Alzheimer’s is a complex disease that defies simple solutions. However, new research into disease mechanisms is yielding a bounty of approaches that promise to prevent the onset of the disease, slow its progression, and even reverse its pathology.

  • Turmeric, the bright yellow spice that is a primary ingredient in curry powder, shows great promise against Alzheimer’s disease, due to a variety of actions, including its ability to:

    • Inhibit and even reverse amyloid-β deposition1
    • Chelate metals such as copper and iron2
    • Reduce brain levels of iNOS (inducible nitric oxide synthase), inflammatory cytokines, and lipid peroxidation3, 4
    • Act as a potent antioxidant4

  • Improving cholinergic function. An invisible, but pernicious hallmark of Alzheimer’s disease is a marked reduction, in certain regions of the brain, in cholinergic function – brain activity that depends on the neurotransmitter acetylcholine (ACh), which is vitally important for memory formation and retention. Cholinergic dysfunction represents an attractive target for medicinal therapy.

    The most important and widely used anti-Alzheimer’s drugs are acetylcholinesterase (AChE) inhibitors, so called because they inhibit the action of acetylcholinesterase, an enzyme that breaks down ACh molecules (a necessary function that can get out of balance). By interfering with the action of this enzyme, the drugs effectively increase the amount of ACh available to the brain’s neurons. Although they can sometimes halt the progress of the disease for a matter of months and slow down its further progress, they cannot stop it altogether or prevent the inevitable outcome. Nor do they affect any of the neuropathologic changes that make Alzheimer’s so devastating. In addition, most such drugs are expensive and can have unpleasant side effects.

    • Fortunately, some safe, natural supplements can also be used to protect mind and memory. One of these, CDP-choline (short for cytidine-5’-diphosphocholine), functions as an intermediate in the biosynthesis of cell-membrane phospholipids. CDP-choline (also known as citicoline) is a precursor to ACh and has shown considerable promise in studies of people with Alzheimer’s, cognitive deficits, and poor memory.5-7
    • Galantamine, a natural substance found in certain flowers, such as the snowdrop, the daffodil, and the spider lily, has also shown promise is delaying the progression of Alzheimer’s by protecting and enhancing cholinergic function. Although galantamine is available as an FDA-approved prescription drug for the treatment of mild to moderate Alzheimer’s disease, it is also available as the nutritional supplement it has been since long before the FDA declared it a “drug.”

      Galantamine differs from the other currently used anti-Alzheimer’s agents in two important ways: 1) it has not just one, but two distinctly different modes of action, both of which increase the brain’s cholinergic activity; and 2) not only is it able to stall the decline in cognitive function, but it can actually to reverse it (to a degree) for some months, thus “buying time” before the patient’s condition eventually declines again.

      These results have been observed in several major clinical trials conducted in the United States and abroad in recent years.8-15 A meta-analysis (a thorough, critical, comparative analysis) of all the significant studies on galantamine confirmed its role as a safe and effective treatment for mild-to-moderate Alzheimer’s disease.16

  • Green tea, a wondrous brew with a broad spectrum of health-giving benefits, contains compounds, such as epigallocatechin gallate (EGCG), that are antioxidant, antibacterial, antiviral, antimutagenic, and anticarcinogenic. Green tea also helps protect against diabetes, atherosclerosis, heart attack, and stroke. It bolsters the immune system, protects against neurodegeneration, and promotes a sense of tranquility (even though, paradoxically, it’s considered to be a stimulant). Green tea also reduces the risk of Alzheimer’s disease by several mechanisms:

    • It inhibits AChE, thus making more of the neurotransmitter ACh available for memory and cognitive function.
    • It inhibits the formation of amyloid-β by blocking the action of the enzyme β-secretase, which catalyzes the breakdown of amyloid precursor protein (APP). Green tea is the only known natural β-secretase inhibitor.
    • It is a powerful antioxidant, capable of preventing much of the free radical-related damage of Alzheimer’s.

  • Antioxidants. Certain vitamins are indispensable because of their antioxidant properties – their ability to neutralize free radicals and other reactive oxygen species (ROS) that can damage our cells. This is especially important for neurons (brain cells), which are more vulnerable to oxidative stress than most other cells. Oxidative damage to neurons is believed to play a crucial role in the development of Alzheimer’s disease. Indeed, oxidative damage may be one of the earliest pathophysiologic events in Alzheimer’s.17 All the more reason to minimize oxidative stress through the use of antioxidant supplements!

    Among the most potent antioxidants are the fat-soluble vitamin E and the water-soluble vitamin C, whose benefits in this regard have been abundantly documented in the scientific literature. These vitamins exert their powerful antioxidant effects not just individually, but also – and perhaps more importantly – through their participation in the human body’s antioxidant network, which includes vitamin E, vitamin C, lipoic acid, coenzyme Q10, and glutathione (all of which can be taken as supplements except glutathione, which is destroyed in the digestive tract). Recent research has shown that the risk for Alzheimer’s disease in elderly people can be sharply reduced with relatively large supplemental amounts of vitamins E and C – but only when they’re taken together!

    Researchers in Italy and Germany evaluated 144 elderly Italians for presence of 13 different antioxidants in their blood. Twenty-five of the study participants had mild cognitive impairment (MCI), an early sign of impending Alzheimer’s; 63 had Alzheimer’s; and 56 were healthy controls. The results showed that, compared with the controls, the MCI patients had significantly reduced levels of 10 of the 13 antioxidants, and the Alzheimer’s patients had significantly reduced levels of 11 of them. In both groups, the levels of vitamins E and C were below normal).18

    Another study by American investigators in 4740 people aged 65 or older found a strong inverse correlation between the risk for Alzheimer’s disease and the use of both vitamin E and vitamin C. The combination of vitamin E + C was strongly protective, reducing the risk by 78%.19

  • B-Vitamins. Swedish researchers have determined that low levels of the B-vitamins folic acid (folate) and vitamin B12 (cyanocobalamin) can double the risk of developing Alzheimer’s disease in elderly people, but only when both vitamin levels were low.20 The reasons are unclear, but may be related, at least in part, to blood levels of homocysteine, which rise as intake of folic acid and vitamin B12 decline. Homocysteine is strongly implicated in the development of atherosclerosis and, therefore, of heart disease. Atherosclerosis affects not only the coronary arteries but also the cerebral arteries (among many others), so it can impair blood flow to the brain. Homocysteine also has a neurotoxic effect that could lead to cell death or neurological and psychiatric disorders such as Alzheimer's disease.

References

  1. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of Abeta oligomers and fibrils and binds plaques and reduces amyloid in vivo. J Biol Chem Dec. 2004; 10.1074/jbc.M404751200.
  2. 2 Baum L, Ng A. Curcumin interaction with copper and iron suggests one possible mechanism of action in Alzheimer's disease animal models. J Alzheimers Dis 2004;6:367-77; discussion 443-9.
  3. Cole G, Yang F, Lim G, Cummings J, Masterman D, Frautschy SA. Curr Med Chem-Immun, Endoc, & Metab Agents 2003;3:15-25.
  4. Zhao BL, Li XJ, He RG, Cheng SJ, Xin WJ. Scavenging effect of extracts of green tea and natural antioxidants on active oxygen radicals. Cell Biophys 1989;14:175-85.
  5. Alvarez XA, Mouzo R, Pichel V, et al. Double-blind placebo-controlled study with citicoline in APOE genotyped Alzheimer's disease patients. Effects on cognitive performance, brain bioelectrical activity and cerebral perfusion. Methods Find Exp Clin Pharmacol 1999;21:633-44.
  6. Alvarez XA, Sampedro C, Lozano R, Cacabelos R. Citicoline protects hippocampal neurons against apoptosis induced by brain beta-amyloid deposits plus cerebral hypoperfusion in rats. Methods Find Exp Clin Pharmacol 1999;21:535-40.
  7. Alvarez XA, Laredo M, Corzo D, et al. Citicoline improves memory performance in elderly subjects. Methods Find Exp Clin Pharmacol 1997;19:201-10.
  8. Raskind MA. Update on Alzheimer drugs (galantamine). Neurologist 2003;9:235-40.
  9. Raskind MA, Peskind ER, Truyen L, Kershaw P, Damaraju CV. The cognitive benefits of galantamine are sustained for at least 36 months: a long-term extension trial. Arch Neurol. 2004;61:252-256.
  10. Tariot PN, Solomon PR, Morris JC, Kershaw P, Lilienfeld S, Ding C. A 5-month, randomized, placebo-controlled trial of galantamine in AD. The Galantamine USA-10 Study Group. Neurology 2000;54:2269-76.
  11. Tariot P. Current status and new developments with galantamine in the treatment of Alzheimer's disease. Expert Opin Pharmacother 2001;2:2027-49.
  12. Pirttila T, Wilcock G, Truyen L, Damaraju CV. Long-term efficacy and safety of galantamine in patients with mild-to-moderate Alzheimer's disease: multicenter trial. Eur J Neurol 2004;11:734-41.
  13. Sano M, Wilcock GK, van Baelen B, Kavanagh S. The effects of galantamine treatment on caregiver time in Alzheimer's disease. Int J Geriatr Psychiatry 2003;18:942-50.
  14. Wilcock GK, Lilienfeld S, Gaens E. Efficacy and safety of galantamine in patients with mild to moderate Alzheimer's disease: multicentre randomised controlled trial. Galantamine International-1 Study Group. Bmj 2000;321:1445-9.
  15. Joffres C, Bucks RS, Haworth J, Wilcock GK, Rockwood K. Patterns of clinically detectable treatment effects with galantamine: a qualitative analysis. Dement Geriatr Cogn Disord 2003;15:26-33.
  16. Olin J, Schneider L. Galantamine for Alzheimer's disease (Cochrane Review). The Cochrane Library. Oxford: Update Software; 2001.
  17. Nunomura A, Perry G, Aliev G, et al. Oxidative damage is the earliest event in Alzheimer disease. J Neuropathol Exp Neurol 2001;60:759-67.
  18. Rinaldi P, Polidori MC, Metastasio A, et al. Plasma antioxidants are similarly depleted in mild cognitive impairment and in Alzheimer's disease. Neurobiol Aging 2003;24:915-19.
  19. Zandi PP, Anthony JC, Khachaturian AS, et al. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study. Arch Neurol 2004;61:82-8.
  20. Wang HX, Wahlin A, Basun H, Fastbom J, Winblad B, Fratiglioni L. Vitamin B(12) and folate in relation to the development of Alzheimer's disease. Neurology 2001;56:1188-94.

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