Vitamins that may be helpful

Several clinical trials have found that acetyl-L-carnitine supplementation delays the progression of Alzheimer’s disease,¹² improves memory,^{13 14 15} and enhances overall performance in some people with Alzheimer’s disease.^{16 17} However, in one double-blind trial, people who received acetyl-L-carnitine (1 gram three times per day) deteriorated at the same rate as those given a placebo.¹⁸ Overall, however, most short-term studies have shown clinical benefits, and most long-term studies (one year) have shown a reduction in the rate of deterioration.¹⁹ A typical supplemental amount is 1 gram taken three times per day.

In a preliminary study, people who used antioxidant supplements (vitamin C or vitamin E) had a lower risk of Alzheimer’s disease compared with people who did not take antioxidants.²⁰ Other preliminary research shows that higher blood levels of vitamin E correlate with better brain functioning in middle-aged and older adults.²¹ The possible protective effect of antioxidants may be explained by the observation that oxidative damage appears to play a role in the development of dementia.²² Large amounts of supplemental vitamin E may slow the progression of Alzheimer’s disease. A double-blind trial found that 2,000 IU of vitamin E per day for two years extended the length of time people with moderate Alzheimer’s disease were able to continue caring for themselves (e.g., bathing, dressing, and other necessary daily functions), compared with people taking a placebo.²³

Vitamin B1 is involved in nerve transmission in parts of the brain (called cholinergic neurons) that deteriorate in Alzheimer’s disease.^{24 25} The activity of vitamin B1-dependent enzymes has been found to be lower in the brains of people with Alzheimer’s disease.²⁶ It has therefore been suggested that vitamin B1 supplementation could slow the progression of Alzheimer’s disease. Two double-blind trials have reported small but significant improvements of mental function in people with Alzheimer’s disease who took 3 grams a day of vitamin B1, compared to those who took placebo.^{27 28} However, another double-blind trial using the same amount for a year found no effect on mental function.²⁹

Phosphatidylserine (PS), which is related to lecithin, is a naturally occurring compound present in the brain. Although it is not a cure, 100 mg of PS taken three times per day has been shown to improve mental function, such as the ability to remember names and to recall the location of frequently misplaced objects, in people with Alzheimer’s disease.³⁰ However, subsequent studies have not validated these results. In one double-blind trial, only the most seriously impaired participants received benefits from taking PS; people with moderate Alzheimer’s disease did not experience significant improvements in cognitive function.³¹ In another double-blind trial, people with Alzheimer’s disease who took 300 mg of PS per day for eight weeks had better improvement in overall well-being than those who took placebo, but there were no significant differences in mental function tests.³² In another double-blind trial, 200 mg of PS taken twice daily produced short-term improvements in mental function (after six to eight weeks), but these effects faded toward the end of the six-month study period.³³

The PS used in these studies was obtained from bovine brain phospholipids. A plant source of PS is also available. However, the chemical structure of the plant form of PS differs from the bovine form. In a preliminary study, plant-derived PS was no more effective than a placebo at improving the memory of elderly people.³⁴ Soy-derived PS was also ineffective in a double-blind study of elderly people with age-related cognitive decline.³⁵

A double-blind trial of 20 to 25 grams per day of lecithin failed to produce improvements in mental function in people with Alzheimer’s disease.³⁶ However, there were improvements in a subgroup of people who did not fully comply with the program, suggesting that lower amounts of lecithin may possibly be helpful. Lecithin supplementation has also been studied in combination with a cholinesterase inhibitor drug called tacrine, with predominantly negative results.^{37 38 39 40}

In a double-blind trial, supplementing with the fatty acids present in fish oil (0.6 grams per day of EPA and 1.7 grams per day of DHA) for six months was not beneficial in people with Alzheimer's disease. However, in the subgroup of people with very mild cognitive impairment, supplementation with these fatty acids slowed the rate of cognitive decline compared with a placebo.⁴¹

DMAE (2-dimethylaminoethanol) may increase levels of the brain neurotransmitter acetylcholine. In one preliminary trial, people with senile dementia were given DMAE supplements of 600 mg three times per day for four weeks. The participants did not show any changes in memory, though some did show positive behavior changes.⁴² However, a subsequent double-blind trial found no significant benefit from DMAE supplementation in people with Alzheimer’s disease.⁴³

In a preliminary report, two people with a hereditary form of Alzheimer’s disease received daily: coenzyme Q10 (60 mg), iron (150 mg of sodium ferrous citrate), and vitamin B6 (180 mg). Mental status improved in both patients, and one became almost normal after six months.⁴⁴

Studies in the test tube have shown that zinc can cause biochemical changes associated with Alzheimer’s disease.⁴⁵ For that reason, some scientists have been concerned that zinc supplements might promote the development of this disease. However, in a study of four people with Alzheimer’s disease, supplementation with zinc (30 mg per day) actually resulted in improved mental function.⁴⁶ In a recent review article, one of the leading zinc researchers concluded that zinc does not cause or worsen Alzheimer’s disease.⁴⁷

A small, preliminary trial showed that oral NADH (10 mg per day) improved mental function in people with Alzheimer’s disease.⁴⁸ Further studies are necessary to confirm these early results.

Some researchers have found an association between Alzheimer’s disease and deficiencies of vitamin B12 and folic acid;^{49 50} however, other researchers consider such deficiencies to be of only minor importance.⁵¹ In a study of elderly Canadians, those with low blood levels of folate were more likely to have dementia of all types, including Alzheimer’s disease, than those with higher levels of folate.⁵² Little is known about whether supplementation with either vitamin would significantly help people with this disease. Nonetheless, it makes sense for people with Alzheimer’s disease to be medically tested for vitamin B12 and folate deficiencies and to be treated if they are deficient.

Most,^{53 54 55 56} but not all,^{57 58} studies have found that people with Alzheimer’s disease have lower blood DHEA levels than do people without the condition. Emerging evidence suggests a possible benefit of DHEA supplementation in people with Alzheimer’s disease. In one double-blind trial, participants who took 50 mg twice daily for six months had significantly better mental performance at the three-month mark than those taking placebo. At six months, statistically significant differences between the two groups were not seen, but results still favored DHEA.⁵⁹ In another clinical trial, massive amounts of DHEA (1,600 mg per day for four weeks) failed to improve mental function or mood in elderly people with or without Alzheimer’s disease.⁶⁰ It is likely that the amount of DHEA used in this trial was far in excess of an appropriate amount, illustrating that more is not always better.

Are there any side effects or interactions?
Refer to the individual supplement for information about any side effects or interactions.

Herbs that may be helpful

An extract made from the leaves of the Ginkgo biloba tree is an approved treatment for early-stage Alzheimer’s disease in Europe. While not a cure, Ginkgo biloba extract (GBE) may improve memory and quality of life and slow progression in the early stages of the disease. In addition, four double-blind trials have shown that GBE is helpful for people in early stages of Alzheimer’s disease, as well as for those experiencing another form of dementia known as multi-infarct dementia.^{61 62 63 64} GBE has been found to be nearly as effective against Alzheimer's disease as donepezil, a prescription drug used to treat the condition.⁶⁵ One trial reported no effect of GBE supplementation in the treatment of Alzheimer’s disease, vascular dementia or age-associated memory impairment.⁶⁶ However, the results of this trial have been criticized, since analysis of the results does not separate those patients with Alzheimer’s disease or vascular dementia from those with age-associated memory impairment. A comparison of placebo-controlled trials of ginkgo for Alzheimer’s disease concluded that the herb compared favorably with two prescription drugs, donepezil and tacrine, commonly used to treat the condition.⁶⁷ Research studies have used 120 to 240 mg of GBE, standardized to contain 6% terpene lactones and 24% flavone glycosides per day, generally divided into two or three portions. GBE may need to be taken for six to eight weeks before desired actions are noticed.

Huperzine A is a substance found in huperzia (Huperzia serrata), a Chinese medicinal herb. In a placebo-controlled trial, 58% of people with Alzheimer’s disease had significant improvement in memory and mental and behavioral function after taking 200 mcg of huperzine A twice per day for eight weeks—a statistically significant improvement compared to the 36% who responded to placebo.⁶⁸ Another double-blind trial using injected huperzine A confirmed a positive effect in people with dementia, including, but not limited to, Alzheimer’s disease.⁶⁹ Yet another double-blind trial found that huperzine A, given at levels of 100 to 150 mcg two to three times per day for four to six weeks, was more effective at improving minor memory loss associated with age-related cognitive decline than the drug piracetam.⁷⁰ This study found that huperzine A was not effective in relieving symptoms of Alzheimer’s disease. Clearly, more research is needed before the usefulness of huperzine A for Alzheimer’s disease is confirmed.

Lesser periwinkle contains the alkaloid vincamine. Supplementation with a semi-synthetic derivative of vincamine, known as vinpocentine, showed no benefit for people with Alzheimer’s disease in a preliminary study,⁷¹ but vincamine itself was shown to be beneficial in a later double-blind trial.⁷²

In a double-blind trial, supplementation with an extract of lemon balm (Melissa officinalis) for 16 weeks significantly improved cognitive function and significantly reduced agitation, compared with a placebo, in people with Alzheimer's disease.⁷³ The amount of lemon balm used was 60 drops per day of a 1:1 tincture, standardized to contain at least 500 mcg per ml of citral.

In a double-blind study of people with Alzheimer’s disease, supplementing with sage for four months resulted in a significant improvement in cognitive function, compared with a placebo.⁷⁴ The amount of sage used was 60 drops per day of a 1:1 tincture. Although it is not known for sure how sage improves cognitive function, it appears to have an effect on acetylcholine, one of the chemical messengers (neurotransmitters) in the brain.

Animal studies have found the Ayurvedic herb bacopa has constituents that enhance several aspects of mental function and learning ability.^{75 76 77} A controlled study found that a syrup containing an extract of dried bacopa herb given to children improved several measures of mental performance.⁷⁸ A double-blind trial in adults found that a standardized extract of bacopa (300 mg per day for people weighing under 200 lbs and 450 per day for people over 200 lbs) improved only one out of several measures of memory function after three months.⁷⁹ Another double-blind trial lasting twelve weeks found 300 mg per day of bacopa improved four out of fifteen measures of learning, memory, and other mental functions in adults.⁸⁰ A third double-blind study found no effects on mental function in a group of healthy adults given 300 mg of standardized bacopa and tested two hours later. Bacopa has not been tested on people with memory problems.⁸¹

Are there any side effects or interactions?
Refer to the individual herb for information about any side effects or interactions.

Blood Flow To Brain May Be Clue To Certain Dementias

ScienceDaily (Aug. 30, 2005) — OAK BROOK, Ill.--The amount of blood flowing into the brain may play a larger role in the development of dementia than previously believed, according to a study in the September issue of the journal Radiology.

Researchers from Leiden University Medical Center in the Netherlands used magnetic resonance imaging (MRI) to examine the brains of elderly patients with and without dementia related to Alzheimer's or Parkinson's disease. As expected, MR images showed that the patients with late-onset dementia had more brain damage compared with young adults and with seniors who had optimal cognitive function. But researchers found that the late-onset dementia group also had a much lower rate of blood flow to the brain than the other two groups.

"Our findings not only support the hypothesis that vascular factors contribute to dementia in the elderly, they are highly suggestive that a diminished cerebral blood flow indeed causes brain damage," said Aart Spilt, M.D., a Leiden radiology resident and lead author of the study. "This gives us a clue to the genesis of dementia."

Dementia is a loss of cognitive functions, such as thinking, remembering and reasoning, that interferes with normal activities. Although many conditions can produce these symptoms, Alzheimer's disease is the most common cause of dementia. Some patients with Parkinson's disease also develop dementia.

In the Dutch study, researchers examined 17 patients with late-onset dementia (dementia occurring after age 75), another 16 seniors of the same age with optimal cognitive function and 15 healthy younger individuals. Researchers used MRI to measure cerebral blood flow and the extent of structural brain damage in each person and then compared the results of the three groups.

Average total cerebral blood flow in the healthy young individuals was 742 milliliters (mL) per minute. Cerebral blood flow in the two elderly groups averaged 496 mL per minute, or 246 mL per minute lower than the younger group. In patients with dementia, average cerebral blood flow was 443 mL per minute, or 108 mL per minute lower than seniors of the same age with optimal cognitive function (551 mL per minute).

Although patients with dementia have been shown to require less cerebral blood flow as the brain becomes less active, Dr. Spilt's research provides some evidence that the decreased blood flow may lead to some types of dementia.

"The findings emphasize the importance of monitoring both high and low blood pressure in older adults," Dr. Spilt said. "Possible causes of low cerebral blood flow include heart failure and a narrowing of cerebral or cervical arteries."

Alzheimer's Disease and Element Imbalances

Scientists are increasingly uncovering the widespread effects of toxic exposure on learning, memory and behavior in humans. Accumulation of heavy metals like lead in the body can dramatically impair cognitive function,1 and the amount of toxins necessary to produce symptoms is turning out to be far less than previously believed.

Aluminum has been shown to specifically damage learning, memory, and cognitive ability and has been suggested as a possible contributing factor in dementia and alcoholic amnesia.2-3 Research on Alzheimer's patients show they are much more likely to exhibit elevated levels of mercury, cadmium, and aluminum.4

Elemental Analysis (Hair, Blood, or Urine) determines levels of toxic and nutritional elements in the body using a hair, blood, or urine sample. Each specimen type provides a unique window on element status. A hair sample, for example, will reflect chronic toxic exposure and long-term nutritional deficiencies, while blood and urine assessment will gauge the effects of more recent imbalances.

References:
1 Zheng YX, Liang YX. Meta-analysis in neurobehavioral toxicological studies. Chung Hua Yu Fang I Hsueh Tsa Chih 1994;28(5):282-283.
2 Davis WM. Is aluminum an etiologic contributor to alcoholic amnesia and dementia? Med Hypotheses 1993:41(4):341-343.
3 Kilburn KH, Warshaw RH. Neurobehavorial testing of subjects exposed residentially to groundwater contaminated from an aluminum die-casting plant and local referents. J Toxicol Environ Health 1993;39(4):483-496.
4 Basun H, Forssell LG, Wetterberg L, Winbland B. Metals and trace elements in plasma and cerebrospinal fluid in normal aging and Alzheimer's disease. J Neural Transm Park Dis Dement Sect 1991;3(4):231-258.

Heavy Metal Anchor Alzheimer's In Your Brain by: Rudy Silva

Heavy metals and aluminum are in every part of our environment and food. These elements are deadly and you will benefit if you are aware of what they do where they come from.

How Heavy Metals Affect the Brain:

Brain tissue has an attraction for heavy metals such as lead, mercury, cadmium, and others. When heavy metals appear in the brain they can interfere with your natural brain chemistry. This interference, overtime, can accelerate the onset of dementia or Alzheimer's.

Aluminum is an element that has been associated with Alzheimer's. Aluminum has been found in high levels in people's brain that have died of Alzheimer's. The evidence points to aluminum been involved with Alzheimer's.

There is a lot of controversy about whether aluminum can bring on Alzheimer's. But because the Aluminum Industry is so powerful, it has blocked and campaigned against any reports that point to aluminum's involvement in dementia or Alzheimer's.

Here is a list of products that contain aluminum:

• Antacids, aluminum wrap, pans, pot, rice cookers, small oven trays, soft drink cans, various food cans, toothpaste tubes, water, roll on deodorants

Here is what heavy metals do:

• Lead - makes you aggressive and hyperactive
• Cadmium - makes you confused and aggressive
• Mercury - gives you headaches, causes memory loss
• Aluminum - is associated with dementia and Alzheimer's Disease

Heavy metals come from air pollution, smoking, pestricides, fillings.

Be aware of how heavy metals and aluminum get into your body, since they will end up in your brain and accumulate along your artery walls with cholesterol. Having loss of memory and other mental abilities is not result of aging. It is a result of poor diet and excess consumption of pollution and toxins.

Minimizing Heavy Metal Damage:

Here is how to minimize heavy metal damage. Take a good electrolytic mineral supplement or eat a lot of fruits and vegetables since they contain a lot of minerals.

The good minerals compete to get absorb in your intestines with the heavy metals. Good minerals will get absorbed leaving behind the heavy metals. These heavy metals will then be excreted out of your body.

Also drinking a lemon and chlorophyll drink is helpful. Chlorophyll attaches to heavy metals and help to remove them from your body. Drink this every morning. Here's how to make this drink. Combine juice of one lemon, 8 oz of distilled water, and 1-2 oz of chlorophyll. (Avianweb - please refer to: Heavy Metal Testing Kits & Chelating Recipe)

Dementia: What Are the Common Signs?

What is Dementia?
Dementia is a problem in the brain that makes it hard for a person to remember, learn and communicate. After a while, this makes it hard for the person to take care of himself or herself.

Dementia may also change a person's mood and personality. At first, memory loss and trouble thinking clearly may bother the person who has dementia. Later, disruptive behavior and other problems may start. The person who has dementia may not be aware of these problems.

What causes dementia?
Dementia is caused by the destruction of brain cells. A head injury, a stroke, a brain tumor or a problem like Alzheimer's disease can damage brain cells. Some people have a family history of dementia.

What are some common signs of dementia?
Dementia causes many problems for the person who has it and for the person's family. Many of the problems are caused by memory loss. Some common signs of dementia are listed below. Not everyone who has dementia will have all of these signs.

• Recent memory loss. All of us forget things for a while and then remember them later. People with dementia often forget things, but they never remember them. They might ask you the same question over and over, each time forgetting that you've already given them the answer. They won't even remember that they already asked the question.
• Difficulty performing familiar tasks. People who have dementia might cook a meal but forget to serve it. They might even forget that they cooked it.
• Problems with language. People who have dementia may forget simple words or use the wrong words. This makes it hard to understand what they want.
• Time and place disorientation. People who have dementia may get lost on their own street. They may forget how they got to a certain place and how to get back home.
• Poor judgment. Even a person who doesn't have dementia might get distracted. But people who have dementia can forget simple things, like forgetting to put on a coat before going out in cold weather.
• Problems with abstract thinking. Anybody might have trouble balancing a checkbook, but people who have dementia may forget what the numbers are and what has to be done with them.
• Misplacing things. People who have dementia may put things in the wrong places. They might put an iron in the freezer or a wristwatch in the sugar bowl. Then they can't find these things later.
• Changes in mood. Everyone is moody at times, but people with dementia may have fast mood swings, going from calm to tears to anger in a few minutes.
• Personality changes. People who have dementia may have drastic changes in personality. They might become irritable, suspicious or fearful.
• Loss of initiative. People who have dementia may become passive. They might not want to go places or see other people.

What if I have any of these signs of dementia?
Talk with your doctor. Your doctor can do tests to find out if your signs are caused by dementia. The sooner you know, the sooner you can talk to your doctor about treatment options.

What if a family member has signs of dementia?
If your family member has some of the signs of dementia, try to get him or her to go see a doctor. You may want to go along and talk with the doctor before your relative sees him or her. Then you can tell the doctor about the way your relative is acting without embarrassing your relative.

Acetylcholine and Memory Defect in Alzheimer's.

One of the characteristic changes that occurs in Alzheimer's disease is the loss of memory and the loss of acetylcholinesterase (AChE) from both cholinergic and noncholinergic neurons of the brain. However, AChE activity is increased around amyloid plaques. ( Sberna, Saez-Valero, Beyreuther, Masters, and Small, 1997 ) This increase in AChE may be of significance for therapeutic strategies using AChE inhibitors.
Amyloid beta-protein (A beta), the major component of amyloid plaques, acts on the expression of AChE. A beta peptides spanning residues 1-40 or 25-35 increased AChE activity in P19 embryonal carcinoma cells. A peptide containing a scrambled A beta ( 25-35 ) sequence did not stimulate AChE expression. Way then an increase in AChE, the increase in AChE expression around amyloid plaques could be due to a disturbance in calcium homeostasis involving the opening of L-type VDCCs. ( Sberna, Saez-Valero, Beyreuther, Masters, Small, 1997 )
The deposit of these beta-amyloid peptides in the brain in form of senile plaque is the key event responsible for Alzheimer pathology. Among various mechanisms that have been proposed to explain the Neuro toxicity of beta-amyloid deposits, beta-amyloid peptides may be indirectly toxic for neurons by activating micro glial cells to produce NO (2). ( Bianchini, 1996 )
The degeneration of the cortex, basal forebrain, and hippocampus, in this way leads to a profound loss of memory.

Acetylcholine receptors are neurotransmitter receptors. Neurotransmitter receptors are proteins that react with extracellular signals, such as acetylcholine, and convert them into intracellular effects (Hucho 1993). They are integral membrane proteins, that is they are within the cell membrane as shown in the figure. ACh receptors are ligand gated ion channels, and they are found on the post synaptic membrane on the target cells.

ACh receptors are one of the chief receptors for excitator neurotransmitters (Alberts et al. 1998). A signal to move a muscle travels from the CNS down a motor neuron to the target muscle cell (www.macalester.edu). The binding of acetylcholine to ACh receptors results in a change in memprane potential of the target cell leading to an action potential in the muscle cell. The acetylcholine is rapidly removed by enzymatic breakdown or reuptake so that when the presynaptic cell stops, the post synaptic cell will stop as well. When the neurotransmitter binds with the receptor, the channel opens and allows Sodium ions into the cell which depolarizes the plasma membrane to create the action potential (Alberts et al. 1998). There are two subtypes of acetlycholine receptors. A predominantly excitatory one in the PNS and another in the autonomic ganglia and CNS. They are typically called muscular and neuronal. There are several subtypes of AChR but the one specified here is the nicotinic AChR. It has two binding sites, and has elaborate pharmacology and toxicology. Because of this, it has been identified, characterized and isolated.

Memory and Acetylcholine

Acetylcholine ( ACh ) was discovered in the 1920s, making Acetylcholine ( ACh ) the first known neurotransmitter. This neurotransmitter can be found in the brain, neuromuscular junctions, spinal cord, and in both the postganglionic terminal buttons of the parasympathetic division of the autonomic nervous system and the ganglia of the autonomic nervous system.
Acetylcholine ( ACh ) is synthesized from acetyl-CoA and Choline. Chemical reactions in brain for the production of Acetylcholine ( ACh ):

ACh receptor sites can be ionotropic ( nicotinic receptor ) or metabotropic ( muscarinic receptor), this make it possible for acetylcholine to produce either an IPSP or an EPSP response.
Only recently it was discovered that the nucleus basalis, particularly in the nucleus basalis of Meynert, is a source of acetylcholine ( ACh ). It was subsequently shown that projections from the nucleus basalis provide the primary source of neocortical acetylcholine ( Mesulam and Van Hoesen, 1976; Lehmann, Nagy, Atmadja, & Fibiger, 1980). There are also cholinergic projections from the adjacent medial septum and diagonal band of Broca to hippocampus ( Squire, 1987 ). All these cholinergic projections together making up a wide source of acetylcholine ( ACh ) in the brain.
Acetylcholine ( ACh ) role in learning and memory is on clear but Deutsch in 1970 believed that because most the acetylcholine ( ACh ) in the neocortex originates in the basal forebrain, that cholinergic synapses themselves were the sites for memory storage. However Squire believes these cholinergic pathways are better suited for some type of modulator role but in what way is yet unclear. The ascending, widely projecting cholinergic pathways seem better suited as a modulator system than as an information-containing, information-storing system (Squire, 1987).

The Environmental Influences on Cognitive Disease

The influences researched include common dietary patterns and toxic chemical exposures, along with insufficient exercise and stress. Some of the key environmental factors found to generate risk in the study were lead, air pollution, and pesticides. Exposure to each was found to greatly increase the risk of developing a cognitive disease. And it’s now believed that these influences can begin having an impact as early as the womb and be carried through life, eventually developing into a neurodegenerative disease.

Report co-author Jill Stein, MD, Greater Boston Physicians for Social Responsibility, says:

"As we explored origins and patterns of chronic degenerative diseases, we discovered a web of conditions in the environment – including nutritional, chemical, physical and social factors – that have a direct influence on the risk of Alzheimer's, Parkinson's and related chronic diseases. It is clear from these findings that our activities in the areas of food and agriculture, energy, chemical use, and social organization are key drivers in the abnormal loss of neurological function in older people throughout the modern world."

The report also finds that nutrition and diet have a sizable impact on the contraction of cognitive diseases—for instance, saturated fat intake have been found to greatly increase the risk of dementia. Infant soy formula, and formulas heavily fortified with iron were also found to be possible contributors.

Unhealthy Environments Can Cause Cellular Alteration
One of the most interesting findings was that these environmental factors are causing an alteration in biochemical pathways at cellular and subcellular levels—and that these physical alterations can lead to Alzheimer’s and Parkinson’s, as well as diabetes, obesity, and cardiovascular disease. According to the report, “This collection of diseases is being driven by dramatic alterations over the past 50 to 100 years in the U.S. food supply, an increasingly sedentary lifestyle, and exposure to toxic chemicals.”

Alzheimer's Disease - What Happens In the Brain

Researchers have discovered changes that take place in the brains of people who have Alzheimer's disease. These include:

• Lower levels of acetylcholine in certain areas of the brain. Acetylcholine is a chemical messenger in the brain (neurotransmitter) needed for some nerve cells to work properly. Other neurotransmitters also are affected.
• Senile plaques, which are clumps of abnormal nerve cells surrounding abnormal protein (amyloid) deposits, and neurofibrillary tangles, which are clumps of material that disrupt the normal structure of nerve cells. Senile plaques and neurofibrillary tangles can be seen during an examination of the brain after the person has died.

These brain changes may cause the memory loss and decline in other mental abilities that occur with Alzheimer's disease. It is not fully understood why these brain changes occur in some people but not in others.

Alzheimer's disease always gets worse over time, but the course of the disease varies from person to person. Some people may still be able to function relatively well until late in the course of the disease. Others may lose the ability to do everyday activities very early on.

• The disease tends to get worse gradually. It usually starts with mild memory loss and progresses to severe mental and functional problems and eventual death.
• Symptoms sometimes are described as occurring in early, middle, and late phases. It is difficult to predict how long each phase will last.
• The average amount of time a person lives after developing symptoms of Alzheimer's disease is 8 to 10 years.

Mild dementia

Usually, a person with mild dementia:

• Becomes confused about where he or she is and gets lost easily.
• Loses the ability to start tasks on his or her own without prompting.
• Avoids new and unfamiliar situations.
• Has delayed reactions and slowed learning ability.
• Begins speaking more slowly than in the past.
• Develops difficulty handling money and paying bills.
• Starts using poor judgment and making inappropriate decisions.
• May have mood swings and become depressed, irritable, or restless.

These symptoms often are more obvious when the person is in a new and unfamiliar place or situation.

Moderate dementia

With moderate dementia, a person typically:

• Has problems recognizing close friends and family.
• Becomes restless and wanders, especially in late afternoon and at night. This is called sundowning.
• Has problems reading, writing, and dealing with numbers.
• Has problems organizing thoughts and thinking logically.
• Can't find the right words to say or makes up stories to fill in the blanks.
• Has trouble dressing.
• Gets upset easily and can be hostile or unwilling to cooperate.
• Has firmly held false beliefs (delusions), suspicion of others (paranoia), and agitation.
• Needs full-time supervision.
• Loses recognition of time.

Severe dementia

With severe dementia, a person usually:

• Can no longer remember how to bathe, eat, dress, or go to the bathroom independently. The person may become bedridden or confined to a wheelchair because he or she has forgotten how to move.
• Loses the ability to chew and swallow.
• Has trouble with balance or walking and may fall frequently.
• Becomes more confused in the evening (sundowning) and has trouble sleeping.
• Cannot communicate using words.
• Loses bowel or bladder control (incontinence).

A person with severe dementia becomes more vulnerable to other illnesses. Death often results from complications of being confined to bed, such as pneumonia.

The Break Down of Alzheimer's Disease

Alzheimer's disease is the most common and severe form of senile dementia. It is a progressive, degenerative disease that attacks the brain, resulting in impaired memory, decreased intellectual and emotional functioning, and ultimately complete physical breakdown. In the United States, it affects approximately 10% of those over the age of 65 and almost 50% of those over the age of 85.

The progression of Alzheimer's is characterized by a number of changes that take place in the brain's biochemistry, structure, and function. Nerves in the Alzheimer's patient's brain die, severing important links between the two sections of the brain (the forebrain and hippocampus) responsible for thinking and memory.

Patients affected by Alzheimer's disease may experience depression, fatigue, occasional forgetfulness to disorientation, and aggressive or paranoid behavior. Typically, Alzheimer's disease is characterized by the following symptoms: progressive memory loss (both short-term and long-term), a decline in the ability to understand vocabulary and words, repetitive questions, problems understanding numbers, spatial and time disorientation, forgetfulness, and an impaired ability to speak fluently.

Factors likely to cause Alzheimer's include heavy metal poisoning, environmental influences, genetics, hormone imbalances, impaired blood flow, and nutritional deficiencies.

There are natural cures for Alzheimer's, as well as non-pharmaceutical ways of preventing the symptom of Alzheimer's from setting in. The Natural Cures website will show you how you can treat Alzheimer's naturally, and well as to show you how you can make lifestyle changes that will improve your general health.