Frequently Asked Questions

Yes, while there is no cure for Alzheimer's disease as yet, there are medications that can help control its symptoms and to help manage conditions such as agitation, depression, or psychosis (hallucinations or delusions), which may occur as the disease progresses:

Cholinesterase inhibitors: People with Alzheimer’s disease have low levels of a key nerve messenger, called acetylcholine, believed to be important for memory and thinking. Four drugs called cholinesterase inhibitors make more of that messenger available by slowing its breakdown, enabling greater cell-to-cell communication and slowing the progress of cognitive impairment in some patients with early- to middle-stage Alzheimer’s disease. The four cholinesterase inhibitors are:

• Razadyne® (galantamine)
• Exelon® (rivastigmine)
• Aricept® (donepezil)
• Cognex® (tacrine)

All four have been approved by the Food and Drug Administration (FDA) for early- to middle-state Alzheimer’s disease; Aricept® is also approved for severe-stage symptoms. Cognex® was the first approved cholinesterase inhibitor but is rarely prescribed today due to safety concerns.

Namenda® (memantine) The first FDA-approved drug for moderate to severe Alzheimer’s disease, Namenda is thought to protect brain cells by regulating a nerve communication chemical, called glutamate, that is released in great quantities by Alzheimer’s-damaged cells. Glutamate is normally involved with learning and memory, but when released in excess by damaged cells, it attaches to “docking sites” called NMDA receptors that in turn accelerate cell damage.

Treatment for mental illnesses People with the later stages of Alzheimer’s disease often experience depression, agitation, paranoia, delusions, and/or hallucinations, which can in turn cause screaming, repetitive questions, hoarding, pacing, hyperactivity, and aggressive behavior.

These symptoms can arise from non-medical triggers as well as medical causes. The former could take the form of a change in the person’s environment (a new place to live, a new caretaker, a change in routine) or from frustration at the inability to communicate. If the trigger can be identified, the environment can be modified to change the behavior.

If non-medical intervention doesn’t work, or the patient becomes a danger to himself or others, a physician should be asked to evaluate the need for medical treatment.

Sources for financial assistance for Alzheimer’s disease prescription drugs can be found at www.ahaf.org/alzheimers/resources/alzheimers-disease.html. Always consult a physician before taking any medications.

Familial Alzheimer’s disease (FAD) or early-onset Alzheimer’s is an inherited, rare form of the disease, affecting less than 10 percent of Alzheimer’s disease patients. FAD develops before age 65, in people as young as 35. It is caused by one of three gene mutations on chromosomes 1, 14 and 21. If even one of these mutated genes is inherited from a parent, the person will almost always develop FAD. All offspring in the same generation have a 50/50 chance of developing FAD if one parent has it.

The majority of Alzheimer’s disease cases are late-onset, usually developing after age 65. Late-onset Alzheimer’s disease has no known cause and shows no obvious inheritance pattern. However, in some families, clusters of cases are seen. Although a specific gene has not been identified as the cause of late-onset Alzheimer’s disease, genetic factors do appear to play a role in the development of this form of the disease. A gene called Apolipoprotein E (ApoE) appears to be a risk factor for the late-onset form of AD. There are three forms of this gene: ApoE2, ApoE3 and ApoE4. Roughly one in four Americans has ApoE4 and one in twenty has ApoE2. While inheritance of ApoE4 increases the risk of developing AD, ApoE2 substantially protects against the disease.

Scientists believe that several other genes may influence the development of Alzheimer’s disease. Two of these genes, UBQLN1 and SORL1, are located on chromosomes 9 and 11. Researchers have also identified three genes on chromosome 10, one of which produces an insulin degrading enzyme that may contribute to the disease. A gene, called TOMM40, appears to significantly increase one’s susceptibility to developing Alzheimer’s when other risk factors are present, such as having the ApoE-4 gene. Several recently discovered genes that influence Alzheimer’s disease risk are CLU (also called APOJ) on chromosome 8, which produces a protein called clusterin, PICALM on chromosome 11 and CR1 on chromosome 1.

Genetic risk factors alone are not enough to cause the late-onset form of Alzheimer’s disease, so researchers are actively exploring education, diet and environment to learn what role they might play in the development of this disease.

Pre-symptomatic Physical conditions connected to Alzheimer’s disease exist in a person’s body long before symptoms are evident. State-of-the-art equipment is being developed to detect subtle signs of Alzheimer’s prior to noticeable memory loss. From the patient’s perspective, Alzheimer’s disease can be described in three general stages of progression:

Mild (stage 1) In addition to minor memory loss and difficulty learning, first-stage Alzheimer’s disease may cause a loss of energy and spontaneity, as well as mood swings, confusion, trouble communicating, and difficulty organizing. Those with Alzheimer’s disease may become withdrawn, avoiding new people and places in preference of the familiar. Understandably, they can also become angry and frustrated.

Moderate (stage 2) During the second stage of Alzheimer’s disease, the patient begins to need help carrying out anything but simple tasks. Recent events and personal histories may be lost and the present confused with the past. There may be difficulty recognizing familiar people, as well as in speaking, reading, writing, and dressing, and difficulty sleeping well. A person with moderate Alzheimer’s disease is clearly becoming disabled.

Severe (stage 3) Third-stage Alzheimer’s disease brings full-blown disability, with possible loss of the ability to feed oneself, to speak, to recognize people, and to control bodily functions. Memory weakens still further and may nearly disappear. The patient’s weakened physical state creates vulnerability to other diseases and breathing problems, especially for those confined to bed.

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.

If you visit a new doctor, bring your medical records; for any doctor, bring a list of over the counter and prescription medicines you are currently taking. If you don't know the names of the drugs, bring the pill bottles with you. A medication or a combination of medications can sometimes cause symptoms that resemble Alzheimer's disease. Also make a list of current medical problems. It's a good idea to show the doctor a list of symptoms, behaviors and any problems carrying out routine activities (for example, paying bills) in yourself or your loved one that concern you.

While an autopsy can confirm the presence of the disease, skilled physicians can correctly diagnose Alzheimer’s disease about 90 percent of the time based on mental and behavioral symptoms, a physical examination, and neuropsychological and laboratory tests. Scientists have recently developed a number of new biomarker and brain scanning techniques that may help to improve diagnosis.

Mentally, having trouble following instructions, losing one’s orientation, displaying poor judgment, and having difficulty managing money, shopping, or driving are all possible symptoms of Alzheimer’s disease.

The physical exam will usually include a general physical, blood tests, and urinalysis. The doctor can use such test results to eliminate other forms of dementia—for instance, certain vitamins and hormones can provoke symptoms of dementia if they are present in too little a quantity. Brain scans can rule out non-Alzheimer’s disease dementia and can reveal structural changes present in Alzheimer’s disease.

The physician will determine whether neuropsychological testing is called for to examine memory, attention, math calculations, language and other intellectual functions.

The place to start is with one’s own physician, who may then suggest specialists to do further testing.

On average, patients with Alzheimer's disease live for 8 to 10 years after diagnosis. However, this terminal disease can last for as long as 20 years.

There is a test currently available that can identify which forms of apolipoprotein (ApoE) are present in the blood. One form, ApoE4, is associated with an already well-studied condition, heart disease, and appears to increase the risk of developing Alzheimer’s as well. However, this blood can only detect whether ApoE4 is present, not if and when the person will develop Alzheimer's.

In 2007, researchers at Stanford University published some promising study results in which 18 blood proteins (and resultant chemical signals) were tested to determine the risk of advancement from mild cognitive impairment (MCI) to Alzheimer’s disease. In the study, the scientists were able to predict whether the subjects would progress to Alzheimer’s with 90% accuracy. However, this study tested a relatively small number of people, and larger studies will need to be undertaken.