This article is a continuation of the first article on Alzheimer’s disease (AD). In part one, we started to look at various natural measures, such as diet and nutritional supplementation, which have demonstrated promising results (relating to improved mental function) in the early stages of AD.*
As mentioned in part one to this article, AD affects between 5 -10% of people over the age of 65 years; with the frequency rising with increasing age. Nutritional status is directly related to cognitive function in the elderly and given the frequency of nutrient deficiency in the elderly population it is likely that many cases of impaired mental function may have a nutritional etiology. 
*Please note - in the advanced stages of AD natural measures are of only limited benefit.
Oxidative Damage & Vitamin E
Considerable evidence indicates that oxidative damage plays a major role in the development and progression of AD. Studies have suggested that antioxidant nutrients offer significant protection against AD; with researchers now showing that antioxidant nutrients especially vitamin E, may help to prevent AD in the same way that they may help against heart disease, cancer, Parkinson’s disease, and other diseases linked to inflammation and excessive oxidation.    
As digestive functions tend to diminish in the elderly population, there is a natural tendency towards fat malabsorption. Since vitamin E is a fat soluble vitamin, neuronal symptoms of vitamin E deficiency are commonly seen in the aged population and because of these known deficiency symptoms, the use of supplemental vitamin E has been investigated to prevent or treat AD. The recommended daily allowance (RDA) of vitamin E is 15mg (22IU).
Intakes as high as 2000IU per day have been shown to slow the progression of Alzheimer dementia. Studies are also showing benefits of using vitamin E with standard pharmacological treatment.
Antioxidants That Can Help
Other antioxidants which have demonstrated an ability to help in the treatment/prevention of (early) AD are lipoic acid (has a positive effect on mitochondrial function and glucose metabolism and is neuroprotective), selenium (supports glutathione production) and coenzyme Q10 (supports oxidative phosphorylation). Melatonin should also be considered for AD.
This hormone is well known for its use in normalising circadian rhythms, sleep cycles and more recently as a powerful antioxidant for cancer therapies. Studies have shown that melatonin treatment protects neuronal cells from heavy metal cobalt damage (a transitional metal found in high levels in AD patients) and avoids beta amyloid release and oxidative damage in AD susceptible individuals.   
Phosphatidylserine is the major phospholipid in the brain; it plays a key role in maintaining cell membrane integrity and fluidity. Normally sufficient levels of phosphatidylserine are manufactured in the brain, but a deficiency of methyl donors e.g. folic acid, vitamin B12, S-adenosylmethionine (SAMe) and/or omega 3 fatty acids (especially docosahexaenoic acid (DHA) – also limits amyloid and oxidative damage), may inhibit the production of sufficient phosphatidylserine. Low levels of phosphatidylserine are associated with impaired mental function and depression. Numerous studies have supported the use of phosphatidylserine in the treatment of age-related cognitive decline, AD or depression.   
Other Treatment Research Findings
Supplementation of choline as phosphatidylcholine in the treatment of AD has had mixed reviews. As discussed in part one of this newsletter various clinical features of AD are believed to arise from cholinergic dysfunction i.e. reduced activity of the enzyme choline acetyltransferase (which synthesises acetylcholine) and neuronal transfer of choline. Although dietary phosphatidylcholine has shown to help increase acetylcholine levels in the brain of normal individuals, the defect in cholinergic transmission in AD means phosphatidylcholine supplementation will not be as beneficial in a majority of AD patients. Unfortunately, providing more choline does not increase the activity of this key enzyme.  
L-Acetylcarnitine has a close structural similarity to acetylcholine and research has shown that it mimics acetylcholine and is of benefit in patients with early-stage AD, as well as those elderly patients who have impaired memory or are depressed. L-Acetylcarnitine has also been shown to act as a powerful antioxidant within the brain cell, stabilise cell membranes and improve energy production within the brain cell.   
There are also many other research findings which strongly suggest that lithium will protect against potential AD and slow the progression of existing cases. Studies have shown that lithium may inhibit the secretion of beta-amyloid protein (a signature protein involved in AD), and prevent damage caused by any beta-amyloid once it has been formed. It may also inhibit over activation of a brain cell protein called tau protein, which contributes to neuronal degeneration in Alzheimer’s disease, as does the formation of neurofibrillary tangles. Lithium inhibits both of these nerve-cell damaging problems.17 (Please see our newsletter on Low Dose Lithium for more information.)
Finally on a lighter note, the old age saying to “use it or lose it” has proved to be true. Research by Dr Michael Valenzuela from the school of psychiatry (University of NSW) has shown that the brain will actually shrink faster if it is not stimulated. In his book (Maintain Your Brain) he refers to brain scans which revealed that people who did not engage in complex mental activity over their lifetime had twice the shrinkage in a key part of their brain in old age.
Those who had been more mentally active over their lives had a larger hippocampus (memory centre of the brain). This is a significant finding because a small hippocampus is a specific risk factor for developing AD. Dr Valenzula goes on to say that "it is vital that everyone is involved in cognitive, social and physical activities in late life such as dancing, tai chi, sailing, travelling and learning a new language, for example."
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