https://www.sandiegohealthdirectory.com/kb en-us Protein that Impairs Memory in Model for Alzheimer's Disease. https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=118 Tue, 27 Jun 2006 03:43:31 GMT https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=118
For the first time, researchers have identified a specific form of amyloid beta protein that causes memory impairment long before amyloid plaques and neurodegeneration appear in a mouse model of Alzheimer's disease (AD). The finding may lead to new ways of diagnosing and possibly even preventing the disease.

The study was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS) and reported in the March 16, 2006, issue of Nature.

Amyloid beta is the main component of amyloid plaques – abnormal clumps of protein that are found in the tissue between nerve cells in people with AD. Researchers have long suspected that amyloid plaques help to trigger the neurodegeneration and cognitive problems found in AD. Most of the known genes and other risk factors for AD increase the accumulation of amyloid beta in the brain and lead to plaque formation. However, recent studies have shown that memory problems develop long before amyloid plaques appear, and that there is no reliable correlation between the number of amyloid plaques and the amount of memory impairment in humans or mice. Other research has suggested that amyloid plaques may actually be beneficial – helping to keep toxic amyloid beta out of the way so that neurons can function. With this idea, researchers have begun to look at smaller clusters of amyloid beta peptides (protein building blocks) to see if they trigger the disease.

In the new study, Karen Hsiao Ashe, M.D., Ph.D., of the University of Minnesota, and colleagues tested mice with one of the gene defects that cause AD to see if any particular form of amyloid beta would correlate with the earliest signs of memory impairment. They found that a form of the protein called A-beta*56 (amyloid beta star 56), which are a cluster of 12 amyloid beta peptides, appeared in the brain at the same time that the mice started to show memory problems.

Furthermore, the number of A-beta*56 clumps in the brain correlated with the degree of memory impairment in the mice.

The researchers then isolated A-beta*56 from the mice and injected it through tubes into the brains of healthy young rats. The rats were then tested to see how well they could remember the location of a platform in a pool of water. This is called the Morris water maze test. The researchers found that the A-beta*56 temporarily interfered with the formation of long-term memories in these rats. Before the injections, the rats could remember spatial information they'd learned. However, when the rats were given injections of A-beta*56 shortly before entering a new maze, their behavior was different.

The animals initially seemed to learn with no problem, but a day later, they could not remember what they'd learned.

"A-beta*56 impaired long-term memory, but not acquisition of spatial information," says Dr. Ashe. The memory impairment was temporary and disappeared by 10 days after the injections.

The researchers found that the level of A-beta*56 in the brain was stable for many months after it first appeared, even though the transgenic mice developed more severe memory impairment as they got older. A possible explanation is that young mice can partially compensate for the toxic effects of A-beta*56 but that they lose this ability as they grow older.

While the study shows that A-beta*56 can interfere with memory, it is still not clear how it does so or whether it triggers the neurodegeneration seen later in the course of AD. The neurodegeneration may result from a different, still-unidentified problem. However, previous studies have shown that amyloid beta reduces the level of a protein called dynamin-1 that is needed for synapses to function correctly. Other research has shown that amyloid beta interferes with release of the nerve-signaling chemical called acetylcholine. Therefore A-beta*56 may prevent neurons from communicating with each other effectively. Researchers suspect that altered synaptic function could trigger neurodegeneration, although this study did not address that possibility.

The finding suggests that screening healthy people for the presence of A-beta*56 might reveal their risk of developing AD in the future and improve early diagnosis of the disease, much as cholesterol screening can reveal who is at risk of heart disease. Investigators might then be able to treat people at high risk of AD using therapies that would delay the disease or prevent it from developing. However, researchers do not yet know if A-beta*56 is present in blood or cerebrospinal fluid - where it could be easily detected - or if it occurs only in the brain.

The new study supports another recent finding by researchers at the University of Pennsylvania, which showed that an antibody, which targets small clusters of amyloid beta, could improve spatial learning and memory in a mouse model for AD. Together, the studies suggest that small clusters of amyloid beta peptides, like A-beta*56, are the cause of memory loss in the early phases of AD.

Dr. Ashe and her colleagues are now studying brains from people who died with cognitive impairment and other conditions to see if those brains contain A-beta*56, and they are looking for other proteins that may cause brain dysfunction. They also are trying to develop a blood test for A-beta*56 that could be used to screen people for risk of AD. Finally, they are looking for antibodies or drugs that might be able to block the effects of the protein or remove it from the brain. They hope to be able to conduct clinical trials of such treatments in the future.

The NINDS is a component of the National Institutes of Health (NIH) in Bethesda, Maryland, and is the nation’s primary supporter of biomedical research on the brain and nervous system. The NIH is comprised of 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and investigates the causes, treatments, and cures for both common and rare diseases. ]]> Many older people worry about becoming more forgetful. They think forgetfulness is the first sign of Alzheimer’s disease. In the past, memory loss and confusion were considered a normal part of aging. https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=38 Mon, 12 Jun 2006 03:03:00 GMT https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=38
A lot of people experience memory lapses. Some memory problems are serious, and others are not. People who have serious changes in their memory, personality, and behavior may suffer from a form of brain disease called dementia. Dementia seriously affects a person’s ability to carry out daily activities. Alzheimer’s disease is one of many types of dementia.

The term dementia describes a group of symptoms that are caused by changes in brain function. Dementia symptoms may include asking the same questions repeatedly; becoming lost in familiar places; being unable to follow directions; getting disoriented about time, people, and places; and neglecting personal safety, hygiene, and nutrition. People with dementia lose their abilities at different rates. Dementia is caused by many conditions. Some conditions that cause dementia can be reversed, and others cannot.

Further, many different medical conditions may cause symptoms that seems like Alzheimer’s disease, but is not. Some of these medical conditions may be treatable.

Reversible conditions can be caused by a high fever, dehydration, vitamin deficiency and poor nutrition, bad reactions to medicines, problems with the thyroid gland, or a minor head injury. Medical conditions like these can be serious and should be treated by a doctor as soon as possible.

Sometimes older people have emotional problems that can be mistaken for dementia. Feeling sad, lonely, worried, or bored may be more common for older people facing retirement or coping with the death of a spouse, relative, or friend. Adapting to these changes leaves some people feeling confused or forgetful. Emotional problems can be eased by supportive friends and family, or by professional help from a doctor or counselor.

The two most common forms of dementia in older people are Alzheimer’s disease and multi infarct dementia (sometimes called vascular dementia). These types of dementia are irreversible, which means they cannot be cured. In Alzheimer’s disease, nerve cell changes in certain parts of the brain result in the death of a large number of cells.

Symptoms of Alzheimer’s disease begin slowly and become steadily worse. As the disease progresses, symptoms range from mild forgetfulness to serious impairments in thinking, judgment, and the ability to perform daily activities. Eventually, patients may need total care.

In multi infarct dementia, a series of strokes or changes in the brain’s blood supply may result in the death of brain tissue. The location in the brain where the strokes occur and the severity of the strokes determine the seriousness of the problem and the symptoms that arise. Symptoms usually begin abruptly and progress in a step-wise fashion with repeated strokes. At this time, there is no way to reverse damage that has already been caused by a stroke. However, treatment to prevent further strokes is very important.

Diagnosis

People who are worried about memory problems should see their doctor. If the doctor believes that the problem is serious, then a thorough physical, neurological, and psychiatric evaluation may be recommended. A complete medical examination for memory loss may include gathering information about the person’s medical history, including use of prescription and over the counter medicines, diet, past medical problems, and general health. Because a correct diagnosis depends on recalling these details accurately, the doctor also may ask a family member for information about the person.
Tests of blood and urine may be done to help the doctor find any problems. There are also tests of mental abilities (tests of memory, problem solving, counting, and language).

A brain CT scan may assist the doctor in ruling out a curable disorder. A scan also may show signs of normal age related changes in the brain. It may be necessary to have another scan at a later date to see if there have been further changes in the brain.
Alzheimer’s disease and multi infarct dementia can exist together, making it hard for the doctor to diagnose either one specifically. Scientists once thought that multi infarct dementia and other types of vascular dementia caused most cases of irreversible mental impairment. They now believe that most older people with irreversible dementia have Alzheimer’s disease.

Treatment

Even if the doctor diagnoses an irreversible form of dementia, much still can be done to treat the patient and help the family cope. A person with dementia should be under a doctor’s care, and may see a neurologist, psychiatrist, family doctor, internist, or geriatrician. The doctor can treat the patient’s physical and behavioral problems and answer the many questions that the person or family may have.

For some people in the early and middle stages of Alzheimer’s disease, the drugs tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne, formerly known as Reminyl) are prescribed to possibly delay the worsening of some of the disease’s symptoms. Another drug, memantine (Namenda), has been approved for treatment of moderate to severe AD. Doctors believe it is very important for people with multi infarct dementia to try to prevent further strokes by controlling high blood pressure, monitoring and treating high blood cholesterol and diabetes, and not smoking.

Many people with dementia need no medication for behavioral problems. But for some people, doctors may prescribe medications to reduce agitation, anxiety, depression, or sleeping problems. These troublesome behaviors are common in people with dementia. Careful use of doctor prescribed drugs may make some people with dementia more comfortable and make caring for them easier.

A healthy diet is important. Although no special diets or nutritional supplements have been found to prevent or reverse Alzheimer’s disease or multi infarct dementia, a balanced diet helps maintain overall good health. In cases of multi infarct dementia, improving the diet may play a role in preventing more strokes.

Family members and friends can assist people with dementia in continuing their daily routines, physical activities, and social contacts. People with dementia should be kept up-to-date about the details of their lives, such as the time of day, where they live, and what is happening at home or in the world. Memory aids may help in the day to day living of patients in the earlier stages of dementia. Some families find that a big calendar, a list of daily plans, notes about simple safety measures, and written directions describing how to use common household items are very useful aids.

Advice for Today

Scientists are working to develop new drugs that someday may slow, reverse, or prevent the damage caused by Alzheimer’s disease and multi infarct dementia. In the meantime, people who have no dementia symptoms can try to keep their memory sharp.

Some suggestions include developing interests or hobbies and staying involved in activities that stimulate both the mind and body. Giving careful attention to physical fitness and exercise also may go a long way toward keeping a healthy state of mind. Limiting the use of alcoholic beverages is important, because heavy drinking over time can cause permanent brain damage.

Many people find it useful to plan tasks; make “things to do” lists; and use notes, calendars, and other memory aids. They also may remember things better by mentally connecting them to other meaningful things, such as a familiar name, song, or lines from a poem.

Stress, anxiety, or depression can make a person more forgetful. Forgetfulness caused by these emotions usually is temporary and goes away when the feelings fade. However, if these feelings last for a long period of time, getting help from a professional is important. Treatment may include counseling or medication, or a combination of both.

Some physical and mental changes occur with age in healthy people. However, much pain and suffering can be avoided if older people, their families, and their doctors recognize dementia as a disease, not part of normal aging.

For More Information

The Alzheimer’s Disease Education and Referral (ADEAR) Center is a service of the National Institute on Aging, part of the Federal Government’s National Institutes of Health. The Center provides information to health professionals, patients and their families, and the public.

U.S. National Institutes of Health]]> This article specifically cites to huperzine A as a treatment for Alzeheimers. It is a published term paper from Stanford. Author unknown. https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=5 Mon, 23 Jan 2006 14:57:38 GMT https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=5
Alzheimer¡¦s Disease (AD) is the leading cause of senile dementia in the US today. The impact of this disease is not confined to the sub-population of those more likely to develop AD but extends to those who must interact with the elderly, namely caretakers and other family members. The effects of the increasing number of AD patients also affects everyone in our society via the rising costs spent on AD patient care.

This disease is a neurodegenerative disorder that is characterized by progressive loss of cognitive functioning, which often results in complete dementia. Patients usually begin with short term memory deficits, constructional apraxia (impairment of basic visual/motor integrative ability) and loss of spontaneity which later continues into dysphasia (impairment of speaking / writing abilities), agnosia (inability to comprehend familiar objects), and general disorientation and behavioral disturbances. AD patients¡¦ brains show atrophy in the cortical gyri due to cell death and loss of neuronal fibers and synapses. (Feldman, et al. 1997)

Conventional therapies include cholinesterase inhibitors that address one of the AD issues, inadequate acetylcholine (ACh) and degradation of these pathways. There is no cure for Alzheimer¡¦s Disease while a high demand for some control over the disease exists. Additionally AD caregivers are often unsatisfied with the conventional therapies because of moderate efficacy and potential side effects. Thus, we see a trend in research to find new cholinesterases and to determine efficacy of alternative therapies such as antioxidant, herbal remedies and combination therapies.

In order to understand the various methods of therapies it is important to understand some of the basic neurochemical characteristics and mechanisms behind AD. AD involves significant damage to some important cortical nuclei as well as deterioration and decrease in number of synaptic connections in the cortex and hippocampus. Acetylcholine neurotransmitter systems seem to be compromised in AD patients. In the cortex, hippocampus, and amygdala there are significant losses of cholinergic neurons and cholinergic markers (i.e. ChAT, AchE). The densities of specific cholinergic receptor subtypes, muscarinic M2 and nicotinic receptors are reduced while other cholinergic receptors are not. This may be due to the possibility that M2 and nicotinic receptors are located presynaptically where they function in modulating the release of other transmitters postsynaptically. Since there is usually damage to cholinergic afferents and retention of postsynaptic cells, it makes sense that there would be this type of differential loss of these receptor subtypes. There is also speculation that other neurotransmitter systems may be compromised in AD. These include the noradrenergic and serotonergic systems, both of which are probably compromised due to the presence of neurofibrillary tangles in the nuclei mainly responsible for the synthesis of these neurotransmitters.

Physiologically speaking, the classical sign of AD are the neurofibrillary tangles (NFT) and AƒÒ amyloid plaques, which develop in areas of the neocortex, hippocampus, amygdala and nuclei of thalamus and hypothalamus. AƒÒ amyloid plaques are aggregations of AƒÒ peptides which have gone through abnormal protein biogenesis. Gene expression for the Amyloid precursor protein is subject to stresses and exogenous factors. At critical points through the process, the amyloid protein is subjected to enzymatic proteolytic cleavages by enzymes called secretases to yield AƒÒ peptides. Errors in this process can yield abnormal Ab peptides, which can then aggregate into amyloid plaques. (Masters, Beyreuther, 1998)

Unfortunately, as yet there is no cure for AD. Subsequently, current focus of treatment is on palliative or symptomatic relief for AD patients. These treatments attempt to improve memory and cognitive functions to allow patients to function more normally in daily tasks. For example, earlier attempts for therapy used drugs that are called nootropics, also called cognitive enhancers. This structurally diverse group of drugs attempted to enhance processes of attention, memory, and learning. Piracetam is the prototype nootropic used (Figure 5). However, clinical trials of this drug showed minimal improvement in a minority of the subjects treated. Most current pharmacological treatments of AD, like nootropics therapy, are based on the cholinergic model of cognitive dysfunction in AD. Many acetylcholinesterase inhibitors (AChEIs) are prescribed to prolong the action of acetylcholine at synapses. In the early eighties, physostigmine was found to produce mild improvements in AD patients but the effects were short-lived. In 1993, tetrahydroaminoacridine, THA or tacrine was approved for use with AD treatment. Subsequent studies of the therapeutic efficacy of tacrine revealed that it has limited clinical value. Also, tacrine produces problematic cholinergic side effects such as nausea, vomiting, salivation, sweating, and lacrimation. Tacrine is even hepatotoxic for some patients. This has led to further studies of alternative therapies for AD.

The search for improved therapies to tacrine began with pharmaceutical research for new AChE inhibitors. One of these searches led to the discovery of the alkaloid compound huperzine A (HupA) found in the Chinese herbal medicine Qian Ceng Ta. This traditional remedy is prepared from the moss Huperzia serrata and has been used in past centuries in China for treating fever and inflammation. More recently, the purified compound has been used as a prescription drug in China for treating dementia. (Skolnik. 1997) Laboratory studies show that HupA is actually a more potent inhibitor of AchE than current medications like tacrine. HupA appears to bind more tightly and specifically to the deep chasm known as the active-site gorge of AChE which guides ACh molecules to the enzyme¡¦s cleaving machinery. In structural analysis of AChE complexed with HupA, researchers found surprisingly that HupA bears no resemblance to ACh and that the HupA/AChE complex binds with so few direct contacts (Figure 1a from Raves et al article). Only one strong hydrogen bond is seen as well as a large number of hydrophobic interactions within the crystalline complex. (Raves, et al. 1997). Comparison between the discussed AChEIs tacrine, HupA and physostigmine are shown (Figures 1-4). All three show the characteristic amino rings and have stable alternating pi bonding. A closer comparison between HupA and tacrine show that they are quite similar because both have primary amine groups as substituents. HupA looks like it could be three connected ring structures if the methyl group and one double bond connected. Then it would be somewhat similar in structure to tacrine. Apparently, though, it is these differences that makes it have higher affinity for the correct binding site on the AChE molecule.

In addition, compared to tacrine, HupA has a longer half-life and lacks cholinergic and hepatotoxic side effects. Studies using cells from the hippocampus and cerebellum of rat embryos have shown that HupA decreases neuronal cell death caused by toxic levels of glutamate. Glutamate activates certain NMDA receptors, which increase the influx of calcium ions followed by activation of proteolytic enzymes and subsequent cell death. These HupA advantages had led to the current clinical trials of efficacy on AD in the US.

Other studies of potential ACh therapies from compounds in herbal medicines also found some interesting results. Trasina (TS), an ayurvedic herbal medicine, is a traditional Indian medicinal plant used to improve memory and intellect. The constituents of Trasina are Withania somnifer, Ocimum sanctum, Eclipta alba, Tinospora cordifolia, Picrorrhiza kurroa, and shilajit. All are plant-derived constituents except shilajit, which is a blackish-brown exudate obtained from steep rocks of different formations found in the Himalayas. Studies were done to determine the efficacy of TS in alleviating the neurodegeneration of ACh pathways. Colchicine was administered to rats to induce cognitive defects. Though TS had minimal effects on cognitive function and cholinergic markers in absence of memory dysfunction, TS was able to attenuate cognitive deficits induced by administered colchicine. This was achieved through what is believed to be the drug¡¦s action of increasing cortical muscarinic ACh receptor capacity. There is some evidence about the actions of individual constituents of Trasina. Shilajit is shown to improve learning acquisition and engram in rats. This effects is significantly more in aged rats. W. Somnifera was found in studies of rats to improve the acquisition and retention of learning. Trasina is still in clinical trials in the US to test for efficacy and side effects in treating AD. (Bhattacharya and Kumar. 1997)

Studies, which do not focus on the cholinergic model of cognitive dysfunction in AD, are also underway. There is increasing evidence from studies to support the hypothesis that oxidative stress may be associated with onset and progression of AD. This has led to attention on antioxidant therapies, which are believed to enhance mental functions and delay cognitive losses with aging. Free radicals, any atom or molecule that contains an unpaired electron, are produced under normal conditions. However, excessive production of free radicals can lead to diseased states because these molecules often interfere with normal bodily functions. AD brains have been shown to exhibit more oxidative reactions than normal. An antioxidant is any substance that is able to protect against the damages of oxidative stress caused by free radicals. Some antioxidants are Vitamin E (high doses), selegine, ginkgo biloba (Egb). Clinical trials of antioxidants in AD are evaluating the efficacy of high dose of vitamin E and selegine in slowing the progression of AD. Preliminary results are promising and indicates need for additional clinical trials and studies. Vitamin E and selegine both do not, however, enhance cognition to the same degree as current available cholinesterase inhibitors. (Pitchumoni and Doraiswamy. 1998).

Ginkgo biloba is an extract from the leaves of the Ginkgo or maidenhair tree, Bai Guo (Chinese). Ginkgo seeds are commonly used in Chinese herbal medicine to relieve wheezing and lessen phlegm. Ginkgo leaves are traditionally used for treating asthma. In Western herbal medicine, ginkgo is used for improvement of circulation especially to the brain and is also used for its antiallergenic and anti-inflammatory actions. The leaves are Ginkgo biloba, as mentioned above, may have some antioxidant involved mechanism in treating AD. The compounds in ginkgo biloba act as scavengers for free radicals. The Egb extract contains several compounds that are thought to act synergistically on preventing oxidative stress and protecting neurotransmission modulation and membrane of neurons. Further studies are needed to fully elucidate the mechanism of EGb. It has undergone several European studies, which report positive results of EGb in the treatment of neurological disorders, and has already been approved in Germany for treatment of dementia. In studies done on AD subjects there was a modest benefit of ginkgo biloba when compared to placebo on cognition. This study compared effects of EGb to placebo in a sample of mild to moderately severe cognitive impairment. It demonstrated through objective tests of cognitive performance that EGb induced noticeable differences in patients¡¦ cognition to caregivers. (LeBars, et al. 1997).

Antioxidants like vitamin E and ginkgo biloba are beneficial because of their simplicity in treatment, ease of access, tolerability and low costs. If further studies indicate that they are complementary to the cholinesterase medications or beneficial alone in prevention of AD onset, some of the heavy burden on caretakers and elderly AD patients themselves would be alleviated. It would also prove beneficial for people who prefer ¡§natural or holistic¡¨ medications over synthetic ones.

While improved pharmacological therapies are still in clinical trials, AD patients and caregivers often use other unproven therapies such as vitamins, home remedies, ¡§smart pills¡¨, and herbal medicines. In a survey study conducted to describe the current use of unproven therapies by AD patients, roughly one-third of the caregivers reported ¡§a little¡¨ improvement with a given therapy. Caregivers who perceived a low level of physician support were not more likely to seek alternative therapies than those who perceived high physician support. This might indicate that the self-reports might not be biased due to bitter feelings toward the medical community. The reports also showed that most of those using these treatments preferred them to conventional medications because they believe that they are more natural and holistic remedies. While conventional treatments have a palliative focus, some of these unproven therapies are believed to retard progression of dementia by improving cognitive functions. Though these therapies seem like a good idea, there are potential negative effects. Since the patients¡¦ physicians do not prescribe these remedies, there maybe be adverse drug reactions with the prescribed medications. The costs of these therapies are often high and can take away from the money supply for other proven beneficial goods or services. We must also consider the ethical issues of companies selling or marketing these unproven therapies to both people with impaired cognition and caretakers who are desperate. (Coleman, et al. 1995). This is just one of the indications that improved medications and therapies must be developed soon for the growing number of AD patients.

Instead of the current monotherapy with AChEIs, perhaps combination therapies should be initiated, given the positive results in studies. Given the multiple pathological and neurochemical deficits in AD, combination therapy seems logical. (Doraiswamy and Steffens.1998). Since the efficacy of cholinesterase inhibitors has been consistently demonstrated for stabilizing or delaying cognitive losses, these medications could be the standard for any combination therapy. Alternative therapies could be used in conjunction to the cholinesterase inhibitors. Conventional AChE inhibitors could be used with a number of different alternative therapies like antioxidants, anti-inflammatory agents, estrogen, selegine, vasoactive agents, ginkgo biloba, and propentofylline (a neuroprotective and glial cell modulator). Some recommendations from a American Psychiatric Association conference in 1997 included a quadruple drug regimen of AChEI, vitamin E, estrogen, and indomethacin. Estrogen and seligiline may enhance the efficacy of AChEIs. Ginkgo biloba and propentofylline could also be used as alternatives. However, there is lack of clinical trial data for these combination therapies.

Also we should explore the possibilities of using therapies that are aimed at decreasing the amount of Ab plaques that develop. Some strategies include:

„h inhibition of Ab forming enzymes

„h inhibition of aggregation

„h promoting dissolution of Ab

„h ameliorating toxicity of Ab

„h suppressing reactive responses to Ab toxicity

These strategies would target the other neurological defect that AD patients suffer. If these are found beneficial combination therapies aimed towards the cholinergic deficits and AƒÒ plaques could further retard the damaging effects of AD.

A myriad of current and future (possible) AD treatments has been discussed. It seems that treatment possibilities would increase if researchers and herbalists internationally would come together and share their ideas and traditional remedies. Many of the possibilities mentioned in this paper have been known to cultures outside of the US for many years before the US researchers began their studies. It is a shame that the US is unable to accept the study results from other countries and must conduct studies for itself before the FDA will review these new possibilites.

Until there is more research at the molecular level and clinical trials, AD patients will have to settle for current medications and beliefs about alternative therapies. Perhaps once we can come to a better stage of medical treatment for Alzheimer¡¦s patients we might be better able to address issues of decreased emotional health many Alzheimer¡¦s patient suffer as a result of their early symptoms. Caretakers would be able to spend time with their patient in a more emotionally supportive way rather than worrying about their patients¡¦ physical and cognitive well beings.


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