Increased Risk of Alzheimer’s / Dementia

Reduced sense of taste or smell

A reduced sense of smell can be one of the first signs of Alzheimer’s Disease.

Periods of confusion/disorientation

A hard-driving personality

A surprising study of elderly people suggests that those who see themselves as self-disciplined, organized achievers have a lower risk for developing Alzheimer’s disease than people who are less conscientious.

A purposeful personality may somehow protect the brain, perhaps by increasing neural connections that can act as a reserve against mental decline, said study co-author Robert Wilson of Chicago’s Rush University Medical Center.

Astoundingly, the brains of some of the dutiful people in the study were examined after their deaths and were found to have lesions that would meet accepted criteria for Alzheimer’s — even though these people had shown no signs of dementia.

“This adds to our knowledge that lifestyle, personality, how we think, feel and behave are very importantly tied up with risk for this terrible illness,” Wilson said. “It may suggest new ideas for trying to delay the onset of this illness.” [General Psychiatry, Oct 1, 2007]

Low Estrogen Levels

Women who use hormone therapy before the age of 65 could cut their risk of developing Alzheimer’s disease or dementia. This possibility is raised by research that will be presented at the American Academy of Neurology’s 59th Annual Meeting in Boston, April 28 May 5, 2007.

The study found women who used any form of estrogen hormone therapy before the age of 65 were nearly 50 percent less likely to develop Alzheimer’s disease or dementia than women who did not use hormone therapy before age 65.

The study was part of the Women’s Health Initiative Memory Study, which is a sub-study of the Women’s Health Initiative (WHI), one of the largest U.S. prevention studies of postmenopausal women. The study looked at prior hormone use in 7,153 healthy women ages 65-79 before they enrolled in the WHI Memory Study. Researchers followed the women’s cognitive health over an average of five years.

In that time, 106 of the women developed Alzheimer’s disease or dementia. Dementia is a general term referring to the progressive decline in a person’s cognitive function. Dementia can affect memory, attention, language and problem solving abilities. Alzheimer’s is the most common type of dementia.

Prior studies have shown that hormone therapy started during the WHI Memory Study increased a woman’s chance of dementia. The reduced risk of dementia was seen only with prior hormone therapy, used before study enrollment. Reduced risk was not affected by other examined factors. “We found that it didn’t matter how old the woman was when she started hormone therapy, how long or recently she took it or what kind of prior therapy she used,” said study author Victor W. Henderson, MD, of Stanford University in Palo Alto, CA, and Fellow of the American Academy of Neurology.

Women who began estrogen-only therapy after the age of 65 had roughly a 50-percent increased risk of developing dementia. The risk jumped to nearly double for women using estrogen-plus-progestin hormone therapy.

Diabetes Type I

According to a new study in Neurology, diabetes mellitus may not only damage the function of the eye, limbs, kidneys, and heart – it may also impair the function of the brain and hasten the process of senile dementia.

Researchers found that diabetes mellitus nearly doubles the risk of developing both vascular dementia and Alzheimer’s disease, according to the Rotterdam Study, a large prospective analysis which tracked dysglycemia and dementia in over 6000 individuals over age 55. Diagnosis of diabetes was based on World Health Organization criteria using a glucose tolerance test.

A related editorial called Alzheimer’s a possible “brain-type diabetes.” Besides damaging important blood vessel networks and increasing the risk of small “silent” strokes deep inside the brain, dysglycemia may be directly involved in the development of the neurofibrillary tangles, the clumping of nerves and fiber tissue inside the brain characteristic of Alzheimer’s.

The researchers noted that advanced glycation endproducts (AGE), proteins damaged by chronically high blood sugar levels, are commonly found inside these tangles. “In brains of AD patients the receptor for AGE appears overexpressed,” they noted. “Activation of this receptor leads to increased oxidative stress that may result in cellular damage.”

Diabetes also disrupts insulin signaling to other cells in the body. This altered signaling may increase the activity of a neuronal enzyme that stimulates phosphorylated tau proteins to build up, a key trigger mechanism cited as one of the earliest signs of Alzheimer’s.

NOTE: This study strongly suggests the important potential role of glycation products and insulin response, not just glucose levels, in the etiology of degenerative disease.

Hypertension

A study in Journal of Neuroimaging (July 2007) suggests that cognitively normal adults exhibiting atrophy of their temporal lobe or damage to blood vessels in the brain are more likely to develop Alzheimer’s disease. Older adults showing signs of both conditions were seven-times more likely to develop Alzheimer’s than their peers.

“Alzheimer’s disease, a highly debilitating and ultimately fatal neurological disease, is already associated with other risk factors such as poor cognitive scores, education or health conditions,” says study author Caterina Rosano. “This study, because it focused on healthy, cognitively normal adults, shows that there other risk factors we need to consider.”

MRI images of participants’ brains were examined to identify poor brain circulation, damaged blood vessels and/or atrophy of the medial temporal lobe. Subjects showing any one or a combination of these symptoms were more likely to develop Alzheimer’s in the following years.

“Similarly to heart disease, brain blood vessel damage is more likely to occur in patients with high blood pressure, high cholesterol or diabetes,” says Rosano. “Since we know that prevention of these conditions can lower risk of heart attack and stroke, it is likely that it would also lower the risk of developing Alzheimer’s.”

Cigarette Smoke Damage

When antioxidant intake of cigarette smokers was evaluated, Alzheimer’s risk was reduced by 35% with vitamin C, 42% with vitamin E, 46% with flavonoids and 51% with beta-carotene. [ JAMA June 26, 2002]

Mercury Toxicity / Amalgam Illness

Part of the increase in the incidence of Alzheimer’s disease may be due to mercury exposure from mercury amalgam fillings, especially those high in copper content. [Environ Contam Toxicol 2001;67. pp.800 806]

Alzheimer's in family members

By age 80, people with Alzheimer’s disease in both parents had a 54% risk, 1.5 times the risk of Alzheimer’s in people with just one affected parent, and 5 times the risk of people with two unaffected parents.

Elevated Total Cholesterol

It is thought that the connection between high cholesterol and Alzheimer’s disease exists in a protein called beta-amyloid, a sticky substance that builds up in the brains of Alzheimer’s patients leading to nerve cell damage and loss of cognitive function. Accumulation of the protein is believed to be related to higher cholesterol levels.

A study in Journal of Neuroimaging (July 2007) suggests that cognitively normal adults exhibiting atrophy of their temporal lobe or damage to blood vessels in the brain are more likely to develop Alzheimer’s disease. Older adults showing signs of both conditions were seven-times more likely to develop Alzheimer’s than their peers.

“Alzheimer’s disease, a highly debilitating and ultimately fatal neurological disease, is already associated with other risk factors such as poor cognitive scores, education or health conditions,” says study author Caterina Rosano. “This study, because it focused on healthy, cognitively normal adults, shows that there other risk factors we need to consider.”

MRI images of participants’ brains were examined to identify poor brain circulation, damaged blood vessels and/or atrophy of the medial temporal lobe. Subjects showing any one or a combination of these symptoms were more likely to develop Alzheimer’s in the following years.

“Similarly to heart disease, brain blood vessel damage is more likely to occur in patients with high blood pressure, high cholesterol or diabetes,” says Rosano. “Since we know that prevention of these conditions can lower risk of heart attack and stroke, it is likely that it would also lower the risk of developing Alzheimer’s.”

A study found people with total cholesterol levels between 249 and 500 milligrams were one-and-a-half times more likely to develop Alzheimer’s disease than those with cholesterol levels less than 198 milligrams. People with total cholesterol levels of 221 to 248 milligrams were more than one-and-a-quarter times more likely to develop the disease.

“We definitely cannot say that this is cause and effect,” Whitmer said. “But we know that total cholesterol levels in midlife are predictive of Alzheimer’s disease later in life. We can only say that it is a risk factor.”

It’s not possible to conclude from the study that LDL cholesterol, the “bad” kind that clogs arteries, is responsible for the relationship, she said. In the 1960s and 1970s, when data on the participants were gathered, no distinction had been made between LDL cholesterol and HDL cholesterol, the “good” kind that helps keep arteries open. [The study was presented at the American Academy of Neurology 60th Anniversary Annual Meeting in Chicago.]

Absence of aerobic exercise or exercising aerobically somewhat

Keeping an active mind and body has been shown to reduce slightly the risk of developing the disease.

Exercising aerobically moderately or exercising aerobically frequently

Keeping an active mind and body has been shown to reduce slightly the risk of developing the disease.

Problem Caused By Being Overweight

Less well known is the fact that if you have a big belly in middle age the chances that you could suffer from dementia are tripled.

Antioxidant Need/Oxidative Stress w/o Supplements

In one study, researchers found that the higher the intake of vitamins C and E, the lower the incidence of Alzheimer’s disease. The conclusion of the researchers was that “high dietary intake of vitamin C and vitamin E may lower the risk of Alzheimer disease.”

In a second study in the same journal, there was a consistent reduction in Alzheimer’s risk with increasing intake of dietary vitamin E. Those with the highest intake of dietary vitamin E showed a remarkable 70% reduction in Alzheimer’s disease incidence. [ JAMA June 26, 2002]

Multiple Mineral, General Requirement

Please see the link with Increased risk of Alzhiemer’s and Multiple Vitamin Need.

Diabetes Type II

According to a study in Neurology, diabetes mellitus may not only damage the function of the eyes, limbs, kidneys, and heart – it may also impair the function of the brain and hasten the process of senile dementia.

Researchers have found that diabetes mellitus nearly doubles the risk of developing both vascular dementia and Alzheimer’s disease, according to a Rotterdam Study that tracked dysglycemia and dementia in over 6,000 individuals over age 55. Diagnosis of diabetes was based on World Health Organization criteria using a glucose tolerance test.

A related editorial called Alzheimer’s a possible “brain-type diabetes.” Besides damaging important blood vessel networks and increasing the risk of small “silent” strokes deep inside the brain, dysglycemia may be directly involved in the development of the neurofibrillary tangles, the clumping of nerves and fiber tissue inside the brain characteristic of Alzheimer’s.

The researchers noted that advanced glycation endproducts (AGE), proteins damaged by chronically high blood sugar levels, are commonly found inside these tangles. “In brains of AD patients the receptor for AGE appears overexpressed,” they noted. “Activation of this receptor leads to increased oxidative stress that may result in cellular damage.”

Diabetes also disrupts insulin-signaling to other cells in the body. This altered signaling may increase the activity of a neuronal enzyme that stimulates phosphorylated tau proteins to build up, a key trigger mechanism cited as one of the earliest signs of Alzheimer’s.

NOTE: This study strongly suggests the important potential role of glycation products and insulin response, not just glucose levels, as being causes of degenerative disease.

A study in Journal of Neuroimaging (July 2007) suggests that cognitively normal adults exhibiting atrophy of their temporal lobe or damage to blood vessels in the brain are more likely to develop Alzheimer’s disease. Older adults showing signs of both conditions were seven-times more likely to develop Alzheimer’s than their peers.

“Alzheimer’s disease, a highly debilitating and ultimately fatal neurological disease, is already associated with other risk factors such as poor cognitive scores, education or health conditions,” says study author Caterina Rosano. “This study, because it focused on healthy, cognitively normal adults, shows that there other risk factors we need to consider.”

MRI images of participants’ brains were examined to identify poor brain circulation, damaged blood vessels and/or atrophy of the medial temporal lobe. Subjects showing any one or a combination of these symptoms were more likely to develop Alzheimer’s in the following years.

“Similarly to heart disease, brain blood vessel damage is more likely to occur in patients with high blood pressure, high cholesterol or diabetes,” says Rosano. “Since we know that prevention of these conditions can lower risk of heart attack and stroke, it is likely that it would also lower the risk of developing Alzheimer’s.”

In a 2011 Japanese study, which included more than 1,000 men and women over age 60, researchers found that people with diabetes were twice as likely as the other study participants to develop Alzheimer’s disease within 15 years. They were also 1.75 times more likely to develop dementia of any kind.

(High) coffee consumption

See the link between Increased Risk of Alzheimer’s and Coffee.

Poorly controlled diabetes

Reasonably controlled diabetes

See the link between Diabetes / Risk and Alzheimer’s disease.

Possible Alzheimer's disease

(Serious) past head injury

Besides age and genetics, most experts agree the evidence is conclusive enough to name serious head injury as a strong risk factor for the disease. Inflammation in the brain can lead to the death of cells which contributes to the disease.

Not keeping one's mind active

Staying mentally active/stimulated appears to reduce the risk.

Keeping one's mind active

Staying mentally active/stimulated appears to reduce the risk.

Glutamine

Glutamine accumulation has also been found in Alzheimer’s disease, Huntington’s disease and high levels of brain glutamine have been associated with a worse prognosis in Lou Gehrig’s disease. Likewise, recent studies have shown that high brain glutamine levels increase brain levels of free radicals and impair the ability of brain mitochondria to produce energy. When the brain produces low energy, excitotoxins, such as glutamate, become even more toxic. It has been shown that the reason for glutamine toxicity under these conditions is because it is converted to the excitotoxin – glutamate. Russell L. Blaylock, M.D.

Fish Oil / Krill

Studies indicate eating a diet high in omega-3 fatty acids, found in fish, may fend off Alzheimer’s. To arrive at this conclusion, researchers studied older mice genetically engineered to develop the disease. The mice were divided into two groups: One group was fed a diet rich in docosahexanoic acid, or DHA, the omega-3 fatty acid found in various types of coldwater fish, and the other group was fed a low-DHA diet; such diets have been associated with impaired mental functioning.

Within five months of the study, a 70% less buildup of amyloid protein, which makes up the plaques in the brain famously attributed to Alzheimer’s, was detected in mice that were fed a diet rich in DHA-fortified foods. These results coordinate with the team’s previous findings that DHA was responsible for protecting the brains of mice from synaptic damage, enabling them to perform better on memory tests. [The Journal of Neuroscience March 23, 2005 25(12): pp.3032-40]

Scientists have discovered the mechanism by which the omega-3 fatty acids found in fish oils can help protect the brain against the cognitive decline associated with Alzheimer’s disease.

Docosahexaenoic acid (DHA), preformed in fish oil, reduces the levels of a protein known to cause damage in the brains of Alzheimer’s patients. They also discovered that a derivative of the fatty acid called neuroprotectin D1 (NPD1) is formed in the human brain, and is essential in protecting against brain cell death. [Journal of Clinical Investigation September 8, 2005]

Two additional studies found that in healthy individuals that a diet high in fish and fish products is associated with better cognitive performance. Higher levels of omega-3 fatty acids were associated with less decline in the speed-related cognitive domains.

It often takes decades for dementia to develop and brain volume to shrink. These studies of the benefits of omega-3 fats on brain function offer an opportunity for early intervention to maintain your brain function and slow progression to dementia. [American Journal of Clinical Nutrition, 86(5), 1259-1260, November 2007] [Scotsman.com News April 6, 2008] Eat your omega-3’s if you want to avoid getting Alzheimer’s. In part, that’s the moral of the story out of new research from Aberdeen University which has found that patients whose diets are high in omega-3 oils do better in mental tests than those who do not have the oils in their diet.

Calling the discovery a “major breakthrough” in the fight against Alzheimer’s, the article in The Scotsman explains how the study was conducted using 58,000 Scots who suffer from the condition.

Lead researcher, Lawrence Whalley, professor of mental health at Aberdeen University, said: “Ten years ago this would have been science fiction. What we are touching on here is how nutrients can interact with specific genes in the body.”

The red herring (excuse the pun) appears to be a crucial gene some individuals possess called APOE e4 that prevents the omega oils from having a healing or preventive effect. Unfortunately, those individuals must pursue other avenues of treatment.

Whalley said: “What emerges from this research is that if you don’t have this gene, omega-3s can make a difference. The next big thing will be to identify what factors can influence how these genes can be switched on and off, and also what to do if you have the gene.”

Maureen Thom, information manager for Alzheimer Scotland, said: “It’s a very welcome and interesting piece of research, very thorough. I would like to see it developed and have results analyzed for a larger number of people. We do advise that everyone should try to stick to a healthy lifestyle and consume omega-3 oils as part of a healthy diet.”

Coffee (Coffea genus)

Research suggests that drinking several cups of coffee each day during middle-age, may significantly reduce the odds of developing Alzheimer’s disease later in life.

Swedish and Finnish researchers studied the association between tea and coffee consumption during middle-age and the incidence of Alzheimer’s disease in late-life. The researchers first questioned people about their tea and coffee drinking habits. A total of 1409 participants were available for the follow-up re-examination approximately 21 years later. At follow-up participants were aged between 65 to 79, and 61 participants were found to be suffering from dementia, 48 of which had Alzheimer’s disease.

Results showed that people who drank coffee whilst middle-aged had a significantly lower risk of developing dementia and Alzheimer’s disease than those who drank little or no coffee. With participants who reported a moderate coffee consumption (3 to 5 cups each day) being 65% less likely to develop dementia/Alzheimer’s disease than those who drank little or no coffee. Tea drinking was uncommon in the study population and the researchers found no association between drinking tea and dementia/Alzheimer’s disease.

“Given the large amount of coffee consumption globally, the results might have important implications for the prevention of or delaying the onset of dementia/Alzheimer’s disease,” said lead researcher, Miia Kivipelto. “The finding needs to be confirmed by other studies, but it opens the possibility that dietary interventions could modify the risk of dementia/Alzheimer’s disease. Also, identification of mechanisms of how coffee exerts its protection against dementia/Alzheimer’s disease might help in the development of new therapies for these diseases.” [A Population-based CAIDE Study. Journal of Alzheimer’s Disease. 2009;16]

Chlorella / Algae Products

One study has shown that among 50 people with Alzheimer’s, aged 70-90, taking 6gm daily of chlorella for 6 months, 68% experienced either a stabilization or improvement in cognitive functions.

Grape Seed Extract / Resveratrol

Although unmodified resveratrol appears to have a weak bioavailability, several studies have clearly demonstrated the in vivo neuroprotective properties of the red wine-derived polyphenol, strongly supporting the notion that natural metabolites of resveratrol may have biological activities. Furthermore, recent findings have shed light on the potential role of resveratrol in transcription- and degradation-dependent anti-amyloidogenic mechanisms, suggesting that natural metabolites or potent synthetic analogues of resveratrol have a therapeutic potential in Alzheimer’s Disease.

Marijuana

New evidence in rats suggests that marijuana may contain compounds that slow the memory loss associated with Alzheimer’s disease.

Marijuana has strong anti-inflammatory effects, and many researchers believe that there is a compelling link between chronic inflammation and the progression of Alzheimer’s, said Gary Wenk, a study co-author and a professor of psychology at Ohio State University.

“Inflammation in the brain is part of aging,” Wenk said. “It happens to almost all of us as we age. But in some cases, this inflammation gets out of hand and causes serious damage.”

“Treatment with a synthetic compound similar to marijuana reduced inflammation in older rats in addition to making the animals “smarter,” said Wenk, who is also a professor of neuroscience and molecular virology, immunology and medical genetics.

“The compound substantially improved the memories of the older rats,” he said. “These animals were able to hold on to key details of a specific task. Untreated older rats, on the other hand, were not.”

The researchers presented their findings October 18, 2006 in Atlanta at the annual Society for Neuroscience meeting.

Evidence suggests that people who regularly smoked marijuana in the 1960s and 1970s rarely develop Alzheimer’s disease, said Wenk, adding that researchers are eager to develop a drug with the anti-inflammatory properties of marijuana, but without the drug’s psychoactive effects.

The colleagues treated young and old rats with WIN-55212-2 (WIN), a synthetic drug similar to marijuana. While the compound improved memory and helped to control inflammation, it is not a candidate for use in humans because it still contains substances that could trigger a high.

Huperzia serrata

Cinnamon (Cinnamonum zeylanicum)

Michael Ovadia, from Tel Aviv University (Israel), and colleagues isolated CEppt, an extract found in cinnamon bark, and introduced the substance into the drinking water of mice that had been genetically altered to develop an aggressive form of Alzheimer’s disease, and fruit flies that had been mutated with a human gene that also stimulated Alzheimer’s disease and shortened their lifespan.

After four months, the researchers discovered that development of the disease had slowed remarkably and the animals’ activity levels and longevity were comparable to that of their healthy counterparts. The extract inhibited the formation of toxic amyloid polypeptide oligomers and fibrils, which compose deposits of plaque found in the brains of Alzheimer’s patients. In a test-tube study, Ceppt was also found to break up amyloid fibers, similar to those seen in Alzheimer’s patients.

Noting that Ceppt caused a “reduction of plaques and improvement in cognitive behavior,” the team concludes that: “Our results present a novel prophylactic approach for inhibition of toxic oligomeric A[beta] species formation in [Alzheimer’s Disease] through the utilization of a compound that is currently in use in human diet.”

A problem remains with the quantity of cinnamon one would need to consume to benefit from its anti-Alzheimer’s properties. “Raw cinnamon also contains substances harmful to the liver,” says Ovadia. “Whereas one may consume six to ten grams per day without damaging the liver, to reap the substance’s medicinal benefits, one would have to consume tens of grams per day at least, which starts to become dangerous. For this reason we developed a means of extracting the active substance from the cinnamon and separating it from the toxic substances.” [Frydman-Marom A, Levin A, Farfara D, Benromano T, Scherzer-Attali R, et al. (2011) Orally Administrated Cinnamon Extract Reduces ß-Amyloid Oligomerization and Corrects Cognitive Impairment in Alzheimer’s Disease Animal Models. PLoS ONE 6(1): e16564. doi:10.1371/journal.pone.0016564]

This extract is not currently available for consumer use.

Ginkgo Biloba

“We found that giving a standardized dose of ginkgo biloba over a period of time does not slow down the incidence rate of dementia or Alzheimer’s disease,” said the study’s lead author, Dr. Steven DeKosky, who was chair of the department of neurology at the University of Pittsburgh School of Medicine and Medical Center at the time of the study.

Coconut

New benefits of coconut oil continue to be discovered. One potential benefit is that it may ease Alzheimer’s. Dr. Mary Newport may have made an important observation about this connection. Dr. Newport’s husband had been diagnosed with early onset Alzheimer’s and was watching her husband quickly deteriorate.

After using drugs that slowed down the effects of Alzheimer’s, she looked into clinical drug trials and found one based on MCTs (medium chain triglycerides, such as found in coconut oil) that not only slowed the progression of Alzheimer’s, but offered improvement. Not being able to get her husband into one of these trials, she began to give him Virgin Coconut Oil, and saw incredible improvement in his condition.

The coconut oil he’d ingested seemed to “lift the fog.” He began taking coconut oil every day, and by the fifth day, there was a tremendous improvement. “He would face the day bubbly, more like his old self,” his wife said. More than five months later, his tremors subsided, the visual disturbances that prevented him from reading disappeared, and he became more social and interested in those around him. [Doctor says an oil lessened Alzheimer’s effects on her husband, St. Petersburg Times, October 29, 2008 ]

You can also watch an interview with Dr. Newport done by CBN here.

Weight Loss

Sugars Avoidance / Reduction

Animal/Saturated Fats Avoidance

Please see the link with Increased risk of Alzhiemer’s and Multiple Vitamin Need.

Processed Foods Avoidance

Keep your weight down, and keep simple sugars and refined carbohydrates to a minimum. Researchers have found that diabetes mellitus (for which these are risk factors) nearly doubles the risk of developing both vascular dementia and Alzheimer’s disease.

Increased Fruit/Vegetable Consumption

News from the Telegraph U.K. says scientists have found that blueberries can increase your attention span in the short term and can maintain a healthy mind in the long term.

According to the report, they found that just one 200g blueberry smoothie was enough to increase powers of concentration by as much as 20 % over the day, and regular consumption of the fruit could lead to a rewiring of a part of the brain that is linked to memory.

The fruit, which is an anti-oxidant, has already been linked to lower heart disease and cancer rates as well as anti-aging. Antioxidants remove free radicals – chemicals that have the potential to cause damage to cells and tissues in the body.

Dr. Jeremy Spencer, a molecular nutritionist at the University of Reading who carried out the latest study, is quoted as saying he believes its affect on the mind has more to do with its ability to increase the blood flow to the brain, and that flavonoid rich foods, which also include chocolate, spinach and some fruit juices, can re-structure the brain and ward off memory loss associated with Alzheimer’s. [reported at the British Science Festival, Sept 2009]

Artificial Sweetener Avoidance

Aspartame use has been reported to trigger symptoms of Alzheimer’s.

NSAIDs

At least twenty studies suggest that Ibuprofen and other NSAIDs – common non-prescription drugs – may slow or prevent the onset of Alzheimer’s disease by as much as 60%. Researchers say it also opens up a new way to think about how Ibuprofen protects the brain.

“We’ve shown that a drug that’s available, that’s been in use for 30 to 40 years, and for which we know the side-effect profiles… can reduce both the inflammatory response to amyloid and the amyloid itself”, says study leader Gregory M. Cole of the University of California in Los Angeles.

Note that NSAIDs can cause serious stomach problems, including bleeding. Investigators therefore hesitate to recommend widespread use of the drugs until they can develop safer versions.

Certain NSAIDs work by decreasing the levels of amyloid-beta 42 rather than by inhibiting cyclooxygenase, as was once proposed. Advil (Ibuprofen) is the most effective, requiring as little as 800mg per day to reduce the risk of Alzheimer’s without serious side-effects. Other NSAIDs require much higher doses to achieve this benefit, while aspirin, Naproxen and celeloxib (Celebrex) were found ineffective.

Conventional Drugs / Information

Researchers found that clioquinol can almost stop the progression of Alzheimer’s disease. They believed that by absorbing the copper and zinc atoms that concentrate in the brains of Alzheimer’s sufferers, clioquinol could stop the onset of dementia before it starts. That could mean that this drug might be of use by a physician who is concerned about Alzheimer’s developing in a high risk patient. [Archives of Neurology December, 2003;60(12):pp.1685-91]

Please also see the link between Alzheimer’s and Conventional Drugs for a report regarding Rember.

Aerobic Exercise

A study (October 2008) coming from Professor Art Kramer, of the US Beckman Institute at the University of Illinois, gives strong evidence that aerobic exercise can actually reverse mental decline.

According to a report in The Telegraph, research suggests that the benefits of regular workouts are seen not only in those undergoing the normal aging process but also in people suffering from Alzheimer’s disease.

Indeed, says the report, the findings of one study suggested that people who exercised for just one hour three times a week over three months increased their brain size to that of someone three years younger.

Writing in the British Journal of Sports Medicine, Professor Kramer, who is quoted as saying he believes that around six months of physical activity would be enough to see a marked improvement in brain power, said: “We can safely argue that an active lifestyle with moderate amounts of aerobic activity will likely improve cognitive and brain function, and reverse the neural decay frequently observed in older adults. The effect of aerobic exercise training on cognitive function also seems to extend to older adults with dementia.”

Also, patients with Alzheimer’s disease have been found to have had lower levels of physical activity earlier in life. Those who exercised regularly throughout life were less likely to contract the disease than those who were inactive. Of course, doctors caution that exercise does not guarantee immunity.

Aluminum Consumption Avoidance

Alzheimer’s Disease has been linked to a number of risk factors, including exposure to aluminum. Now from France comes a report that drinking water with high aluminum concentrations may indeed increase the risk of developing Alzheimer’s and dementia. High sources of aluminum in the diet include: aluminum cooking utensils, aluminum-containing antacids, tap water (which may have aluminum sulfate added to remove particulate and organic matter).

Researchers determined that a concentration of aluminum in drinking water above 0.1mg/liter may be a risk factor of dementia and Alzheimer’s disease. Nearly 2,700 individuals were followed for an 8-year period to identify new cases of probable Alzheimer’s or other dementing illness. The sample was divided into 77 drinking water areas, with surveys conducted to determine concentrations of aluminum, calcium, and fluorine in each water supply. The study authors point out that their findings support those of several other studies linking aluminum to Alzheimer’s, but add that “this result needs to be confirmed using a higher number of exposed subjects.” [American Journal of Epidemiology 2000;152: pp.59-66.]

One of our doctors comments: This is another reason to make sure that you limit your water intake to filtered or bottled. Aluminum is certainly an issue, but probably not as significant as chlorine exposure. Unless you have well water you will also need a filter for your shower as most of us will probably absorb more toxins from bathing or showering than we will from drinking tap water.

Estrogen Replacement

Estrogen replacement therapy may help reduce risk or delay its occurrence, but does not help once disease is established. One reason for the confusion is the use of synthetic estrogens: natural estrogens should exert a protective effect. One study found that the risk of Alzheimer’s disease and related dementia for women who had used estrogen was found to be about one third below that of women who had never used estrogen. The risk also decreased with increasing dosage and duration of estrogen therapy. The lowest risk was observed in long-term users taking high doses.

Suggestions that the decline in estrogen levels in women at menopause might somehow make them more vulnerable to the disease have prompted interest in the hormone as a possible treatment and research has suggested that women who take estrogen are less likely to develop Alzheimer’s.

However, a new study found that once the mind-robbing disease sets in, the female hormone offers no benefit. A year of estrogen did nothing to slow the progression of the disease or improve mental functioning in 120 older women with mild to moderate Alzheimer’s. Overall, the results of this study do not support the role of estrogen in the treatment.

In another study, women aged 60 and older were given either a low estrogen dose, a high dose or a placebo every day for a year. Instead of showing any improvement, those taking estrogen in fact fared worse than the placebo group in a rating of dementia. [JAMA February 23, 1999 283: pp.1007-1015] [One of our doctors comments: I am really surprised that this study did not receive more widespread news coverage. When the drug companies had the initial studies published suggesting that estrogen will help protect against Alzheimer’s it was all over the news. I was immediately confronted by many patients who felt my recommendation to avoid estrogens was unwise. Now the evidence is in that estrogen does NOT help Alzheimer’s but actually worsens it. I am delighted that JAMA continues to take a leadership role in publishing these landmark articles which refute the drug companies’ position. Unfortunately, the conventional media still appears to be sold out – hence the lack of notification of the results of this study.

There are times when estrogen is necessary. I believe if phytoestrogens are unable to stop the hot flashes then it would be wise to use small amounts of estrogens to stop them. Waking up every night with hot flashes is a surefire prescription for depression and increased risk of disease. Thus in this case the estrogen is the lesser of two evils. It should be used for the shortest time possible and always with the intent of weaning oneself off of it.]

Testosterone

The popular image of this sex hormone is primarily as a muscle-building machismo-inducing substance that “pumps men up”, yet clinical research is uncovering important roles for testosterone in many other diverse areas of health and physiology, including the brain. New evidence suggests that testosterone may enhance memory function and protect against the development of Alzheimer’s disease.

Neuroscientists from Rockefeller University and Weill Medical College of Cornell University recently discovered that when neural cells from the brains of rats are exposed to testosterone, the cells don’t produce as much Amyloid beta-peptide (AB-peptide). The accumulation of AB-peptide can cause plaque deposits to form in the brain. These deposits are believed to play a major role in the development of Alzheimer’s disease.

Testosterone in addition appears to improve certain cognitive abilities in men, such as verbal and spatial memory function. Levels of bioavailable testosterone are especially important, researchers emphasized, because these levels decline most rapidly as men and women age.

Since high levels of testosterone have been linked with prostate cancer in men and endometriosis in women, however, they urged caution when using replacement therapy, carefully weighing the risks and benefits for each patient.

Increasing levels of adrenal hormones such as cortisol, which rise in response to stress and aging, may also play an important role in Alzheimer’s. High levels of these hormones can damage the hippocampus region in the brain, causing

learning impairment and memory loss. Testosterone, however, shows the potential to reverse some of this damage.

Melatonin

Ensure normal melatonin levels. Melatonin, a powerful antioxidant and heavy-metal-chelating agent, has been shown to protect against heavy metal exposure which is in turn implicated in Alzheimer’s Disease.

After exposing nerve cells to inorganic mercury, neurobiologists observed a toxic reaction that reduced cellular levels of the antioxidant glutathione by 30%, triggered the release of plaque-forming ß-amyloid peptides, and spurred the hyperphosphorylation of tau-protein – all pivotal mechanisms in the development and progression of Alzheimer’s.

However, they found that if the cells were first incubated with melatonin – a powerful antioxidant and heavy-metal-chelating agent – they were protected from these damaging effects. In fact, despite being exposed to toxic doses of mercury, the cells treated with melatonin often showed metabolic status comparable to that of mercury-free cells.

These results provide strong experimental evidence that mercury toxicity may be involved in Alzheimer’s development and that melatonin shows a marked potential to neutralize this toxic-induced pathology, by boosting antioxidant defense and binding to heavy metals.

Eye Doctor / Ophthamologist

2010 (London, England)—A simple and inexpensive eye test could aid detection and diagnosis of major neurological diseases such as Alzheimer’s at an earlier stage than is currently possible, according to new research by UCL (University College London) scientists.

The research, led by Professors Francesca Cordeiro & Stephen Moss and published today in Cell Death & Disease, demonstrates a new technique that enables retinal, and therefore brain cell death, to be directly measured in real time. The method, demonstrated in an animal model, could not only refine diagnosis of neurodegenerative disorders and help track disease progress; it could also aid the assessment and development of new treatments. (Photo by Rick Furber)

The technique uses fluorescent markers that attach themselves to the relevant cells and indicate the stage of cell death. The retina is then observed using a customized laser ophthalmoscope. Until now, this kind of technique has only been used in cells in the lab, rather than in live animals. This research is therefore the first ever in vivo demonstration of retinal nerve cell death in Alzheimer’s Disease.

Professor Cordeiro, UCL Institute of Ophthalmology, said: “The death of nerve cells is the key event in all neurodegenerative disorders—but until now it has not been possible to study cell death in real time. This technique means we should be able to directly observe retinal nerve cell death in patients, which has a number of advantages in terms of effective diagnosis. This could be critically important since identification of the early stages could lead to successful reversal of the disease progression with treatment.

“Currently, the biggest obstacle to research into new treatments for neurodegenerative diseases is the lack of a technique where the brain’s response to new treatments can be directly assessed—this technique could potentially help overcome that.”

Although this paper outlines the technique in animal models (rats and mice), Professor Cordeiro’s team are further along with work using the same technique to detect and assess glaucoma, and will be conducting their first patient trials later this year.

She added: “The equipment used for this research was customized to suit animal models but is essentially the same as is used in hospitals and clinics worldwide. It is also inexpensive and non-invasive, which makes us fairly confident that we can progress quickly to its use in patients.

“Few people realise that the retina is a direct, albeit thin, extension of the brain. It is entirely possible that in the future a visit to a high-street optician to check on your eyesight will also be a check on the state of your brain.”

A report in the London Daily Telegraph also quoted Dr. Cordeiro as saying: “If you catch Alzheimer’s Disease early enough you can slow it down and even reinvigorate the cells.”

Tests, General Diagnostic

MRI scans can be used to diagnose Alzheimer’s disease, even before the onset of symptoms of dementia, say researchers.

Alzheimer’s disease is currently diagnosed by a process of elimination as many other diseases cause similar symptoms, furthermore a diagnosis of Alzheimer’s disease cannot be confirmed until after the patient has died by autopsy. However, results of a study by Ranjan Duara and colleagues at the Florida Alzheimer’s Disease Research Center (ADRC) has added to a growing body of evidence which suggests that MRI scans of the brain can be used to diagnose the neurodegenerative disease.

The researchers used a visual rating system to evaluate the extent of atrophy, or shrinkage, present on MRI scans in three parts of the medial temporal lobe of the brain which are vital for conscious memory. They then compared the MRI brain scans of 260 people, which included people with probable Alzheimer’s disease, people with varying degrees of mild cognitive impairment (MCI), and a control group of normal elderly with no symptoms of memory loss. Results showed that by using the rating system they could accurately distinguish those with probable Alzheimer’s disease from those with MCI, and from those in the control group. Furthermore, the scans even enabled the researchers to identify brain atrophy in some participants who did not have symptoms of memory loss at the start of the study, but who went on to develop memory problems several years later. Thus suggesting that MRI scans could enable doctors to identify those who will get Alzheimer’s long before they become symptomatic.

“This study demonstrates that MRI brain scans are accurate enough to be clinically useful, both in diagnosing Alzheimer’s disease itself at an early stage and in identifying people at risk of developing Alzheimer’s,” said Huntington Potter, PhD director of the Florida ADRC.

News release: MRI brain scans accurate in early diagnosis of Alzheimer’s disease. University of South Florida Health. December 18th 2008.

Test / Monitor Hormone levels

Make sure estrogen and testosterone levels are normal.

Test for Heavy Metals

Avoid mercury, and detoxify if levels are found elevated. See discussion of Melatonin for details.

Lithium (low dose)

There are many research findings that strongly suggest that lithium will protect against potential Alzheimer’s disease and slow the progression of existing cases. Researchers have reported that lithium inhibits beta-amyloid secretion, and also prevents damage caused by beta-amyloid protein once it’s been formed. Beta-amyloid peptide is a signature protein involved in Alzheimer’s disease: the more beta-amyloid protein, the worse the Alzheimer’s becomes. Overactivation of a brain cell protein called tau protein also contributes to neuronal degeneration in Alzheimer’s disease, as does the formation of neurofibrillary tangles Lithium inhibits both of these nerve-cell damaging problems.

Zinc

Maintain adequate zinc status: Reduced levels of zinc are being linked to Alzheimer’s disease. In one study, 38 elements were evaluated by neutron activation and mass spectrometry in the post-mortem brain tissue of eleven Alzheimer’s patients and six controls. An increase was found in aluminum, silicon and calcium; a significant decrease was found in zinc and selenium. The lower level of zinc in all areas of the tissue studied correlates with reports indicating low serum levels of zinc in other dementia studies. [Reduction of Zinc and Selenium in Brain Alzheimer’s Disease: Corigan, et al., Trace Elements in Medicine, 91;8(1): pp.1-5]

Software Programs

The Improvement in Memory with Plasticity-based Adaptive Cognitive Training (IMPACT) study was funded by the Posit Science Corporation, which owns the rights to the Brain Fitness Program, tested in the study.

Elizabeth Zelinski, PhD, of the USC Davis School of Gerontology and Glenn Smith, PhD, of the Mayo Clinic were principal investigators on the study, published with colleagues from the University of California, San Francisco, Stanford, and California State University, Los Angeles.

Of the 487 healthy adults over the age of 65 who participated in a randomized controlled trial, half used the Brain Fitness Program for 40 hours over the course of eight weeks. The Brain Fitness Program consists of six audio exercises done on a computer, and is intended to “retrain the brain to discriminate fine distinctions in sound, and do it in a way that keeps the user engaged,” Zelinski explained.

The other half of participants spent an equal amount of time learning from educational DVDs followed by quizzes.

Those who trained on the Brain Fitness Program were twice as fast in processing information with an average improvement in response time of 131 percent. The active control group did not show statistically significant gains, the researchers found.

According to the researchers, participants who used the Brain Fitness Program also scored as well as those ten years younger, on average, on memory and attention tests for which they did not train. Many participants also reported significant improvements in everyday cognitive activities such as remembering names or understanding conversations in noisy restaurants.

“The changes we saw in the experimental group were remarkable—and significantly larger than the gains in the control group,” Zelinski said. “From a researcher’s point of view, this was very impressive because people got better at the tasks trained, [and] those improvements generalized to standardized measures of memory and people noticed improvements in their lives. What this means is that cognitive decline is no longer an inevitable part of aging. Doing properly designed cognitive activities can enhance our abilities as we age.”

This program is expensive, so one should investigate fully before purchasing.

Reading List

A team of national researchers, led by Emory University, has developed a rapid screening test to detect mild cognitive impairment (MCI) – often the earliest stage of AD. The findings are published in the online edition of Journal of Alzheimer’s Disease.

The study shows that the combination of a very brief three-minute cognitive screening test, called the Mini-Cog (MC), with a Functional Activities Questionnaire (FAQ) – administered to a family member or friend – could accurately identify individuals with MCI and undiagnosed dementia.

“Since current medications can only delay the onset of Alzheimer’s disease but are not able to reverse its devastating effects, a test like this is key to help individuals detect this devastating disease earlier and maintain a good quality of life for as long as possible,” says James Lah, MD, associate professor of neurology, Emory University School of Medicine and lead investigator of the study.

The new screening instrument, referred to as the MC-FAQ, allowed the researchers to correctly classify the 204 participating elderly individuals as cognitively normal, demented, or mildly cognitively impaired with a high degree of accuracy (83%). Approximately 30 percent of participants had MCI and 32% were very mildly demented.

According to Lah, screening for MCI is notoriously difficult and typically requires 40-60 minutes or more of formal neuropsychological testing to achieve 80 percent accuracy or higher. Specific accuracy for classifying people as MCI with the MC-FAQ was 74%.

“While this may not seem overly impressive, it is quite remarkable for a 3-minute investment,” says Lah. “The MC-FAQ is also extremely inexpensive, easy to administer and score, and requires no special training.”

The MC portion of the screening consisted of a simple clock drawing task and three-item recall that typically took the research participant less than five minutes to complete. The FAQ was completed by a reliable informant, generally a spouse, other family member or close friend while the research participant was performing other tasks. [Journal of Alzheimer’s Disease, November 2008 (Volume 15:3)]

Please note: If you decide to try this test and, you find the results of the test suspicious, please don’t jump to any conclusion until you consult with your personal care physician.

There are three parts to the test.

First, name three objects and then ask the person being tested to repeat them back to you (for example, chair, house, apple). If the person cannot repeat the three objects after a few tries (cannot learn them), please consult a physician immediately. If the person can complete this task move on to the following.

Second, ask the person to draw a clock. The clock should include the shape and the numbers on the clock. Pretty much like a simple clock you see on a wall.

Third, ask the person to repeat the words/objects from the first part of the test.

If the person is unable to repeat any of the words, they might be categorized as mildly cognitively impaired or suffering from dementia. The key word so far – might.

If the person can repeat all three words the person is not “probably suffering from dementia”.

If the person cannot draw the clock or if it looks abnormal they would fall into the category of “probably” suffering from mild cognitive impairment or dementia.

You should note that many people that cannot past this test might be suffering from some other illness. This is why it is necessary to consult your doctor and a memory specialist.

The person you are testing could be suffering from depression, hypothyroidism, or any number of illnesses that can present as Alzheimer’s or dementia. This is why it is necessary to get a complete battery of tests performed by a medical professional prior to any “official” diagnosis.

Lecithin / Choline / GPC

Study participants received 1200mg GPC daily for six months. On a variety of assessment scales for Alzheimer’s disease (AD), GPC patients scored more favorably than patients from the control group, all of whom received placebo. The mental status of patients on GPC therapy improved, while those receiving the placebo worsened. These findings are comparable to the results obtained with the use of the prescription drugs Aricept (donepezil HCl) Exelon (rivastigmine tartrate) and Reminyl (galantamine hydrochloride) in the treatment of AD patients, and with fewer side effects. [Mech Ageing Dev 2001 Nov: 122(16): pp.2041-2055]

In another study, Richard Wurtman, from Massachusetts Institute of Technology (MIT; Massdachusetts, USA), and colleagues have formulated a mixture of three naturally occurring dietary compounds: choline, uridine and docohexaenoic acid (DHA).

Choline can be found in meats, nuts and eggs, and omega-3 fatty acids are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Uridine is produced by the liver and kidney, and is present in some foods as a component of RNA. Docohexaenoic acid (DHA) is an omega-3 fatty acid, best known for its role in promoting cardiovascular health. Collectively, these three nutrients are precursors to the lipid molecules that, along with specific proteins, make up brain-cell membranes, which form synapses. To be effective, all three precursors must be administered together.

The researchers followed 259 patients for six months. Patients, whether taking the nutrient blend or a placebo, improved their verbal-memory performance for the first three months, but the placebo patients deteriorated during the following three months, whereas the nutrient blend patients continued to improve. Further, electroencephalography (EEG) studies revealed changes in brain-activity patterns throughout the study: as the trial went on, the brains of patients receiving the nutrient blend started to shift from patterns typical of dementia to more normal patterns. Because EEG patterns reflect synaptic activity, the researchers submit that synaptic function increased following treatment with the nutrient blend. [“Nutrient Cocktail” Improves Alzheimer-Related Memory Decline. Posted on Aug. 3, 2012, 6 a.m. in Alzheimer’s Disease Dietary Supplementation Fatty Acids, Lipids & Oils]

DHA (docosahexaenoic acid)

Over 1200 patients participated in an epidemiological study which showed that people with high DHA levels were 45% less likely to develop dementia than people with low DHA levels. This suggests that proper DHA intake may reduce the risk of developing Alzheimer’s. The best source of preformed DHA is fish oil.

Please see the link between Alzheimer’s, Increase Risk and Lecithin/Choline also.

Essential Fatty Acids

Please see the link from Increased Risk of Alzheimer’s and Fish Oil.

Acupuncture

The Chinese consider acupuncture to be an effective therapy for Alzheimer’s disease. There is solid evidence that acupuncture increases certain neurotransmitters in the brain and can actually stimulate nerve regeneration. Increased serotonin levels probably explain why acupuncture is so effective in controlling pain and managing stress. Acupuncture also promotes blood circulation to the brain and improves memory and concentration so there is good reason for people who have Alzheimer’s, or who are at risk for developing it, to try acupuncture.

Vitamin E

Ensure sufficient antioxidant intake. A study of more than 5,000 men and women found that people who consumed very high amounts of dark green, yellow, and red vegetables appear to reduce their risk of dementia by about 25%. Several studies have shown that vitamin E, an anti-oxidant, can slow progression of Alzheimer’s.

Dietary vitamin E is rich in the gamma tocopherol fraction of vitamin E, whereas vitamin E supplements consist primarily of alpha tocopherol. It is the gamma tocopherol fraction of vitamin E that has been shown to be the critical factor in suppressing free radicals. The brain is especially vulnerable to the toxic effects of free radicals because of its high-energy output. Notably, in this study, only those with a genetic predisposition for contracting Alzheimer’s disease (those whose genetic structure was without the APOE epsilon 4 allele) showed the remarkable protective benefit from dietary vitamin E. [ JAMA June 26, 2002]

There is a conflicting study of Japanese men living in Hawaii that did not show any protective benefit from supplemental vitamin C or E over a period of 5.2 years. [JAMA 2002;288(18): pp.2266-8]

Vitamin Folic Acid

There is growing evidence suggesting that low blood folate levels can increase the risk of getting Alzheimer’s.

In an ongoing study searching for new clues to the aging process, researchers took blood samples of nuns between the ages of 78-101years old living in a convent in Mankato, Minnesota. After 30 of the nuns died, researchers examined their brains for signs of atrophy and compared the results with previous blood nutrient levels.

In brain samples showing numerous Alzheimer’s disease brain lesions, researchers found that significantly lower blood levels of folate corresponded with more severe atrophy of the neocortex, the region of the brain containing a rich supply of nerve cells.

Although the study was small, and did not attempt to prove a causal effect, it supports previous evidence linking defects in B-vitamin metabolism with age-related dementia and Alzheimer’s. “Optimal folate concentration may in fact be higher in old age or when diseases such as Alzheimer’s are present,” commented the researchers.

Low folate levels can trigger a build-up of the amino acid homocysteine, which has been linked to higher risk of Alzheimer’s and accelerated atrophy of the medial temporal lobe in Alzheimer’s patients.

“There seems little doubt now that there is an association between the evolution of certain brain diseases associated with cognitive decline in the elderly and vitamin deficiencies associated with hyperhomocysteinemia,” a related editorial resounded.

Although the full extent to which B-vitamin metabolism influences the actual causal mechanisms of dementia is still not clear, “the potential therapeutic options [implicated by these discoveries] are exciting”, the authors posited.

The nuns provided a unique population sample to study because they all had similar long-term diet and exercise habits. Researchers found strong evidence of biochemical individuality among the group, despite their similar lifestyle and eating habits. Blood nutrient levels varied widely, reflecting differences in “drug-nutrient and disease-nutrient interactions or differences in the intake, absorption, and metabolism of the nutrients.”

NOTE: As this study suggests, even people with similar diets may show striking differences in nutrient metabolism related to various physiological functions. Assessing each patient is the best way to gauge the effectiveness of nutrient intervention strategies.

Sources:

Snowdon DA, Tully CL, Smith CD, Riley KP, Markesbery WR. Serum folate and the severity of the atrophy of the neocortex in Alzheimer disease: findings from the Nun Study. Am J Clin Nutr 2000;71: pp.993-8.

Weir DG, Molloy AM. Microvascular disease and dementia in the elderly: are they related to hyperhomocysteinemia? Am J Clin Nutr 2000;71: pp.859-60.

Vitamin B Complex

Optimize your B-complex status, especially folic acid and B12. In one study, 76 Alzheimer’s patients had lower blood levels of folic acid and vitamin B12 than 108 age-matched control subjects. In addition, researchers found that Alzheimer’s patients had higher blood levels of homocysteine, which is already implicated in atherosclerosis. Folic acid and B12 supplementation is known to reduce homocysteine levels.

A two-year clinical trial in England has shown that B vitamins, including B-6, B-12 and folic acid, slow down mild cognitive impairment (MCI), a condition which is a major risk factor for Alzheimer disease and other forms of dementia.

Dr. Gustavo C. Román, medical director of the Alzheimer & Dementia Center at the Methodist Neurological Institute in Houston, said that patients who already exhibit signs of dementia and test positive for high levels of homocysteine are more likely to respond well to the large doses of B vitamins. Homocysteine is an amino acid in the blood, and high blood levels are linked to an increased risk of developing Alzheimer disease.

Román has seen the impact of these B vitamins in his patients and found that injections of B-complex vitamins are more effective than oral supplements.

“I’m not saying that everyone who takes B vitamins will prevent dementia,” Roman said. “But in the right dosage and for the appropriate patients, the vitamin B-12 treatment could be a step toward modifying disease progression.”

Approximately 50 percent of people diagnosed with MCI go on to develop Alzheimer disease within five years. More than five million Americans are estimated to have Alzheimer disease, the most common form of dementia.

Vitamin Niacinamide

An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.

Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.

“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”

Scientists found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.

Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer’s patients.

“Microtubules are like highways inside cells. What we’re doing with nicotinamide is making a wider, more stable highway,” Green said. “In Alzheimer’s disease, this highway breaks down. We are preventing that from happening.”

The study appeared online Nov. 5, 2008 in the Journal of Neuroscience.

Vitamin C (Ascorbic Acid)

Both vitamin E and vitamin C supplements reduced the incidence of Alzheimer’s disease in a 1998 study. This study followed 655 individuals over 65 years of age for an average of over 4 years. The anticipated rate of Alzheimer’s did not occur in those individuals taking larger amounts of either vitamin. The lower levels of vitamin C and E found in some supplements did not provide this protection in this study. A reasonable protective benefit could be expected with 400 IU of vitamin E or 500mg or more of vitamin C. [Alzheimer Dis. Assoc. Disord.1998:12(3): pp.121-126] This was confirmed by a later study. [JAMA 2002;287(24): pp.3223-3229]

However, there is a conflicting study of Japanese men living in Hawaii that did not show any protective benefit from supplemental vitamin C or E over a period of 5.2 years. [JAMA 2002;288(18): pp.2266-8]

Vitamin B3 (Niacin)

A small increase in the intake of niacin was associated with a reduced risk of Alzheimer’s disease in a study

of 815 elderly adults followed for an average of just over 2 years. The difference occurred with 22mg per day consumed compared to 12mg per day. The dietary intake of other B-vitamins was not associated with this reduced risk. [Gerontological Society of America 55th Annual Scientific Meeting, November, 2002]

Vitamin B12 (Cobalamine)

Low levels of vitamin B12 have been linked to an increased risk Alzheimer’s disease. [Neurology, May 2000] It remains unclear as to whether B12 supplementation will reduce the risk.

All ages of Alzheimer’s patients have been found to have lower serum B12 levels, compared to normals and patients with other forms of dementia in several other studies.

Supplementation of B12 and/or folic acid may result in complete reversal in some patients, but there is generally little improvement in patients who have had Alzheimer’s symptoms for longer than six months. Some scientists hypothesize that prolonged low levels of vitamin B12 may lead to irreversible changes.

Researchers have known for some time that there is a genetic marker, called e4 allele, which indicates a high risk

for dementia. About 15% of the population has this marker. It’s also well-known that people who have dementia or

Alzheimer’s, as well as many older people in general, often have low levels of vitamin B12. Evidence points to a clear link between e4 allele and vitamin B12. People who had the high-risk genotype plus low levels of vitamin B12 had a significantly poorer memory than any other combination that was tested. Simply raising the levels of vitamin B12 showed a marked

improvement, even though the genetic condition still exists. [American Psychological Association, 5 April 2004]

See also the link with Alzheimer’s risk and the use of B complex.