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Inflammatory Process in Alzheimer's Disease

by Manuela Malaguti Boyle(more info)

listed in alzheimer's and dementia, originally published in issue 185 - August 2011

Alzheimer's disease (AD) is a progressive degenerative disorder characterized by memory loss,
intellectual decline and definitive cognitive impairment. The incidence of dementia in Western
Countries, of which AD is the major cause, is estimated to be approximately 10% of the population
over the age of 65 and 47% of the population over 80 of age.[1] More than 33% of women and 20% of men aged 65 and older will develop dementia during their lifetime.[2]


The specific cause of AD is not fully understood, and it is likely that multiple causes exist. It is interesting mentioning that in 2002, a study reported in the Archives of Neurology, the eating habits of 980 dementia-free elderly participants were followed for a four year period. Those with apolipoprotein-producing gene (e-4) in the highest 25% of fat consumption had double the risk of developing Alzheimer's as those eating the lowest amount of fat. The presence of  the e-4 gene can be determined y a simple blood test. If present, the predisposition can be modified by dietary factors, so that the disease is less likely to manifest.[3]  So far,  no efficient treatment for the patients has been found. Another study conducted in 2001 by Dr Jorge Barrio of UCLA  found  that a PET brain scan in conjunction with intravenously injective radioactive tracer chemical can identify those with Alzheimer's. The tracer chemical is retained longer in the areas of the brain where the amyloid plaque is present and can be viewed via PET. This system allows physicians to diagnose AD with almost total certainty.[4]

In 1906, the German neuropathologist Alois Alzheimer's microscopically identified the two specific markers characterizing the disease that now bears his name: sticky, abnormal clumps (amyloid plaques) that form within the empty space between brain cells with tangled bundles of fibers (tau neurofibrillary tangles) that erupt from within the clumps. Another characteristic of the disease is the loss  of the nerve cells in the areas responsible for memory and other higher mental abilities.

Symptoms typically begin slowly, and progress over a period of 5 - 20 years, with the average life span of the affected person averaging from 8 to 10 years following the initial diagnosis.[2] At the beginning the individual might experience absentmindness such as difficulties in remembering familiar names, dates and times of activities. As the disease progresses into its later stages, thought process becomes increasingly less clear, with clear difficulties in speaking, reading, writing and comprehension of everyday activities. Anxious or aggressive behaviour usually occurs, alongside mood swings, disorientation and depression.[5]

The clinical features of Alzheimer's disease have been associated to cholinergic dysfunction due to reduction of the activity of the enzyme choline acetyl transferase. This dysfunction is caused by the excitatory amino acids glutamate or aspartate, which, in turn, provokes excessive production of nitric oxide (NO) inflammatory molecules. This excitotoxicity causes the presence of the tangles associated with Alzheimer's disease.[5]

Other possible causes or contributing factors are:

  • Heavy metal toxicity;
  • Oxidative/free radical damage;
  • Inflammation and inflammatory cytokines;
  • Viral infection;
  • Low mitochondrial function;
  • Nutrients deficiency (B3, folic acid, B12).

Heavy Metal Toxicity
There are many extrinsic factors leading to Alzheimer's, particularly mercury. Many people are not aware that the major exposure to mercury occurs in the mouth from silver amalgams fillings. This source of mercury has a direct impact on the brain in some sensitive individuals, particularly those with low nutrient levels of B5 and sulphur compounds such as methionine, cysteine, lipoic acid and thiamine as mercury can bind to these compounds and compromise their function. Lipoic acid and Bioflavonoids such as quercetin and rutin are good chelators of mercury.[2] Aluminium is another metal that has been shown to cause neuronal malfunction and cell death. Aluminium competes with magnesium binding sites in the biological system, thus an individual who is marginally or low in magnesium can accelerate the accumulation of aluminium in the brain. Zinc deficiency increases this accumulation. Once in the brain, aluminium increments free radical production by causing excessive stimulation of the neurons (exitoxicity) and their consequential death. Studies on the absorption of aluminium from drinking water confirm that a significant amount of aluminium reaches the brain particularly if ingested along with organic acids such as malic, citrate, oxalic and lactic acid. Citric acid is usually high in soft drink.[6] Aluminium can be removed from the body by taking desferrioxamine, trivalent ion chelators. Ingestion of aluminium, implicated as a probable cause of AD, should be avoided. This would include antiperspirants (nearly all contain aluminium salts); aluminium-containing anti-acids (such as Mylanta and others); aluminium cans and aluminium cookware (that can leach aluminium ions into the food).[6]

Oxidative Stress
A cell's surface can rust and this process weakens the structure and alters the properties and function of the cell. Fortunately, the cell has a defence system against this rusting, called the
'antioxidant defence system'. It is a series of molecules that prevent free radicals binding with critical component of the cell. These antioxidants include beta-carotene, vitamins C, E, B2, B3, A, selenium, glutathione, CoQ10, Superoxide Dismutase (SOD) and many others.[7]

Inflammation and Inflammatory Cytokines
As the nerve cell death of Alzheimer's sufferers is linked to the build-up of beta amyloid plaque, the brain immune system (microglia) interacts with the amyloid, producing a number of cytokines such as tumour necrosis factor and gamma interferon. The result of this inflammatory state sees a large amount of free radicals that further contribute  to the destruction of nerve cells. The use of free radicals scavenger is consequently recommended. It is important considering that many Alzheimer's patients suffer with an impaired Phase II detoxification pathway, thus nutrients such as methionine, sulphate and taurine are also indicated.[8]

Viral Infection
Herpes simplex often migrates to the brain and in people who carry the protein ApoE4, it has been linked to the onset and development of Alzheimer's disease. ApoE4 causes cognitive decline by reducing the androgen receptors level in the brain, hence Alzheimer's disease patients are affected more by decline in DHEA.[9]

Low Mitochondrial Function
The two major activities within the mitochondrial are the Krebs' Cycle and the Electron Transport Chain.  The latter is the main determiner of intracellular reactive oxygen species (ROS) production. The efficiency of a person's electron transport chain determines the amount of ROS production and studies point that this capacity is determined by genetic make-up. The coupling of these two functions is the ensuing Mitochondrial Oxidative Phosphorylation, which in the brain has to work optimally to produce the maximum amount of energy from a glucose molecule. If any blockage occurs due to free radicals, toxins, radiation or ageing, the cell will die prematurely.

Free radicals can be quenched by supplementing with acetyl-l-carnitine, B complex, magnesium, manganese, vitamin E, CoQ10 and nicotinamide adenine dinucleotide (NAD). These nutrients are powerful allies in controlling neurodegeneration and forestalling the progression of Alzheimer's disease.[5]

Nutrients Deficiency
Nutritional deficiency accelerates the deterioration of Alzheimer's disease in patients showing a lack of B3, B6, B12, folic acid, linoleic and linolenic acid and zinc. Deficiency in these nutrients is known to be a factor in development of dementia.[2]

The major fuel of the brain is glucose broken in carbon dioxide and water. A disturbance in glucose utilization is considered to be a significant factor in brain disease. The breakdown of glucose requires B group vitamins, zinc, magnesium and oxygen to ensure effective utilization of the fuel. Furthermore, many Alzheimer's patients are gluten/alpha gliadin sensitive, as well as being low in thyroxine. As reported in the Journal of Neuroscience in 2001, curcumin, an extract of the spice turmeric, reduces inflammation and amyloid plaque deposits in animals. The study's author reported that although long term use of ibuprofen suppressed inflammation and amyloid plaque related pathology in an Alzheimer's transgenic mouse model, excessive use of NSAIDS can cause gastrointestinal, liver and kidney toxicity.[10]

With low-dose administration of curcumin, insoluble beta-amyloid and plaque burden can be significantly reduced by 43-50%. Other natural, side-effect free anti-inflammatory includes fish oil (such as cod liver oil), ginger, flax seed oil and feverfew. Seanol, an abstract of brown algae, is also a powerful anti-inflammatory. A healthy diet rich in fruits, vegetables, whole grains, nuts and seeds will go a long way in helping maintaining normal brain function. Taking 1,000 mg of vitamin C and up to 1,000 IU of vitamin E had 78% reduced risk of developing AD.[2]

The ingestion of pesticides and other toxic chemicals either by inhalation, through skin absorption or oral ingestion, should be consciously and persistently avoided.[9]

1. Pangalos MN, Jacobsen SJ and Reinhart PH. Disease modifying strategies for the treatment of Alzheimer's disease targeted at modulating levels of the beta-amyloid peptide. In Biochem. Soc. Trans.33(4): 553-8. 2005.
2. Osiecki H. The physician handbook of Clinical Nutrition, 7th Edition. Bioconcept. Australia pp. 531. 2005.
3. Luchsinger JA. Caloric Intake and the risk of Alzheimer's disease. Archives of Neurology. (59) 1528-1563. 2002.
4. Barrio JR. Molecular Imaging Probes.. PET: Molecular Imaging of Biology  5 (6) 404-417. 2003.
5. Cousins N. Anatomy of an Illness. New York. Bantam Books. 1989.
6. Walter J, Papolla M and Bazan NG. A dysfunction in Cholesterol and Lipid Metabolism. Alzheimer's Disease Journal 25 (3): 475-483. 2005.
7. Anekonda TS. Can herbs provide a new generation of drugs for treating Alzheimer's disease? Brain Res Review 50(2); 361-76. 2005.
8. Abalan F. Alzheimer's disease: the Nutritional Hypothesis. Journal of Orthomolecular Medicine 3 (1): 13-17. 1988.
9. Zandi PP. Reduced risk of Alxheimer's disease in users of antioxidant vitamin supplements. Archives of Neurology 61:82-88. 2004.
10. Lim GP. The curry spice curcumin reduces oxidative damage and amyloid pathology in Alzheimer's transgenic mouse. Journal of Neuroscience 21 (21): 8370-8377. 2001.


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About Manuela Malaguti Boyle

Manuela Malaguti Boyle ND BA BHSc(Comp Med) Grad Dip Nut Adv Dip Nat GCRN BNA (UK) ATMS NHAA (Australia) IFM (US) is a Naturopathic Physician and Clinical Nutritionist, trained in Australia and United Kingdom. Her area of expertise is nutritional therapy as a viable treatment for mental illness. She continuously researches how nutrition impacts the nervous system function and brain cognition. Manuela firmly believes that 'junk food gives rise to junk thoughts' and she seeks to help patients improve their state of mind and coping abilities. Nutritional interventions safely complement standard drug treatments. Manuela's articles have appeared in several publications both in United Kingdom and Australia. She is currently consulting at the Centre for Complementary and Alternative Medicine Centre, 19 Tanglin Road Singapore. Manuela may be contacted via

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