Alzheimer’s Disease (AD) is the commonest type of dementia. It mostly affects people over 65. Dementia is the name given to a group of diseases which affect thinking, memory and other functions of the brain. Brain cells are destroyed leading to confusion, loss of memory, behaviour and personality changes. The onset of the illness is often gradual, and it gets progressively worse. These brain changes cannot be reversed.
Dementia can also be the result of a stroke, head injury, or infectious diseases such as Creutzfeld Jacob disease and HIV (the virus that causes AIDS) infection. AD is very rare in people under 65. It is slightly more common in women than men. According to the Alzheimer’s Association in the US, one in 10 people 65 years of age and nearly half of those over 85 suffer from the disease. Today, about 500,000 people in Britain have AD. In America, the number is 4 million. Worldwide, there are an estimated 12 million people with the disease. That number is predicted to double by the year 2050. As more people in developing countries survive into old age, the number of those with AD is increasing dramatically and will soon far outstrip the number of people with AD in industrialized nations.
Brief History of Alzheimer’s Disease
Alzheimer’s disease was discovered in 1901 when a 51-year-old woman Auguste D, sought help in a psychiatric hospital for being paranoid and forgetful. The doctor who was in charge of treating Auguste was Dr. Alois Alzheimer.
The term, Alzheimer’s Disease (AD) was first used in 1910 in the 8th edition of textbook Compendium der Psychiatrie by Emil Kraepelin. He reported that autopsy showed changes typical of “the most serious form of senile dementia”. One-third of the cells in the cortex were destroyed. But there was some confusion about how to interpret the disease. Although the changes in the brain did indeed suggest senile dementia, the relative youth of the patient argued that the disease was a new one. For that reason, Kraepelin characterized it as pre-senile dementia. Thus began a lasting argument about AD that was only recently resolved. Was Alzheimer’s disease senile dementia or something else? And was it part of the normal aging process?
In the 1960s, people began to realize that AD was not rare, as previously thought, but indeed the predominant cause of dementia and a common illness. Senility, which was considered to be a normal part of aging was now seen as abnormal, the result of disease or other illness, and possibly treatable.
One of the effects of AD is that the synaptic connections in the brain-the spaces between brain cells where communication takes place-are lost. Some of the cells that are destroyed supply a chemical substance called acetylcholine to portions of the brain concerned with memory. So the first drugs developed for AD were aimed at boosting the action of acetylcholine, or preventing it from breaking down in the first place. In 1993, the US Food and Drug Administration approved the first drug to treat AD. This drug, and two others that have been approved since, may relieve some of the symptoms of AD. But to the extent that they work, they work only in the early stages of the disease. And they are temporary solutions at best. Thus far, no treatment has been found to cure the disease or to slow its progression.
The way doctors define disorders is based on their clinical experience and what that experience leads them to expect. When dementia was first defined as a disorder, it was considered a problem of the elderly. It was not expected that such symptoms would commonly affect people who were younger. When that proved to be the case, the condition was considered exceptional or atypical. Because it was unexpected and atypical, this suggested that the disease process might be a different one.
Why does the name you give to something matter? It matters because failing to realize that you are looking at a single disease process instead of two unrelated ones has implications for how you investigate and treat a disease. In the case of AD, better understanding of the underlying disease process showed that even though the disorder progressed with age, when it began at a younger age, it was still the same disease as the disorder affecting the elderly. A better idea of the disease process reshaped prior understanding, based on clinical patterns, with a new understanding based on observable changes in the cells of the central nervous system.
Although AD gained acceptance as a disease state, it did not attract much attention at first. One reason was the emphasis on a psychological explanation for the symptoms of dementia that resulted from the influence of Sigmund Freud. A second reason was that Kraepelin’s description of the disease did not offer much hope for treatment.
Until 1936, AD was commonly diagnosed based both on the pattern of symptoms observed by the doctor, and by examination of brain tissue after death. But when it became clear that many non-demented people also showed plaques and tangles, diagnosis began to be made on the basis of clinical criteria alone.
In recent years, AD has burst to the forefront of public consciousness. For one thing, people are now living longer than ever before, and AD is a disease primarily of old age. Also, the surge in population following the Second World War has contributed to an increasingly older population worldwide. Finally, most people with AD do not die of the disease but of complications from it, such as pneumonia. For a long time, owing to a lack of awareness about AD, someone who contracted pneumonia as a complication of AD would have their cause of death listed as pneumonia. Better diagnosis of AD has led to greater recognition of the impact of the disease.
In the last two decades criteria for diagnosing AD have become stricter, and ways of imaging the brain hold out the promise of even more accurate diagnoses. Furthermore, researchers have made progress in understanding the genetic basis of AD. Between 1991 and 1995, new molecular cloning techniques made it possible to identify defects called mutations associated with AD in four genes.
Genes exist to make proteins, which direct all of the workings of the body. The first finding in AD genetics was the discovery that a mutation in the gene that makes the so-called amyloid precursor protein results in overproduction of the protein. Research in the 1980s on families in which AD struck at an early age helped to locate this gene on chromosome 21 in 1991. But these mutations are extremely rare, and worldwide they account for less than 5% of all cases of AD.
In 1995, researchers identified mutations in genes called presenilin 1 and 2 that cause 50% of early onset cases of AD. Genes to account for the remaining cases of early-onset AD remain to be identified. One form of a fourth gene, called ApoE, does not always cause AD but can increase a person’s chance of getting the common version of the disease that occurs in people over 65. Research continues into other genes involved in both early- and late-onset AD.
All people with Down’s syndrome develop plaques and tangles by their 40s, which puts them at increased risk of developing dementia as their life expectancy increases. So findings in AD genetics are also being used to help understand how Down’s works.
Timeline of Events Related to Alzheimer’s Disease:
|1907||Dr. Alois Alzheimer describes two cases of "presenile" dementia with extensive plaques and neurofibrillary tangles.|
|1968||Researchers show that the severity of dementia in AD seems more closely related to the density of plaques and tangles and not to cerebrovascular changes.|
|1984||Researchers at the University of California at San Diego discover that amyloid plaques consist largely of peptide fragments.|
|1991||Mutations in gene for amyloid precursor protein discovered in several families with early-onset AD.|
|1992||Tacrine is approved by the US Food and Drug Administration (FDA) as the first treatment for mild-to-moderate AD.|
|1993||Discovery of gene (ApoE4) that increases the risk of the more typical form of AD, which appears late in life.|
|1995||Mutations in presenilin genes found to cause an aggressive form of early-onset AD.|
|1996||Donepezil hydrochloride is the second drug approved by the FDA to treat early-stageAD.|
|1997||Research suggests vitamin E may slow the progression of AD.|
|1999||An experimental vaccine is shown to reverse AD-like symptoms in mice.|
|2000||FDA approves third drug (rivastigmine) for treatment of early-stage AD. Phase I clinical trials begun in US and UK to test the safety of an amyloid vaccine in human subjects.|
Common Symptoms of Alzheimer’s Disease Include:
- Loss of short-term memory – forgetting appointments, names and deadlines, even forgetting what has just been said.
- Mistakes and confusion – when performing familiar or even mundane tasks.
- Difficulty in thinking things through – not being able to add up the shopping bill or understand a simple argument.
- Disorientation – getting lost in places that should be familiar, perhaps even wandering around, unable to find the way home.
- Odd decisions – like wearing the wrong clothes for the season.
- Confusion with time – not knowing the day of the week, the date or even the hour.
- Mood swings – sudden changes of mood for no reason, often resulting in great anger, sadness, happiness or other emotions.
- Changed personality – confident people may become fearful, relaxed people may become anxious or paranoid.
Causes of Alzheimer’s Disease – Brain Function, Genetics & Research
The cause of dementia and Alzheimer’s disease is not known and there is no effective treatment. Most of the time, it is not possible to predict who will get the disease – it occurs randomly in people over 65. 5% of cases of AD occur in much younger people and appear to be linked to faulty genes. One of the genes that causes this kind of AD is located on the same gene that causes Down’s syndrome. All people with Down’s syndrome develop the brain changes associated with AD by the time they are 40. But not all of them develop dementia. It is most likely that Alzheimer’s disease is caused by a variety of factors. From various post-mortem studies, researchers have found that a person’s brain with AD contains abnormal levels of plaques or deposits which tangles between or within cells. These plaques prevent brain from functioning properly.
In addition, AD causes a decrease in vital brain chemicals (called neurotransmitters) that help nerve cells to communicate with each other. As the damage to the brain increases, cells die and the connections between them are broken. Plaques and tangles are also found, in smaller amounts, in the brains of people who show no signs of dementia. No one knows what causes the abnormal build-up of deposits that results in AD, though several different theories are being investigated. Researchers in the fields of epidemiology, genetics and molecular and cell biology continue to make headway in understanding some of the mechanisms underlying the disease.
What we do know is that AD affects important areas of the brain such as the hippocampus, which is involved in memory, and the cerebral cortex, which governs language and other thought processes. The nerve cells in these areas, and the connections between them, are destroyed, and the brain begins to waste away.
Patients without dementia show some of the same kinds of brain changes that occur in people with AD. The difference is that some of these changes are more marked in people with AD. At present, the only way to really tell whether a person has AD is to examine brain tissue after death.
Gumming up the works
The hallmarks of AD are clusters of proteins that accumulate within and between nerve cells. It is not understood how these deposits damage cells, nor do researchers have a clear idea how they contribute to dementia. But even if they turn out not to cause AD directly, they are biological markers of the disease that may help to trace its mechanism.
Very early in the course of AD, waxy protein deposits called plaques begin to build up between cells. Most elderly people have some waxy plaque buildup, but in people with AD the plaques are extensive, and they are concentrated in the hippocampus and the cerebral cortex. Cells around the plaques often look abnormal. Plaques mostly contain protein fragments called beta-amyloid peptide.
Proteins get their instructions from genes, and if the gene suffers a defect, called a mutation, the protein the gene codes for may also be defective. Beta-amyloid precursor protein (beta-APP) is a protein that is widely present in the body, though its precise role is unknown. As it matures, the protein is cut in several ways, creating fragments of beta-amyloid protein, a small number of which are toxic. However, mutations in the gene that codes for beta-APP cause something to go haywire in the cutting process and to generate an excess of the toxic form of the protein fragment. This toxic form is the beta-amyloid peptide that is found in the plaques of AD.
Beta-amyloid peptide may injure nerve cells in several ways, from disrupting calcium regulation (which kills cells) to triggering an inflammatory response from the body’s immune system that makes any existing damage worse. But how these mechanisms relate to the dementia of AD is not clear. Moreover, researchers disagree whether plaques cause AD by destroying cells, or whether they result from damage to cells caused by something else.
Protein clusters found inside nerve cells are called neurofibrillary tangles. These structures resemble threads twisted around each other. The tangles consist mainly of a protein called tau, which ordinarily works with another protein called tubulin to support the structure of cells and to provide a track for transporting nutrients and other cellular components through the cell. For a long time, tau was believed not to be important in AD. But study of a disorder called fronterotemporal dementia suggests that abnormal processing and buildup of tau may contribute to dementia by clogging up the cell and interfering with its function.
Attacking the Messenger
For everything they do, brain cells use a variety of chemical messengers called neurotransmitters to communicate. For example, as part of the normal flow of information, the neurotransmitter acetylcholine is produced in some cells (particularly those of the hippocampus) and broken down in other areas by an enzyme called acetylcholinesterase.
In AD, however, the amount of acetylcholine produced is much lower, hampering communication between cells. As if that were not enough, acetylcholinesterase continues to do its job. It is as though an arm-wrestling partner continues to arm wrestle after you have stopped resisting. Drugs called cholinesterase inhibitors aim at blocking the enzyme, to increase the amount of acetylcholine and improve memory and concentration. But to the extent the drugs help at all, they are only of benefit in the early stages of the disease. Once brain cells have been destroyed, the drugs are useless.
Genetic Causes and Risk Factors in AD
About 5% of people with AD have a special family history of the disease. In these cases, not only is more than one family member affected, but the disease often strikes people in their thirties and forties. For this reason, it is called early-onset AD. Up to 50% of cases of early-onset AD are caused by defects in three genes (beta-APP, and presenilin 1 and 2). The remainder of early-onset cases are probably also caused by defective genes, but those genes have yet to be found.
Late onset AD-the more common form of AD that strikes people over 65-also runs in families in about 10-25% of cases, though the pattern is less distinct. Defective genes different from the ones that cause early-onset AD are believed to be implicated, but for now they are unknown. In the vast majority of cases of late-onset AD, there is no clear family history of the disease. Although genes have been linked to a person’s risk of getting this form of AD, they do not appear to cause it.
The gene that makes beta-APP was found on human chromosome 21. Geneticists were helped in this discovery by research on families with early-onset AD and on people with Down’s syndrome, who show the signs of AD by age 40. (People with Down’s have an extra copy of chromosome 21.)
The next task was to look for mutations that might result in an excess of beta-amyloid peptide. Indeed, in several families with familial early-onset AD, mutations were found in the beta-APP gene that either increased the amount of both versions of the peptide, or increased production of the toxic version.
Mutations in the beta-APP gene are responsible for less than 1% of all cases of early-onset AD.
Presenelin 1 and presenilin 2
Defects were also found in a set of genes that interfere with how beta-APP is cut. Disruptions in these genes, called presenelin 1 and presenilin 2, cause about 50% of early-onset familial AD. These mutations act indirectly to increase production of beta-amyloid peptide, expecially the toxic version. They are located on chromosome 14 and chromosome 1, respectively.
A fourth gene that possibly has a wider effect than the amyloid gene is a gene that everyone carries called ApoE. ApoE helps the body metabolize fats and is located on chromosome 19. People who have a particular type of the gene (ApoE4)-anywhere from 6 to 37% of the population-have a greater risk of developing the more typical form of AD that occurs after 65.
Unlike APP and the presenilin genes, ApoE4 does not work by increasing production of beta-amyloid peptide. But it may increase a person’s risk for AD in a number of other ways. One theory is that ApoE4 and beta-amyloid compete to occupy the space between brain cells. A housekeeping molecule responsible for clearing the area around cells has an easier time removing ApoE than amyloid. Thus, amyloid begins to accumulate and to make mischief. Also, people who inherit ApoE4 from both parents are more likely to develop AD before the age of 70 (as opposed to 80-85, which is the average age at which late-onset AD strikes). But having the ApoE4 gene does not necessarily mean a person will get AD, nor does not having the gene mean they won’t.
Environmental causes of AD
Many environmental factors have been presumed to play a role in AD, but findings from studies of low education, smoking, vascular disease and diabetes have been inconclusive. Recently, an analysis of head injuries suggests that people who suffer serious head injuries in early adulthood may be at greater risk of developing AD. Other environmental agents under investigation as causes of AD include viruses, and diet and lifestyle factors.
Only humans develop AD, so for a long time, finding a small animal in which the disease could be studied at all was a major obstacle to progress in research. Also, because most of what is known about AD comes from examining human brain tissue after death, scientists know much more about the later stages of the disease than the earlier stages. What is needed is an animal model that reproduces all the characteristics of AD as closely as possible.
Fortunately, scientists have been able to engineer mice with mutant genes that cause amyloid plaques like those affecting the brains of people with AD. These mice also display learning and memory problems as they age. But unlike human nerve cells affected by AD, the mouse nerve cells remain healthy. And the mice do not develop neurofibrillary tangles. Still, work with these mice is very helpful in studying the role of environmental factors, and in assessing treatments based on replacing cells lost or damaged by the disease. Refining the mouse models will shed additional light on how AD works.
Peering into the brain
A major goal of research in brain-imaging techniques is to find ways to improve early detection of AD. Already, computerized tomography (CT) and magnetic resonance imaging (MRI) are sometimes used in diagnosing AD to rule out other causes of dementia, such as tumours or damage from stroke. These techniques can also show how parts of the brain shrink as the disease progresses.
Other techniques, such as single-photon emission computerized tomography (SPECT) and positron emission tomography (PET) highlight patterns of brain activity. Like CT and MRI, they may improve the accuracy of diagnosis. But primarily they are used as research tools to study how the work of healthy brains differs from the work of brains with AD.
At present, it is not possible to detect plaques and tangles using brain-imaging techniques.
Is There Any Hope?
Unfortunately, there is no cure for AD, but there are drugs that can slow down the progress of the disease and help with the symptoms which are part of the illness, such as aggression, depression, etc.
The only licensed medication for Alzheimer’s is called cholinergic therapy. Drugs like donepezil, rivastigmine and galantamine, can maintain (and possibly restore) cognitive and other functions in some people. But they may only work for a short time. On the whole these drugs are quite well tolerated, though some people can experience side-effects.
Alzheimer’s disease is a progressive illness – with symptoms such as memory loss and impaired thinking that gradually get worse. This is followed by loss of ability to do everyday things, behavioural difficulties and gradual loss of interaction with what happening So far there is no cure, and no treatment that will stop the condition developing. However, certain drugs can slow down the progress of the disease and improve a person’s thinking and functioning. Three of these cholinergic drugs (listed below) are now recommended treatments.
While physical treatment may be limited, there is much that can be done for the psychological health of people with Alzheimer’s disease and their carers. Seeking early diagnosis and receiving information about the condition early in the illness helps patients and carers prepare for what lies ahead, rather than discover things alone by default. Support groups, specialist dementia services and talking treatments can be of immense benefit for people learning to live with the condition. It is important for carers to get support and to look after their own physical and mental health. People with Alzheimer’s disease may have other problems alongside it, such as psychosis, depression or a physical illness such as pneumonia. If these are treated effectively, the quality of life for people with Alzheimer’s and their carers can be greatly improved. Researchers are working to find new, more effective ways to treat Alzheimer’s Disease.
Currently, at least two dozen drugs to treat AD are undergoing clinical trials in the US. Some of these drugs are cholinesterase inhibitors, which only show benefit in mild-to-moderate cases of AD, and which cannot halt or cure the disease. An alternative approach aims at preventing the degeneration of brains cells caused by beta-amyloid peptide. For example, researchers are seeking to interfere with the production of beta-amyloid peptide, to keep the peptide from accumulating even if it is produced and to block the toxic effects of the peptide. Other areas of investigation include the following:
Anti-inflammatory Drugs: It may be possible to slow the progress of AD with anti-inflammatory agents similar to ibuprofen and aspirin. Since the 1990s, many studies have shown that AD occurs much less frequently in people with arthritis than in the general population. Researchers reasoned that the antiflammatory drugs that people with arthritis take somehow repair the cellular damage that leads to AD. A number of antiinflammatory drugs are under trial or investigation for treating AD.
Oestrogen: Women on hormone replacement therapy also have a reduced incidence of AD, and researchers hoped that oestrogen might prove effective both in preventing and in treating the disease. Findings from one effort, the Alzheimer Disease Cooperative Study, were disappointing. But other trials of oestrogen are still under way.
Antioxidants: Just like a car engine generates pollutants, cells as they function generate toxic molecules called free radicals. Usually the body controls this process, known as oxidative stress, by producing antioxidants that counteract free radicals. But in certain situations oxidative stress overwhelms the body’s defenses and triggers a chain reaction in which cells, particularly nerve cells, become damaged. Oxidative stress is believed to be a contributing factor to AD, and clinical trials of antioxidants such as vitamin E and ginkgo biloba are ongoing.
Vaccines: Trials of a vaccine intended to immunise patients against accumulation of beta-amyloid plaques are under way in both the US and UK. These studies are based on research using mice that have a version of AD characterised by amyloid plaques. Injecting the mice with a vaccine made of beta-amyloid peptide reduced the number of plaques. Preliminary results of these phase I trials, which test safety, suggest that the vaccine is well tolerated in human recipients.
Drug Treatments for Cognitive Problems
Cholinergic drugs are the most common drugs for cognitive problems in Alzheimer’s disease. They aim to preserve the chemical neurotransmitter acetylcholine (decreased in Alzheimer’s), by stopping an enzyme called acetylcholinesterase, (the enzyme that normally breaks it down) from working.
Problems with Cholinergic Drugs:
THEY MAY HAVE SIDE-EFFECTS: such as nausea, diarrhoea and abdominal pain in some people. 7
THEY DO NOT WORK FOREVER: Their effects usually wear off in the short to mid term. The progress of the disease may be slowed down for several months (especially in people with mild Alzheimer’s disease) but is not stopped.
THEY MAY INTERACT WITH OTHER DRUGS: It is important to check that all drugs taken (prescription and over-the-counter) are compatible.
THEY MAY INHIBIT THE RELEASE OF ACETYLCHOLINE IN THE LONG RUN: Cholinergic drugs work to increase amounts of acetylcholine in the brain. There’s a danger that the brain will adapt to these increases, and will consequently produce less acetylcholine. In these cases, an effect could be worsening cognitive problems, especially if the drug is stopped too precipitously.
Drug Treatments for Co-existing Conditions
People with Alzheimer’s disease often experience physical and mental health problems alongside it, including depression, sleep disturbances, behavioural problems and psychosis. Once physical causes are eliminated, and if behavioural methods and support do not help these problems, then drug treatment may be given.
Antipsychotics: These drugs may be given to people with Alzheimer’s disease who are aggressive or agitated. They are also given for psychotic symptoms such as delusions or paranoia. However there is not a lot of published evidence in this area except for one drug.
Typical antipsychotics are best not used as there is evidence they worsen the disease and little evidence that they are that effective. 11 12 Before any drugs are used, a thorough assessment is made of the person’s social and environmental situation, and a physical examination carried out to check they are not in pain. This would usually be carried out by a doctor, in collaboration with experienced community staff. Any drugs used should be reviewed to ensure they are having the desired effect, and because these behavioural problems wax and wane in Alzheimer’s disease, reviewed again after about four months to ensure they are still needed.
Anticonvulsants: The use of mood stabilisers has increased in recent years, in spite of little published proof of their benefit. It would be appropriate to use these drugs where agitation or distress was not directly caused by psychotic phenomena (where an antipsychotic would be a better option), and this seems to be where anecdotal reports claim they do well, on their own or to supplement other therapies.
Anti-depressants: Many people with Alzheimer’s disease experience an episode of depression. This is happens at any stage of the illness, not just early – and the reason is not fully understood. This is a rarely used drug and most of time they have a high number of side effects and adverse events in patients with Alzheimer’s disease. Cognitive problems such as memory loss can be a sign of depression as well as Alzheimer’s, and anti-depressants can improve these problems. But older people can be more susceptible to side-effects of anti depressants than younger people and care taken accordingly.
Sleeping Tablets: These are often given for night time disturbance, or day/night reversal that is sometimes seen.
Talking Therapies and Support
Emotional and practical support, understanding and advice is essential to both the person with Alzheimer’s and their carer(s). People respond to their condition in very different ways and so treatment should be geared to the individual.
Talking therapies such as counselling can help people cope with the demands of caring for someone with Alzheimer’s disease. It can also help people with Alzheimer’s, especially in the early stages of the disease.
Specialist dementia services and groups can improve the quality of life of sufferers and carers by providing information, support, understanding and respite care. Groups and services helpful for people with dementia may include:
Reminiscence Therapy encourages people to talk about past events, often assisted by photos, music, objects and videos of the past. There has been very little research in this area but it can temporarily improve the mood and cognitive skills of people with Alzheimer’s.
Creative Therapies such as music, dance, crafts, art and gardening are stimulating and can help people express themselves and make sense of their environment.
Behaviour Therapies usually offered by psychologists working in the memory assessment services, but also from occupational therapy and occasionally physiotherapy services. Behavioural therapies may be useful in offering guidance on dealing with (and preventing) difficult behaviours.
Carers themselves constantly come up with ingenious solutions to everyday problems, hence the value of meeting in carers groups. Some people respond to dementia by becoming angry and argumentative, whereas other people will be passive and depressed. Most people are affected by their environment. Simple behavioural techniques can identify contributing factors that may help to stop problem behaviour or allow the carer to cope with it. A study of carer training in New York showed a delay in the sufferer going into a nursing home of almost a year, when the carer was better able to understand what was happening.
Nutritional supplements can be useful in Alzheimer’s Disease:
Vitamin E: Found in foods such as eggs, vegetables, vegetable oils, fruits and nuts. It is possible that Vitamin E might slow functional decline in people with moderate Alzheimer’s disease. A study in USA showed a delay in entering nursing homes in people taking Vitamin E. This has convinced many professionals to take Vitamin E themselves, but the dose in the study was very high and most take less. The study needs to be repeated, but antioxidants like Vitamin E are good for the body in general, so it is a worthwhile strategy to ensure an adequate intake.
Ginkgo Biloba Extract: Sometimes called Egb 761, ginkgo can cause a moderate improvement in people suffering memory loss, cognitive impairment and Alzheimer’s-type dementia. No one is exactly clear how it works, possibly a combination of antioxidant and an increase in blood flow through the brain. In studies in the general population the drug seems to have a protective effect and it is widely taken.
These treatments can be easily obtained from health food shops, but medical advice should be sought beforehand because:
They may interfere with other, prescribed therapies.
They may produce adverse effects under certain conditions e.g., vitamin E may be associated with blood clotting problems in vitamin K deficient people.
Aromatherapy massage and other complementary therapies: some people with Alzheimers Disease (and their carers) find these therapies useful for agitation, anxiety and sleep disturbances. They can also relieve physical discomfort. A guide to complementary therapy is available from the Alzheimer’s Society
What can I do to help myself (or a family/friend) with Alzheimer’s Disease?
It is important to see your family doctor (General Practitioner/GP) if you have any of the symptoms or experiences listed above. If you are worried about a friend or relative, offer to go with them to their GP. It can be difficult to see a doctor when there is the possibility of bad news, but Alzheimer’s disease shares symptoms with many other conditions, ranging from depression to a brain tumour. Many of these are treatable, especially if caught early.
Although Alzheimer’s can’t be cured, if you get diagnosed and treated at the early stages of the illness, the progress of the disease can be slowed down. Early diagnosis also means that you and your carers can prepare yourselves and your financial and legal affairs for the future. If a doctor suspects you have Alzheimer’s disease, he or she will usually refer you to a psychiatrist or a neurologist. An occupational therapist may also be involved in helping you with your daily routines and activities.
In general, a relative or partner often has a very active role in looking after someone with Alzheimer’s disease. Groups, run by organizations like Alzheimer’s Association in USA, offer great support and located in several areas. They run carer’s support groups and respite care. Reminiscence groups that focus on early memories (for example by showing slides of past major events) offer members a chance to retrieve old memories (which are often still intact) and a chance to bond with others in a similar situation.
The Future – Where is Research Headed?
A vaccine has shown promising results in specially bred mice, and trials are underway in humans in the UK and USA – and it is early days yet to predict how successful this will be. Methods to prevent Alzheimer’s are still a long way off but researchers are working on a number of different approaches to treating Alzheimer’s disease, as interest in the area increases.
Investigations are presently underway to test new anticholinesterase cholinergic drugs. A build-up of reactive molecules called free radicals may play a major role in Alzheimer’s disease. Antioxidants neutralise free radicals and may help prevent or treat Alzheimer’s.Oestrogen was first linked to Alzheimer’s disease when it was noticed that post menopausal women undergoing hormone replacement therapy seemed less likely to develop the disorder. This is an observation rather than definitive proof, and treatment studies to date have been disappointing. It is an interesting and plausible treatment option, but longer term studies and further research in to understanding the interaction between oestrogen and the brain are needed – and ongoing. It is not recommended that oestrogen be used as a treatment in Alzheimer’s disease, but it is another factor to weigh up if considering HRT for other reasons.
Anti-inflammatory drugs have also been associated with a reduction in the frequency of Alzheimer’s disease in patients with longstanding arthritis, which has sparked interest in their potential to treat Alzheimer’s.
Other research on AD has focused on a number of different factors that may put people at risk for developing AD, such as lower education, aluminium poisoning and weakened immunity. But none of these findings is conclusive. Race, culture, environment and lifestyle do not appear to have any effect on a person’s risk of development AD. Conversely, there is some evidence that a severe blow to the head can cause the disease. But injury alone is not sufficient, and many people who develop AD have never sustained a blow to the head.
Research is also continuing into developing mouse and rat models that will reproduce every aspect of AD. Although mice with the same mutations found in humans do develop amyloid plaques, they do not lose neurons anywhere near the extent that humans do, nor do their brains form neurofibrillary tangles. Development of an appropriate animal model is not only critical for finding drugs to treat the disease, but also other treatments, such as implanting healthy cells into the brain to replace damaged ones.
Perhaps the most important finding to come from research over the years is to recognize that AD is not part of normal aging but a real disease. In other words, AD is primarily a disease of old age, but simply living a long time is not enough to cause it. AD appears to have many causes, which makes it complicated. But that also opens up the possibility of different therapeutic approaches, as well as different ways of preventing the disease.
References & Citations: