Alzheimer's Disease
What is it?
Alzheimer’s disease is a type of mental deterioration in which sufferers experience a steady and progressive loss of intellectual function due to degenerative changes in the brain. It is the fourth leading cause of death in the USA; and by the age of 80, around one person in three has the disease. Approximately two million people in the USA are currently affected by the disease with women twice as susceptible as men. As the population ages, experts estimate that by 2050 there will be almost 9 million sufferers.
Changes in the brain in Alzheimer’s disease
In Alzheimer’s disease, there is general destruction of nerve cells in several key areas of the brain devoted to mental functions. Nerve fibers grow tangled and protein deposits known as plaques build-up in the nerve cells. These plaques are usually made up of compounds known as beta amyloid peptides, which are toxic to nerve cells. There is also a reduction in brain neurotransmitters, including acetylcholine.
Symptoms of alzheimer's disease
The most common early symptom of Alzheimer’s disease is memory loss. This develops gradually and at first almost imperceptibly, with symptoms that resemble ordinary memory lapses. Other intellectual functions such as comprehension and language skills also deteriorate until the person loses the ability to learn and remember anything new. Familiar places and people become unrecognizable and ordinary activities become increasingly difficult. Sufferers often become irritable, restless and easily agitated. They may become disorientated and wander off and get lost. In the later stages of the disease, they are unable to carry out daily activities and become dependent on others for basic needs such as eating and washing.
When symptoms occur before age 65, the disease is referred to as presenile dementia of the Alzheimer’s type; and after 65 as senile dementia of the Alzheimer’s type. The average time a person survives with the disease is seven years, although some patients may live for up to 20 years.
Diagnosis of alzheimer's disease
The only way to definitely confirm the presence of Alzheimer’s disease is to perform a brain biopsy which is obviously not possible when the person is alive. Because of this, a physician diagnoses the disease based on physical, neurological and psychiatric signs. However, diagnosis is difficult as the symptoms of the disease are similar to those seen in other disorders; such as other types of dementia, anemia, depression, drug side effects and nutritional deficiencies. Alzheimer’s disease is often diagnosed when these other causes have been ruled out. Research has shown that Alzheimer’s disease is often unrecognized.1 Advances in technology such as brain imaging and testing may make it easier to diagnose the disease.
Causes of alzheimer's disease
Although people are more likely to develop Alzheimer’s disease as they grow older, it is not a natural result of the aging process. There is currently an enormous amount of research being carried out into possible causes, identification and treatment of Alzheimer’s disease. It seems likely that several factors are involved in the development of the disease.
Genetic factors
Family history and twin studies suggest that there is likely to be a genetic component to Alzheimer’s disease. It seems that several gene mutations are linked to the disease. Recent research in this area has centered around a blood protein known as APO-E which acts as a natural antioxidant and protects nerve cells against free radical damage. It occurs in several different forms and, as with all proteins, these forms are determined by genes. People with one particular form of the gene, known as APO-E4 seem to be at higher risk of Alzheimer’s disease. Patients with the gene are also likely to get the disease at an earlier than average age. Scientists are also discovering other genetic factors which appear to increase the risk of Alzheimer’s disease. These discoveries may lead to a test which could identify those at risk of the disease in its early stages, thus enabling treatment to be started before damage to brain cells progresses too far.
Oxidative damage and inflammation
Research suggests that abnormalities in oxidative metabolism may play an important role in Alzheimer’s disease. Free radicals may be involved in the formation of the plaques of beta amyloid protein seen in the brains of Alzheimer’s patients. People with Down Syndrome are more susceptible to Alzheimer’s disease and there is evidence that the neuronal degeneration seen in Down Syndrome may be due to oxidative damage.
Inflammation may also be an important part of the Alzheimer’s disease process. Anti-inflammatory drugs such as ibuprofen appear to reduce the risk of developing the disease.2
Environmental toxins
Some experts believe that environmental toxins contribute to Alzheimer’s disease. Research indicates that Alzheimer’s disease is more prevalent in certain cultural environments. Results from the Honolulu-Asia Aging Study showed that Japanese men who live and grow old in Hawaii are twice as likely to develop Alzheimer’s disease as Japanese men who live and grow old in Japan.3 The reasons for this are unknown, although environmental and dietary factors may play a part.
Some experts believe that aluminum may play a role in the development of Alzheimer’s disease. The plaques and tangles in the brains of people with Alzheimer’s disease often contain aluminum compounds. Foods made with baking powder as well as some antiperspirants and antacids contain aluminum compounds, which can also be absorbed from pots and pans used to cook acidic foods. But aluminum is one of the most common substances on earth, and very little of it is absorbed by healthy bodies. Neither people with peptic ulcers who use large amounts of antacids nor metal workers constantly exposed to aluminum have an especially high rate of Alzheimer’s disease. It seems likely that the accumulation of aluminum in plaques and tangles is probably a result rather than a cause of the brain damage that produces dementia.
Researchers have found that children of young fathers are more susceptible to the disease. Studies suggest that the rate of Alzheimer’s disease declines steadily with increase in the father’s age: the child of a 15-year-old is at four times higher risk than the child of a 65-year-old.
Treatment of alzheimer's disease
There is currently no known cure for Alzheimer’s disease and it has not been possible to stop or reverse the brain damage that occurs. Most available drugs only have a temporary effect on the progression of the disease. Those that have been used include hydergine, piracetam, acetyl-L-carnitine, selegiline, tacrine and donezepil. Other drugs now being investigated include anti-inflammatory drugs, hormone replacement therapy and nerve growth factors. Other types of drugs have been used to treat the common symptoms of the disease such as anxiety, depression and disturbed sleeping patterns.
As it is likely that Alzheimer’s disease involves several steps, it is possible that therapy may one day involve the combined use of several types of drugs with small effects on individual steps.
There are several studies which suggest that estrogen therapy can reduce the risk of Alzheimer’s disease in postmenopausal women, possibly due to its action as an antioxidant or its effect on nerve growth factors.
Alzheimer's Disease and diet
Poor nutrition is related to Alzheimer’s disease, although whether this is a cause or a result of the disease is not clear. A diet which is lacking in essential vitamins and minerals may increase the risk of Alzheimer’s disease. Loss of interest in food and inability to prepare and eat nutritious food in the later stages of the disease may also contribute to deterioration of a patient’s condition.
The results of a recent study suggest that a high fat diet may be linked to the development of Alzheimer’s disease.4 Researchers found that in countries where people eat diets high in fat, there is a higher prevalence of Alzheimer’s disease. However, it is likely that other factors also play a part.
In another study, researchers at Case Western Reserve University are investigating lifestyle histories of 104 Alzheimer’s disease patients and 223 people who do not have the disease. Preliminary results after five years are showing that those people without the disease are consuming significantly greater amounts of antioxidant nutrients: alpha carotene, beta carotene, lutein, lycopene and vitamin C; and significantly more servings of fruits and vegetables.5
Other types of dementia
The second most common cause of dementia is multi-infarct dementia. This is also irreversible and results from a series of small strokes that damage arteries supplying blood to the brain. Diet may play a role in preventing and controlling this form of dementia through effects on blood pressure and other risk factors.
The third most common cause of dementia appears to be excessive alcohol intake, due to the direct effects of alcohol on nerves and also to the effects of alcohol on nutritional status. Alcoholic dementia may be at least partially reversible with abstinence and good nutrition. Other causes are vitamin B12 and folic acid deficiencies; these are reversible dementias. In all types of dementia, adequate nutrition may improve physical wellbeing and improve the quality of life.
Vitamins, minerals and alzheimer's disease
Antioxidants
As there is evidence that oxidative damage plays a role in the tissue injury seen in Alzheimer’s disease,6 antioxidants may have a role to play in preventing the brain from free radical damage. Studies have shown that certain parts of the brains of Alzheimer’s disease sufferers may be more susceptible to free radical damage than those without the disease. Antioxidant supplements may reduce this susceptibility.7
Patients with Alzheimer’s disease have been shown to have lower levels of vitamins A, C, E and zinc.In one study, serum concentrations of vitamins A and E and major carotenes were determined in patients with Alzheimer’s disease, multi-infarct dementia and control subjects. The results showed that both Alzheimer’s and multi-infarct dementia patients had significantly lower levels of vitamin E and beta carotene than controls.8
Vitamin E
As an antioxidant, vitamin E may have a role to play in preventing the oxidative damage seen in Alzheimer’s disease. In a 1997 study done in the US, researchers looked at the effects of vitamin E and the drug, selegiline, on the clinical deterioration seen in Alzheimer’s disease. The study involved 341 patients who were divided into four groups. One group received selegiline, another received 1000 IU (670 mg) of vitamin E, another group received both, and the last group received a placebo. The patients were followed to see when they reached one of the following endpoints: death, institutionalization, inability to do certain basic activities of daily living, or severe dementia. The results showed that treatment with either selegiline or vitamin E slowed progression of the disease.9
Vitamin B12
Vitamin B12 deficiency can produce symptoms which include confusion, memory changes, delirium and depression. Alzheimer’s disease sufferers may be prone to vitamin B12 deficiency10 and some studies have shown a relationship between vitamin B12 levels and the severity of mental impairment in Alzheimer’s disease.11
In another study, intravenous vitamin B12 was shown to improve intellectual functions such as memory, emotional functions and communication in patients with Alzheimer’s disease. Improvements in cognitive functions were relatively constant when the vitamin B12 levels in the cerebro-spinal fluid were high. Improvements in communication functions were seen when a certain level of vitamin B12 was maintained for a longer period.12
Thiamin
Some studies have found lower levels of thiamin in the brains of Alzheimer’s disease patients, which has an impact on mental function.13 Clinical data suggest that high dose thiamin may have a mild beneficial effect in some patients with Alzheimer’s disease but it does not appear to halt the progress of the disease.14 Thiamin appears to increase the effect of the neurotransmitter, acetylcholine, in the brain.
Zinc
The metabolism of zinc may be altered in Alzheimer’s disease.15 Results from the Nun Study, a study of aging and Alzheimer’s disease, showed that low zinc levels in the blood were associated with more senile plaques in the brains of those who died from the disease.16 In another study zinc supplements (27 mg per day) led to improvements in memory, understanding and communication in eight out of ten patients who took them.17
Choline
Levels of acetylcholine are lower in Alzheimer’s disease sufferers due to the reduced activity of the enzyme which synthesizes it. Choline, which is part of the vitamin B complex, is involved in the synthesis of acetylcholine and some studies have detected improvements in mental performance after treatment with it.18,19 However, results of studies have been mixed. Choline and lecithin (which contains choline) may only be useful in the initial stages of the disease.
Acetyl-L-carnitine
Acetyl-L-carnitine is a compound which is involved in energy metabolism in the cell. It also acts as an antioxidant and may enhance or mimic the function of acetylcholine. There are several studies which suggest that it may delay the progression of Alzheimer’s disease.20 In a small double-blind trial published in 1995, seven patients with probable Alzheimer’s disease received 3 g/day of acetyl-L-carnitine for one year, while five similar patients were given a placebo. Patients treated with acetyl-L-carnitine showed significantly less deterioration on mental status tests than did patients receiving the placebo.21
Herbal medicine and alzheimer's disease
Several studies have suggested that the herb, Ginkgo biloba is beneficial in the treatment of Alzheimer’s disease. In a study reported in the Journal of the American Medical Association in 1997, US researchers conducted a 52-week, randomized double-blind, placebo-controlled trial involving mildly to severely demented outpatients with Alzheimer disease or multi-infarct dementia. They used tests to assess the cognitive functioning of the patients and also included assessments by the caregivers of the patients as part of the outcome measurement. The results showed that the ginkgo extract stabilized and, in a substantial number of cases, improved the cognitive performance and the social functioning of demented patients for six months to one year.22