.