* Alzheimer’s disease is a brain disease of unknown cause that leads to dementia.

* Most patients with Alzheimer’s disease are over 65 years of age.

* There are 10 classic warning signs of Alzheimer’s disease: memory loss, difficulty performing familiar tasks, problems with language, disorientation to time and place, poor or decreased judgment, problems with abstract thinking, misplacing things, changes in mood or behavior, changes in personality, and loss of initiative.
» Read more: Alzheimer’s Disease At A Glance

A variety of clinical research trials are underway with agents that try either to decrease the amount of Aβ1-42 produced or increase the amount of Aβ1-42 removed. It is hoped that such therapies may slow down the rate of progression of Alzheimer’s disease. As of June 2007, it is not known how well such therapies may work.
» Read more: Potential and future therapies for Alzheimer’s disease

Symptoms of Alzheimer’s disease include agitation, depression, hallucinations, anxiety, and sleep disorders. Standard psychiatric drugs are widely used to treat these symptoms although none of these drugs have been specifically approved by the FDA for treating these symptoms in patients with Alzheimer’s disease. If these behaviors are infrequent or mild, they often do not require treatment with medication. Non-pharmacologic measures can be very useful.
» Read more: Treatment of psychiatric symptoms

Glutamate is the major excitatory neurotransmitter in the brain. One theory suggests that too much glutamate may be bad for the brain and cause deterioration of nerve cells. Memantine (Namenda) works by partially decreasing the effect of glutamate to activate nerve cells.
» Read more: Partial glutamate antagonists

The management of Alzheimer’s disease consists of medication based and non-medication based treatments. Two different classes of pharmaceuticals are approved by the FDA for treating Alzheimer’s disease: cholinesterase inhibitors and partial glutamate antagonists. Neither class of drugs has been proven to slow the rate of progression of Alzheimer’s disease. Nonetheless, many clinical trials suggest that these medications are superior to placebos (sugar pills) in relieving some symptoms.

Cholinesterase inhibitors

In patients with Alzheimer’s disease there is a relative lack of a brain chemical neurotransmitter called acetylcholine. (Neurotransmitters are chemical messengers produced by nerves that the nerves use to communicate with each other in order to carry out their functions.) Substantial research has demonstrated that acetylcholine is important in the ability to form new memories. The cholinesterase inhibitors (ChEIs) block the breakdown of acetylcholine. As a result, more acetylcholine is available in the brain, and it may become easier to form new memories.

Four ChEIs have been approved by the FDA, but only donepezil hydrochloride (Aricept), rivastigmine (Exelon), and galantamine (Razadyne – previously called Reminyl) are used by most physicians because the fourth drug, tacrine (Cognex) has more undesirable side effects than the other three. Most experts in Alzheimer’s disease do not believe there is an important difference in the effectiveness of these three drugs. Several studies suggest that the progression of symptoms of patients on these drugs seems to plateau for six to 12 months, but inevitably progression then begins again.

Of the three widely used AchEs, rivastigmine and galantamine are only approved by the FDA for mild to moderate Alzheimer’s disease, whereas donepezil is approved for mild, moderate, and severe Alzheimer’s disease. It is not known whether rivastigmine and galantamine are also effective in severe Alzheimer’s disease, although there does not appear to be any good reason why they shouldn’t.

The principal side effects of ChEIs involve the gastrointestinal system and include nausea, vomiting, cramping, and diarrhea. Usually these side effects can be controlled with change in size or timing of the dose or administering the medications with a small amount of food. Between 75% and 90% of patients will tolerate therapeutic doses of ChEIs.

Alzheimer’s disease is invariably progressive. Different studies have stated that Alzheimer’s disease progresses over two to 25 years with most patients in the eight to 15 year range. Nonetheless, defining when Alzheimer’s disease starts, particularly in retrospect, can be very difficult. Patients usually don’t die directly from Alzheimer’s disease. They die because they have difficulty swallowing or walking and these changes make overwhelming infections, such as pneumonia, much more likely.
» Read more: What is the prognosis for a person with Alzheimer’s disease?

As of June 2007, there is no specific “blood test” or imaging test that is used for the diagnosis of Alzheimer’s disease. Alzheimer’s disease is diagnosed when: 1) a person has sufficient cognitive decline to meet criteria for dementia; 2) the clinical course is consistent with that of Alzheimer’s disease; 3) no other brain diseases or other processes are better explanations for the dementia.
» Read more: How is the diagnosis of Alzheimer’s disease made?

The biggest risk factor for Alzheimer’s disease is increased age. The likelihood of developing Alzheimer’s disease doubles every 5.5 years from 65 to 85 years of age. Whereas only 1%-2% of individuals 70 years of age have Alzheimer’s disease, in some studies around 40% of individuals 85 years of age have Alzheimer’s disease. Nonetheless, at least half of people who live past the 95 years of age do not have Alzheimer’s disease.
» Read more: What are risk factors for Alzheimer’s disease?

The cause(s) of Alzheimer’s disease is (are) not known. The “amyloid cascade hypothesis” is the most widely discussed and researched hypothesis about the cause of Alzheimer’s disease. The strongest data supporting the amyloid cascade hypothesis comes from the study of early-onset inherited (genetic) Alzheimer’s disease. Mutations associated with Alzheimer’s disease have been found in about half of the patients with early-onset disease.
» Read more: What are causes of Alzheimer’s disease?

The criteria for dementia are conservative meaning that a patient must have had considerable decline in the ability to think before a diagnosis of dementia is appropriate. The progression of Alzheimer’s disease is so insidious and slow that patients go through a period of decline where their memory is clearly worse than its baseline, yet they still do not meet criteria for dementia. This transitional syndrome is called Mild Cognitive Impairment (MCI). Individuals affected with MCI have cognitive impairment that is demonstrated on formal neuropsychological testing but are still able to function well. Formal neuropsychological testing usually means that the patient is administered a battery of standardized tests of memory and thinking. Some of these tests are something like the IQ tests we may have taken in school. When these tests were developed they were administered to hundreds or thousands of people so that statistics are available to say how a person’s score compares to a sample of healthy persons of the same age. If a person scores in the top 50%, it means that he or she did better than at least 50% of other normal people who took the test. Persons with lower scores – often in the bottom 7% – are considered to have MCI.

There are several forms of MCI. Perhaps the most common is associated with impairment in memory but not in the ability to plan and reason. Persons with this type called “amnestic MCI” (amnestic comes from “amnesia” and means no memory) have a high risk of developing Alzheimer’s disease over the next few years. Persons with preserved memory but impaired reasoning or impaired judgment (call non-amnestic MCI) have a lower risk of developing Alzheimer’s disease.

As treatments are developed that decrease the risk of developing Alzheimer’s disease or slow its rate of progression (as of June 2007, no such medication has been approved by the FDA), recognition of amnestic MCI will be increasingly important. It is hoped that medications will be developed that will slow the rate of progression of MCI to Alzheimer’s disease or completely prevent the development of Alzheimer’s disease.