Questions & Answers

Medicare is a federal health insurance program for people age 65 or older who receive Social Security retirement benefits. To receive assistance from Medicare, a person must meet specific eligibility requirements. Medicare covers some, but not all, of the services a person with Alzheimer's disease may require. For example, the program does not cover long term healthcare. Medicaid is a federal program for certain individuals and families with low incomes and resources, typically administered by state agencies; eligibility and benefits vary from state to state. Medicaid can cover all or a portion of nursing home costs. A person with Alzheimer's can qualify for long term care only if there are minimal income and cash assets. Medicaid may be applied for by calling each state's Department of Human Services or Medicaid Assistance Program.

First, visit your regular family physician. The physician will probably do a variety of tests to determine the probability of Alzheimer's. Specialists such as neurologists, gerontologists and geriatric psychiatrists may also be involved in the evaluation process.

Dementia is a progressive deterioration of intellectual function due to the death of brain cells. Dementia can be caused by medical conditions such as hypothyroidism or stroke, drug toxicity or brain injury. Some conditions are treatable, and others cause irreversible brain damage. Alzheimer’s disease (AD) is irreversible, and in western countries, it accounts for more than half of dementia cases. Currently, the only way to diagnose AD definitively is through a brain autopsy. However, on living patients, physicians can correctly diagnose AD about 90 percent of the time based on mental and behavioral symptoms, a physical examination, and neuropsychological and laboratory tests.

A physician will normally take a history of mental and behavioral symptoms, using information provided by the patient and the family. In nearly 75 percent of cases, AD starts with the inability to remember recent events and to learn and retain new information. Early stage AD patients experience memory problems that interfere with daily living and steadily worsen. Other early AD symptoms can include difficulty managing money, driving, orientation, shopping, following instructions, abstract (conceptual) thinking and finding the right words. There may also be other problems, such as poor judgment, emotional instability and apathy. AD can be distinguished from other types of dementia in part by the symptoms exhibited, the extent to which these symptoms occur and the speed with which the disease progresses.

A physical examination will be performed to help identify and rule out other potential causes of dementia. This exam will normally include a general physical, blood tests and urinalysis. Through a blood test, for example, the physician can measure thyroid function; hypothyroidism or failure to produce sufficient thyroid hormones is common in the elderly and can cause dementia. Dementia may also be the result of a vitamin B12 deficiency which is common in the elderly, and can be measured through blood tests. Physicians may use brain scans (such as magnetic resonance imaging or MRI) to rule out other possible causes of dementia, including brain tumors, stroke, blood accumulation on the brain surface or other conditions. In addition, brain scans can show characteristic structural changes present in AD. Physicians may administer an electroencephalogram (EEG) to measure the electrical activity in the brain. Occasionally, spinal fluid may be tested through a lumbar puncture.

Neuropsychological tests identify behavioral and mental symptoms associated with brain injury or abnormal brain function. The neuropsychological tests used will depend on the symptoms and the dementia’s state of advancement. Usually, physicians start with a brief screening tool, such as the Mini-Mental Status Examination (MMSE), to help confirm that the patient is experiencing problems with intellectual functions. The MMSE includes tests of memory, attention, mathematical calculation and language. If a patient has severe dementia, further neuropsychological testing beyond the MMSE is usually not necessary. However, for patients with mild intellectual deficits, more tests may be needed to determine whether the patient is simply showing signs of advanced age or is developing AD. The patient may be referred to a neuropsychologist, who will administer a battery of tests to identify more specific deficits.

Currently, there is no cure for Alzheimer's disease (AD). However, there are medications that can help control its symptoms. In addition, treatments are also available to help manage agitation, depression, or psychotic symptoms (hallucinations or delusions), which may occur as the disease progresses. Consult a physician before taking any medications.

FDA-Approved Drugs

There are five Food and Drug Administration (FDA)-approved drugs that can control symptoms and slow the progression of AD. Four, called cholinesterase inhibitors, Cognex® (tacrine), Aricept® (donepezil), Exelon® (rivastigmine), and Razadyne® (galantamine), slow the metabolic breakdown of acetylcholine, an important brain chemical involved in nerve cell communication. These drugs make more of this chemical available for communication between cells. This slows the progression of cognitive impairment and can be effective for some patients with AD. These four medications are all approved for the treatment of mild to moderate symptoms of Alzheimer’s disease. In 2006, the FDA approved Aricept for the management of severe AD symptoms. The fifth medication, Namenda® (memantine), is approved for the treatment of moderate to severe AD. Namenda appears to protect the brain's nerve cells against excess amounts of glutamate, a messenger chemical released in large amounts by AD-damaged brain cells.

The effectiveness of these drugs varies from person to person, and some drugs may be better tolerated than others by certain individuals. Side effects include nausea, dizziness, headache and fatigue. All medications are taken orally. However, in 2007, the FDA approved the ExelonPatch (rivastigmine transdermal system) to deliver this drug through the skin. Cognex, though effective, has more adverse side effects and although still available, is now rarely prescribed.

Medications to Control Depression, Anxiety and Psychotic Symptoms

For patients in the middle stages of AD, there are also medications to control depression, anxiety and psychotic behavior, including paranoid thoughts, delusions and hallucinations. These individuals can also exhibit aggression, hyperactivity and combativeness. Medications for these symptoms are considered when non-medication alternatives have failed and/or these symptoms put the AD patient or others in danger.

Potential Treatments for AD

Many potential AD treatments are being investigated in laboratories and tested in human clinical trials. Scientists continue basic research on therapies that could potentially clear the protein plaques in the brain. The safety and efficacy of possible treatments are being tested on humans, including drugs that could remove plaques, immunotherapy with beta amyloid antibodies, non-steroidal anti-inflammatory drugs (NSAIDs) and statins (drugs used to lower cholesterol). The protective effects of estrogen, antioxidants (Vitamins A, C and E), ginkgo biloba and omega 3 fatty acids (found mainly in fish such as tuna and salmon) are also being tested in trials. To date, no consistent results have emerged from various studies, but further research and future results from rigorous trials should help clarify the benefit of these and other treatments.

Immunotherapy

In 1999, studies revealed that injection of beta amyloid itself, called active immunization, caused laboratory mice to produce antibodies against the protein and reduced its accumulation. Spurred on by the potential of immunotherapy, some pharmaceutical companies started human clinical trials in 2001. However, in 2002, the trials were halted when about six percent of participants developed a potentially serious side effect, acute encephalitis (inflammation in the brain). Autopsies of several participants who died of other causes revealed that a large amount of beta amyloid had been cleared from their brains, their brain volume was lower, and lower levels of tau, another protein related to AD, were found in their spinal fluid. Further, for the living trial participants who developed antibodies, there was evidence of better memory, attention and concentration. More recently, some pharmaceutical companies have begun further human trials using passive immunotherapy, in which antibodies to a protein rather than the protein itself are given to the recipient.

NSAIDs (non-steroidal anti-inflammatory drugs)

Studies suggest that brain inflammation may play a role in damage due to Alzheimer’s disease, and early observations indicated that NSAIDs could potentially slow disease progression. However, studies and human clinical trials have produced conflicting results.

A large trial of three NSAIDs, Aleve® (naproxen), Vioxx® (rofecoxib) and Celebrex® (celecoxib) showed that these drugs did not delay the advance of the disease. Trials of naproxen and Celebrex were suspended before completion due to concerns about an elevated risk of stroke and heart attack for participants.

In early 2008, researchers examining data from the U.S. Veterans Affairs Health Care System found that long-term (5-year) NSAID use, particularly the use of ibuprofen, appeared to protect against Alzheimer’s. Another study looking at results from six previous investigations suggested that naproxen, ibuprofen and aspirin may reduce the risk of Alzheimer’s disease.

More recently, a 2009 study published in the journal Neurology showed that NSAIDs do not prevent Alzheimer's disease or other forms of dementia. In fact, the risk of developing dementia in the study's very elderly population was 66 percent higher among heavy users of NSAIDS than among people who used little or no NSAIDs.

Each of these studies was performed in unique clinical populations including differences in sizes of the study and ages of the participants. More clinical trials will be necessary to fully understand how NSAIDs impact Alzheimer’s disease. While additional studies are underway, individual patients should continue to consult with their doctors on the relative benefits and risks of treatments involving NSAIDs.

Statins

Several clinical trials are underway to test whether statins, cholesterol-lowering drugs, may help slow progression of AD.

Estrogen

Research suggests that estrogen taken to manage the symptoms of menopause may also protect the brain. Therefore, scientists have been interested in whether estrogen could reduce the risk or slow the advance of AD. However, clinical trials of those already diagnosed with AD, showed that estrogen had no impact on its progression. Other studies indicate that women who begin using estrogen after age 60 to 65 are at increased risk of developing dementia, as well as heart attack and stroke. Estrogen is now only recommended for short term use to treat menopausal symptoms. Recent research has helped clarify the neuroprotective role of estrogen taken by younger women before menopause. According to a study published in August 2007, scientists from the Mayo Clinic found that women who had one or both ovaries removed prior to menopause had an increased long-term risk of dementia or cognitive impairment. However, those who underwent ovary removal, but also had estrogen treatment until at least age 50 did not experience this higher risk. These findings suggest that if taken before menopause, the neuroprotective benefits of estrogen may outweigh the risks of side effects, such as heart problems, stroke and cognitive impairment. Women of any age should consult with a physician about the individual risks and benefits of undergoing or considering hormone replacement therapy.

Antioxidants

Vitamin E may offer some protection against cell damage caused by free radicals. However, research has produced conflicting results and further rigorous scientific study will be needed to clarify the role of this antioxidant. Ongoing clinical trials are investigating whether vitamins E and C can slow the progression of AD. Another clinical trial is examining whether Vitamin E and/or selenium can prevent AD or cognitive decline. In April of 2005, the New England Journal of Medicine published results of a study that compared the use of vitamin E, Aricept (donepezil - an Alzheimer's disease treatment) and a placebo in delaying progression from mild cognitive impairment (MCI) to Alzheimer’s disease. People with MCI experience memory problems, but are able to function independently; however, MCI is often a transitional stage that leads to the serious cognitive decline of Alzheimer's disease. The study found that over the course of three years, none of the treatments affected the advance of the disease.

Ginkgo biloba

Ginkgo biloba, an extract from the leaves of the ginkgo tree, is said to have antioxidant and anti-inflammatory properties. It may also increase blood flow in the brain. However, the results of a large multicenter clinical trial led by the University of Pittsburgh School of Medicine, and published in the Journal of the American Medical Association in November of 2008, found that Ginkgo biloba does not reduce the risk of developing Alzheimer’s disease or dementia in either healthy older individuals or in those with mild cognitive impairment. A similar clinical trial is underway in Europe.

Omega-3 fatty acids

Omega-3 fatty acids are found mainly in “oily” fish such as salmon and albacore tuna, but are also present in certain nuts and oils. Scientists believe they may have a protective effect on the brain. Clinical trials are underway to test whether these fatty acids can slow the both cognitive and functional decline in those with mild to moderate AD.

Before taking any medications, over-the-counter drugs, supplements or herbs, visit a physician for a full medical evaluation. The American Health Assistance Foundation does not endorse any medications, vitamins or herbs. A qualified physician should make an informed decision based on each person's medical history and current prescriptions.

You may want to consider brain donation at a research institution near your home. As part of the donation process, the researchers will perform a brain autopsy, which is presently the only way of truly confirming a diagnosis of Alzheimer’s disease. Brain autopsies for an Alzheimer’s diagnosis can be expensive (they can cost as much as $1500 or more by some estimates), but this cost is covered by the research institution if you should choose to donate your husband’s brain (or brain tissue) to them. Generally, however, you will be responsible for any costs associated with the transport of your husband’s body, such as the cost of transporting the body to the research institution where the autopsy is performed, and then from the institution to the funeral home.

Brain donation is an invaluable gift to medical science, as it helps to provide insight into the anatomical and biochemical basis of dementia and Alzheimer’s disease. Most often, only a small sample is required, so the body is not disfigured in the autopsy process. If this is something that you are truly interested in, you should contact a program near you to find out more specific details and to begin the donation process. Because for research purposes it is important to perform the autopsy as soon as possible after death, many of the programs require that the necessary consent and arrangements be made in well in advance.

Some programs accepting brain donations include:

• Baylor College of Medicine Brain Donation Autopsy Program
• Boston University Alzheimer's Disease Center
• Northwestern University Brain Endowment program
• University of Pennsylvania Center for Neurodegenerative Disease Research

Additionally, a list of brain banks in several states that can perform postmortem diagnosis of Alzheimer's disease and may accept brain tissue for donation has been compiled by the Alzheimer Research Forum.

It is difficult to say how exactly Alzheimer’s disease (AD) will affect your employment (at least initially) because I do not know the details of your disease state or your job. Suffice to say, many people who have been diagnosed with the early onset form of AD (which typically afflicts patients under 65 years of age) and are in the early stages of the disease, continue to work for some time following their diagnosis, again depending on how rapidly the disease progresses and the nature of their employment. It is good to continue working for as long as you can, because it helps to provide a sense of normalcy and routine in your life. It is important that you do inform you boss of your diagnosis when you feel ready (preferably sooner rather than later); however, it may be important for you to obtain the input of an attorney specializing in these issues.*

Alzheimer’s disease is considered a disability and is therefore encompassed by the Americans with Disabilities Act (ADA). Therefore, your employer cannot fire you on account of your diagnosis alone. Under the ADA, your employer is obligated to provide reasonable accommodations to allow you to work, which may mean changing job titles or positions. For example, if your current position requires a high level of responsibility, then perhaps a more suitable position would be one with less accountability. If however, you employer has made a reasonable attempt to accommodate your disability but there really is nothing else they can give you to do and/or you can no longer fulfill the requirements of the job, then your employer may ask you to leave. You do not want to be a potential liability to your employer, so it is a good idea sit down with your boss initially and then periodically to reassess your health status and your role/position within the company.

You and your physician can determine when would be the best time for you to leave your job, such as when you can no longer reasonably perform the functions associated with your job. Clearly, if any injury or harm could come to yourself or others as a direct result of your not being able to satisfy the job requirements (such as if you are a pilot, pharmacist, bus driver, or machinist, for example), then you may want to consider finding a different job with less responsibility. As for your primary caregiver, the Family Medical Leave Act (FMLA) will allow your caregiver to take up to 12 weeks of unpaid, job-protected leave per year to care for a disabled or incapacitated relative. Your caregiver must be considered an "eligible" employee, meaning he or she must have worked for his or her employer for at least 12 months (or 1,250 hours), and the employer must employ at least 50 employees at the caregiver’s worksite or within 75 miles of the worksite. For more information on FMLA, please see the Department of Labor.

*If you would like to obtain the input of an attorney, please contact Eldercare Locator, which is a public service of the Administration on Aging, a Department of Health and Human Services and is a nationwide service that connects older Americans and their caregivers with information on senior services. Their toll-free number is 1-800-677-1116; they can provide you with direction in finding resources in your community.

Several independent research studies have reported an association between high cholesterol serum levels and Alzheimer’s disease. Consistent with these reports, other research findings also suggest that the best way to lower your risk of developing Alzheimer’s disease involves a combination of measures normally thought of as good for maintaining a healthy heart, such as eating a healthy diet low in saturated and trans-fats, exercising regularly, reducing stress, and of course, lowering serum cholesterol levels.

Primidon (trade name: Primidone) is an antiepileptic agent currently only indicated for the treatment of seizures, seizure disorders, and essential tremor (such as is found in patients with Parkinson’s disease).

Unfortunately, there are no formal studies that have looked at the combined effects of these drugs on the treatment of AD or PD. This is mostly due to the fact that the patient population that could potentially benefit from the combined use of both of these drugs—i.e., patients having dementia associated with Parkinson’s disease—is relatively small compared to the larger general group of patients having Alzheimer’s disease, non-dementia-associated PD, and other neurodegenerative diseases and disorders.