Alzheimer's disease, the most common form of dementia, is a progressive disorder characterized by widespread loss of brain cells called neurons, beta-amyloid deposits in the cerebral blood vessels, development of plaques and the presence of neurofibrillary tangles. These changes, occurring in the association area of the cerebral cortex, the hippocampus and the middle and temporal lobes, are accompanied by decreased concentrations of the neurotransmitter acetylcholine. In my opinion, it appears that a deficiency in antioxidant status may accelerate the progression of Alzheimer's disease, and making an effort through diet or supplements to have adequate antioxidant status can reduce the risk for Alzheimer's disease.

Alzheimer's statistics : Recent US census figures suggest that by 2050, the number of people with Alzheimer's disease will triple. Americans are living longer, healthier lives and only the mortality rate from Alzheimer's disease is increasing among the top 10 causes of death, the U.S. federal government reported on Wednesday. Alzheimer's disease moved to seventh place from eighth place among the leading causes of death in 2004, passing influenza and pneumonia.

Natural options for Alzheimer’s Disease treatment - Alternatives to Alzheimer's Medication
While scientists have not fully determined the actual causes of Alzheimer’s disease, a number of treatment options have been proposed or tried over the years. Although much more research needs to be done in order to find out the role of these supplements in Alzheimer's disease, I think it is appropriate to give them a try since this condition currently has no cure or effective treatment. You are not likely to find this information in any official Alzheimer's disease association or Alzheimer's foundation. Some natural options for Alzheimer's disease treatment or prevention include (discuss with your doctor first):

It is nearly impossible to know which of the above nutrients or herbs, or combinations thereof are helpful as a treatment, prevention, or alternative Alzheimer's disease medication. It may be a trial and error process until the right combination or dosage is found. It is also very difficult to predict how these supplements interact with Alzheimer's prescription drugs. One has to be cautious with some of these supplements, particularly galantamine and huperzine since they can be quite potent. Also, when taking multiple supplements, make sure to reduce the dose of each one since they add on to each other and one could have insomnia or feel overstimulated.

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Exercise and Alzheimer's disease
Walking, gardening and generally being physically active after age 65 appears to ward off dementia, including Alzheimer's disease.

Alzheimer Prevention with Juices
Drinking fruit and vegetable juices frequently could help reduce the risk of Alzheimer's disease in individuals at risk for developing the disease. There is evidence from both lab and animal studies that high levels of reactive oxygen species -- harmful byproducts of normal metabolism -- may be involved in the development of Alzheimer's disease. While vitamins and polyphenols contained in plant foods exert antioxidant effects and thus blunt the action of oxidants, certain ways of preparing these foods can deplete their nutrient content. Juicing, however, can preserve much of the antioxidant content of fruits and vegetables. The American Journal of Medicine, September 2006.

Alzheimers medication - Alzheimer's treatment
Several Alzheimer's drugs are available including cholinesterase inhibitors such as donepezil, rivastigmine, and galantamine. I am not convinced an Alzheimer medication of this sort offers a long term solution or cure for Alzheimer's disease.

Alzheimer's symptom and sign - Diagnosing Alzheimer's Disease
There are several symptoms common to Alzheimer disease patients. These symptoms include: trouble remembering things...at first, only short-term memory may be affected. The individual may forget an appointment or the name of a new acquaintance. A person may also forget where they left things. Eventually, long-term memory is also impaired.
     Mood or personality changes could occur. A person may suddenly become angry or sad for no apparent reason. Or someone who was social and outgoing may become withdrawn.
    Trouble completing ordinary tasks is another symptom of Alzheimer's disease. Simple tasks that once caused no difficulty may become much more challenging. For example, the individual may forget how to dress, use the oven, etc.
     Difficulty expressing thoughts and disorientation. We all know what it's like to be driving and momentarily forget where you are going. But those with Alzheimer's disease may get lost in their neighborhood. They may also lose track of dates and the time.
     Unusual behavior. The individual may wander, become agitated, hide things, wear too few or too many clothes, become overly suspicious, or engage in unsafe behaviors.

Cause of Alzheimers Disease
There is a very high genetic cause for Alzheimer's disease.
     Nerve signals travel across synapses with the help of chemicals known as "neurotransmitters," including one called acetylcholine. Nerve cell destruction causes a reduction in acetylcholine, leading to impaired transmission of nerve signals and poor communication between nerve cells called neurons. In addition to acetylcholine, the brain of Alzheimer’s disease patients have areas of abnormal protein called "plaques" and "tangles," the names reflecting what these abnormalities in the brain look like under the microscope. The underlying cause of Alzheimer's – what actually triggers the changes in the brain – is still not fully known but could partly be due oxidation and damage to nerve cells over time. It is likely that no single factor is responsible, but rather that it is due to a variety of factors, which may differ from person to person. People whose parents or brothers and sisters develop the disease appear to be at greater risk of developing it themselves, so there may be a genetic component. However, no straightforward pattern of inheritance has been found. It is known that head injury is a risk factor, and also that Alzheimer’s disease often affects people with Down’s syndrome. Some researchers have suggested that people who exercise their brains (for example, doing crosswords and other mental agility exercises) are less likely to develop the disease. And Omega 3 fatty acids, contained in oily fish such as mackerel and salmon may, also help to prevent dementia. But there is no completely solid evidence to show how environmental factors influence the chance of getting Alzheimer’s.
     Australian scientists say they have identified a toxin that plays a key role in the onset of Alzheimer's disease. The toxin, called quinolinic acid, kills nerve cells in the brain, leading to dysfunction and death. Quinolinic acid may not be the cause of Alzheimer's disease, but it plays a key role in its progression.

Amyloid, Obesity, and Alzheimer's Disease
As body fat increases, so do blood levels of a protein fragment linked to Alzheimer's disease, which may explain the reported association between obesity and the brain-wasting disease. Obesity by itself, even in otherwise healthy middle-aged people, is associated with elevated levels of the amyloid peptide that builds up and causes Alzheimer's. Amyloid is normally made all throughout the body at various lengths. Researchers at Edith Cowan University in Joondalup, Western Australia investigated whether levels of the peptide, plasma amyloid-beta 42,were related to body mass index (BMI) or fat mass in 18 healthy adults. As BMI rose, so did amyloid-beta 42 blood levels. The same was true for fat mass. But there was no relationship between BMI or fat mass and another peptide, amyloid-beta 40, which is not associated with disease. Obesity-linked conditions like diabetes and heart disease may also increase Alzheimer's risk, but when the team adjusted the data for levels of insulin, cholesterol, and inflammation in an attempt to account for their influence, the fat-amyloid-beta 42 relationship remained. This suggests that it's the fat itself -- not the diseases that excess weight can cause -- that may be increasing levels of the dangerous protein. To learn more about amyloidosis.

Neurofibrillary tangles and Gait
Brain lesions known as neurofibrillary tangles, such as those seen in Alzheimer's disease, are also associated with impaired gait in older subjects with or without dementia. The more tangles an older person had in the substantia nigra - an area of the brain associated with Parkinson's disease -- the more problems there is with gait. In addition to, or even instead of, problems with memory, persons with Alzheimer's disease may have problems with walking and balance.

Alzheimer's Test
Concentrations of three proteins in the fluid that bathes the brain and spine are associated with the initial stages of Alzheimer's disease in people with mild cognitive impairment. Researchers measured levels of three proteins related to Alzheimer's disease -- AB42, T-tau, and P-tau181 -- in cerebrospinal fluid samples from 137 patients with mild cognitive impairment and 39 controls. During 4 to 6 years of follow-up, 56 of the subjects with mild cognitive impairment remained cognitively stable, 3 died, 57 developed Alzheimer's disease, and 21 progressed to other forms of dementia. According to the investigators, baseline concentrations of T-tau and P-tau181 were significantly higher, and AB42 significantly lower, among patients who developed Alzheimer's disease compared with controls, cognitively stable patients with mild cognitive impairment, and patients who developed other forms of dementia.

Alzheimer's Disease Research Update - Alzheimer's Clinical Trial
Curcumin inhibits formation of Abeta oligomers and fibrils, binds plaques and reduces amyloid in vivo.
J Biol Chem. 2004 Dec 7. Yang F, et al. University of California Los Angeles, North Hills, CA
Alzheimer's disease involves amyloid (Abeta) accumulation, oxidative damage and inflammation, and risk is reduced with increased antioxidant and anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has potent anti-inflammatory and antioxidant activities and can suppress oxidative damage, inflammation, cognitive deficits, and amyloid accumulation. These data suggest that low dose curcumin effectively disaggregates Ass as well as prevents fibril and oligomer formation, supporting the rationale for curcumin use in clinical trials preventing or treating Alzheimer's disease.

Atypical antipsychotic drugs used to treat Alzheimer's disease and other types of dementia for relatively brief periods, less than 8 to 12 weeks, may be associated with a small increased risk of death.

A high concentration of silica in drinking water seems to protect against Alzheimer's disease.

Consuming a diet rich in the omega-3 fatty acid docosahexanoic acid (DHA) may help prevent or treat Alzheimer's disease. In the study, reported in The Journal of Neuroscience, mice that ate DHA-enriched chow showed less beta-amyloid build-up in the brain than mice fed regular chow. Beta-amyloid is a protein that forms the characteristic brain plaques seen in patients with Alzheimer's disease." These results suggest that dietary DHA could be protective against beta-amyloid production, accumulation, and potential downstream toxicity," senior author Dr. Greg M. Cole, from the University of California at Los Angeles, and colleagues note. Research has linked high levels of DHA in the diet with a reduced risk of Alzheimer's disease. Still, the studies have shown an association, but don't prove that eating a diet high in DHA actually reduces amyloid levels and prevents Alzheimer's disease. To show this, animal studies are often needed. Cole's team used a mouse model of Alzheimer's disease and fed the animals low- or high-DHA chow or regular chow. The animals were fed the assigned diet until 22.5 months of age, at which point brain tissue was obtained and tested for amyloid build-up. The high-DHA diet reduced total amyloid level by 70 percent compared with the other diets. Moreover, brain plaques were reduced by 40 percent.

Britain's agency charged with assessing whether drugs and procedures are worth their cost has issued a preliminary ruling against all of the four main drugs licensed for treating Alzheimer's disease. The National Institute for Clinical Excellence (NICE) said that Aricept, Exelon, Reminyl, and Ebixa should not be reimbursed by the national health service. It advised that people taking the drugs "may be continued on therapy until it is considered appropriate to stop," the institute said in preliminary recommendations. Some 52,500 patients are taking the medicines in Britain. Although not a cure, clinical trials have shown that they can slow the progress of symptoms of the illness. The recommendations follow an unfavourable review of the four drugs' clinical effectiveness and cost effectiveness by NICE's appraisals' committee. The committee said the clinical gains with the drugs called acetylcholinesterase inhibitors were small and the evidence on outcomes of importance to patients and caregivers, such as quality of life and time to institutionalisation, was "limited and largely inconclusive." It also concluded that the evidence for the clinical effectiveness of memantine, which is licensed for more severe Alzheimer's disease, was "insufficient."

Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change.
American Journal of Clinical Nutrition, Vol. 81, No. 2, 508-514, February 2005
High intake of vitamin E  (tocopherol) from food, but not from supplements (which usually contain -dl-tocopherol), is inversely associated with Alzheimer disease. Objective: We examined whether food intakes of vitamin E, -tocopherol equivalents (a measure of the relative biologic activity of tocopherols and tocotrienols), or individual tocopherols would protect against incident Alzheimer disease and cognitive decline over 6 y in participants of the Chicago Health and Aging Project. Design: The 1993–2002 study of community residents aged 65 y included the administration of 4 cognitive tests and clinical evaluations for Alzheimer disease. Dietary assessment was by food-frequency questionnaire. Results: Tocopherol intake from food was related to the 4-y incidence of Alzheimer disease determined by logistic regression in 1041 participants who were clinically evaluated (n = 162 incident cases) and to change in a global cognitive score determined by mixed models in 3718 participants. Higher intakes of vitamin E and -tocopherol equivalents were associated with a reduced incidence of Alzheimer disease in separate multiple-adjusted models that included intakes of saturated and trans fats and docosahexaenoic acid. - and -Tocopherol had independent associations. In separate mixed models, a slower rate of cognitive decline was associated with intakes of vitamin E, -tocopherol equivalents, and - and -tocopherols. Conclusion: The results suggest that various tocopherol forms rather than - tocopherol alone may be important in the vitamin E protective association with Alzheimer disease.

Researchers at Mount Sinai School of Medicine have found that a low carbohydrate diet that reduced total caloric intake by 30% prevented the development of a fundamental feature of Alzheimer's disease in mice genetically engineered to develop the disease. The study is the first to demonstrate that a change in diet can slow and possibly prevent Alzheimer's diseases.

Pharmacotherapeutic approaches to the prevention of Alzheimer's disease.
Am J Geriatr Pharmacother. 2004 Jun;2(2):119-32.
Alzheimer's dememtia (Alzheimers disease) is the most common cause of cognitive impairment in older patients and is expected to increase greatly in prevalence. Interventions that could delay disease onset would have a major public health impact. OBJECTIVE: The objective of this article is to review evidence from epidemiologic studies and controlled trials addressing whether Alzheimers disease can be prevented. Data were gathered through a comprehensive, systematic search of MEDLINE using focused search criteria and spanning a 6-year period from January 1998 through January 2004; a hand search of reference lists from these studies and reviews; a review of the Cochrane Database of Systematic Reviews; and a hand search of relevant journals. Selection of articles was based on the clinical focus. RESULTS: Preventive interventions for Alzheimers disease include vitamins, nonsteroidal anti-inflammatory drugs, and agents that protect the endothelium (eg, statins). Good control of hypertension with angiotensin-converting enzyme inhibitors and long-acting dihydropyridines also confers neuroprotective benefits. CONCLUSIONS: The paradigm that Alzheimers disease is pharmacologically unresponsive is shifting as more effective pharmacotherapies for prevention and treatment rapidly emerge. Our understanding of the molecular mechanisms of neurodegeneration will soon allow us to more specifically target and interrupt the processes that contribute to this progressive dementia.

Alzheimer's disease, oxidative injury, and cytokines.
J Alzheimers Disease. 2004 Dec;6(6):651-657.
Alzheimer's disease is infrequently a genetically driven disease. Rather it is the product of free radical injury inflicted over decades after an initial insult to the central nervous system (CNS). The brain is uniquely sensitive to oxidative injury. A variety of insults to the CNS are now associated with Alzheimer's disease. These include hypertension, diabetes, and head trauma. These then cause a cytokine cascade and microlocalized inflammation in the CNS, that in time results in clinical Alzheimer's disease. By the ninth decade of life over half of the population manifests Alzheimer's disease. Prevention or reversal of Alzheimer's disease will lie in administration of effective antioxidant therapy with specific treatments when etiologies are known.

Docosahexaenoic acid protects from dendritic pathology in an Alzheimer's disease mouse model.
Neuron. 2004 Sep 2;43(5):633-45.
Learning and memory depend on dendritic spine actin assembly and docosahexaenoic acid (DHA), an essential n-3 (omega-3) polyunsaturated fatty acid (PFA). High DHA consumption is associated with reduced Alzheimer's disease risk, yet mechanisms and therapeutic potential remain elusive. Here, we report that reduction of dietary n-3 PFA in an Alzheimer's disease mouse model resulted in 80%-90% losses of the p85alpha subunit of phosphatidylinositol 3-kinase and the postsynaptic actin-regulating protein drebrin, as in Alzheimer's disease brain. The loss of postsynaptic proteins was associated with increased oxidation, without concomitant neuron or presynaptic protein loss. n-3 PFA depletion increased caspase-cleaved actin, which was localized in dendrites ultrastructurally. Treatment of n-3 PFA-restricted mice with DHA protected against these effects and behavioral deficits and increased antiapoptotic BAD phosphorylation. Since n-3 PFAs are essential for p85-mediated CNS insulin signaling and selective protection of postsynaptic proteins, these findings have implications for neurodegenerative diseases where synaptic loss is critical, especially Alzheimer's disease.

Drinking tea appears to affect the brain in a similar way as drugs prescribed for Alzheimer's disease, UK researchers report. The team, based at Newcastle University's Medicinal Plant Research Centre, investigated the properties of green and black tea, as well as coffee, in a series of laboratory experiments. The results showed that both types of tea inhibited the activity of enzymes associated with the development of Alzheimer's disease. Coffee, however, had no significant effect, according to a report in theOct, 2004 edition of Phytotherapy Research. The teas inhibited the activity of acetylcholinesterase -- the same mechanism of action used by drugs such as Novartis' Exelon and Pfizer's Aricept. The teas also hindered the activity of the butyrylcholinesterase, which has been found in senile plaques in the brains of Alzheimer's disease patients. Green tea obstructed the activity of beta-secretase, which also plays a role in the production of senile plaques.

The benefits and risks associated with cholinesterase inhibitor therapy in Alzheimer's disease.
Expert Opin Drug Saf. 2004 Sep;3(5):425-40.
The 'second-generation' cholinesterase inhibitors (ChEIs), donepezil, galantamine and rivastigmine, are a class of medications that are currently approved for the treatment of mild-to-moderate Alzheimer's disease (Alzheimer's disease). These medications have proven efficacy in improving cognition, behaviour, activities of daily living, and global functioning in mild-to-moderate Alzheimer's disease. They have also been shown to reduce caregiver stress and to delay time to nursing home placement. Two separate meta-analyses have indicated that ChEIs confer a modest but significant therapeutic benefit in the treatment of Alzheimer's disease, despite higher rates of treatment discontinuation and side effects than placebo. There is growing evidence to support their efficacy in treating moderate-to-severe Alzheimer's disease. ChEIs are generally well-tolerated, with side effects that tend to be dose-related and are most problematic during dose titration. The most common adverse effects, related to cholinergic stimulation in the brain and peripheral tissues, include gastrointestinal, cardiorespiratory, extrapyramidal, genitourinary, and musculoskeletal symptoms, as well as sleep disturbances. Few clinically significant drug-drug interactions with ChEIs have been identified. Three head-to-head disease trials of ChEIs in the treatment of Alzheimer's disease have been published to date, but are limited due to their open-label design, rates of titration, and the drug dosage levels utilised. Further study is needed to examine other indications for ChEIs, as well as their combination with newer treatments, such as memantine.

Alzheimer's fact : People who spent most of their lives in jobs that involve little brain work appear more likely to eventually develop Alzheimer's disease.

A recent report suggests high copper levels in tap water may play a role in causing Alzheimer's disease. Those at risk for Alzheimer's (i.e. family history) may consider drinking distilled water.

For women, maintaining high levels of "good" HDL cholesterol may be one of the most effective strategies for fending off Alzheimer's disease, according to new research.

Data from the ongoing Women's Health Study indicate that women with the highest HDL levels -- ranging from 60 to 75 -- have half the risk of becoming mentally impaired as those with the lowest levels.

Alzheimer's fact : High intake of niacin, particularly from food sources, may reduce the risk of Alzheimer's dementia disease and age-related cognitive decline.

Drugs for early Alzheimer's disease, which pharmaceutical companies and campaigners have lobbied the UK government to provide to large numbers of elderly patients with Alzheimer's dementia across the country at a cost of over £39m a year, have little effect on their memory and do not stop the distressing deterioration of their lives or preventing Alzheimer's disease progression, according to an important study published July 2004. The five-year study, paid for by the NHS and not the drug companies, found that the drugs are a waste of the scarce resources available for the condition, said the lead re searcher Roger Gray, director of Birmingham University's clinical trials unit. alzheimers disease information

Estrogen pills appear to slightly increase the risk of Alzheimer’s disease and other forms of dementia in postmenopausal women, a study found, echoing recent findings involving estrogen-progestin supplements. The findings contradict the long-held belief that estrogen pills can help keep older women’s minds sharp. The results came from a government study called the Women’s Health Initiative and were published in The Journal of the American Medical Association. The research involved nearly 3,000 women, ages 65 to 79, who had had hysterectomies and had taken daily estrogen-only pills, sold by Wyeth Pharmaceuticals as Premarin, for an average of about five years. alzheimers care

Clinical efficacy and safety of huperzine Alpha in treatment of mild to moderate Alzheimer disease, a placebo-controlled, double-blind, randomized trial
Zhonghua Yi Xue Za Zhi. 2002 Jul 25;82(14):941-4.
To evaluate the clinical efficacy and safety of huperzine Alpha in treatment of patients with mild to moderate Alzheimer disease METHODS: Two hundred and two patients with the diagnosis of possible or probable Alzheimers disease from 15 centers the nationwide were randomly divided into two groups: huperzine Alpha group (n = 100, given huperzine Alpha 400 micro g/day for 12 weeks) and placebo group (n = 102 ). RESULTS: In comparison with the baseline data, there was an improvement of 4.6 points in cognition; an improvement in behavior and mood with 59.2% of the Alzheimer disease patients being on the mend clinically. CONCLUSION: A safe and effective medicine, huperzine Alpha remarkably improves the cognition, behavior, ADL, and mood of Alzheimer disease patients. 

A high concentration of silica in drinking water seems to protect against Alzheimer's disease
Blue Green Algae has a cholinesterase inhibitor

Alzheimer's disease info emails
Q. I just got your Mind Power Rx for my mother, who has early stage Alzheimer's disease. Then today I noticed your article on galantamine.  Would it be OK to give her both supplements together, or do they have the same basic function?
      A. Mind Power Rx does not contain a cholinesterase inhibitor like galantamine or huperzine. However, if your doctor decides to combine them, half a capsule of each would be preferable as a starter

Email from a doctor who says: I have a patient who was not doing well on Aricept and Namenda until we added nicotine patch and sage extract. He is my poster child! Sage contains several cholinesterase inhibitors and could help Alzheimer's disease.

Saw Palmetto has important phytosterols
AHCC

Q. Are insulin and Alzheimer's related? Any info would be helpful.
     A. I don't see a direct link between insulin and Alzheimer's disease. I am not sure if those with diabetes have a higher incidence of Alzheimer's.

Q. What are your suggestions on prevention of Alzheimer's disease? I have a family history of Alzheimer's diease. My mom has it and my grandmother died from the diease.
     A. Leading a healthy lifestyle with a good diet, exercising, keeping the mind busy, getting good sleep, and perhaps taking low doses of antioxidants could all be helpful.

Q. Are Alzheimer's disease medications of any help? I read in a book that they weren't.
     A. According to Alzheimer's articles in medical journals, these pharmaceutical medications do not appear to be worthwhile, whether in the early stage of Alzheimer's final stage. They do not stop the progression of Alzheimer's disease.

Q. What's the difference between Alzheimer's and dementia ?
     A. Alzheimer's is a form of dementia. There are many other causes of dementia.

Q. What are the studies with stem cells and Alzheimer's?
     A. I have not kept abreast of stem cell research and Alzheimer's.

Q. My mom has Alzheimer's, is a flu shot okay to give?
     A. I don't see why not.