Alzheimer’s disease (AHLZ-high-merz) is a progressive brain disorder that gradually destroys a persons memory and ability to learn, reason, make judgments, communicate and carry out daily activities.
As Alzheimer’s progresses, individuals may also experience changes in personality and behavior, such as anxiety, suspiciousness or agitation, as well as delusions or hallucinations.
Although there is currently no cure for Alzheimer’s, new treatments are on the horizon as a result of accelerating insight into the biology of the disease. Research has also shown that effective care and support can improve quality of life for individuals and their caregivers over the course of the disease from diagnosis to the end of life.
Alzheimer’s is the leading cause of dementia, a group of conditions that all gradually destroy brain cells and lead to progressive decline in mental function. Vascular dementia, another common form, results from reduced blood flow to the brains nerve cells. In some cases, Alzheimer’s disease and vascular dementia can occur together in a condition called “mixed dementia.” Other causes of dementia include frontotemporal dementia, dementia with Lewy bodies, Creutzfeldt-Jakob disease and Parkinson’s disease. Progression of Alzheimer’s disease.
Alzheimer’s disease advances at widely different rates. The duration of the illness may often vary from 3 to 20 years. The areas of the brain that control memory and thinking skills are affected first, but as the disease progresses, cells die in other regions of the brain. Eventually, the person with Alzheimer’s will need complete care. If the individual has no other serious illness, the loss of brain function itself will cause death.
Experts have documented common patterns of symptom progression that occur in many individuals with Alzheimer’s disease and developed several methods of staging based on these patterns. Progression of symptoms corresponds in a general way to the underlying nerve cell degeneration that takes place in Alzheimer’s disease.
Nerve cell damage typically begins with cells involved in learning and memory and gradually spreads to cells that control every aspect of thinking, judgment, and behavior. The damage eventually affects cells that control and coordinate movement.
Staging systems provide useful frames of reference for understanding how the disease may unfold and for making future plans. But it is important to note that all stages are artificial benchmarks in a continuous process that can vary greatly from one person to another. Not everyone will experience every symptom and symptoms may occur at different times in different individuals. People with Alzheimer’s live an average of 8 years after diagnosis, but may survive anywhere from 3 to 20 years.
The framework for this section is a system that outlines key symptoms characterizing seven stages ranging from unimpaired function to very severe cognitive decline.
Within this framework, we have noted which stages correspond to the widely used concepts of mild, moderate, moderately severe, and severe Alzheimer’s disease. We have also noted which stages fall within the more general divisions of early-stage, mid-stage, and late-stage categories.
Early-stage Alzheimer’s can be diagnosed in some, but not all, individuals with these symptoms. Friends, family, or co-workers begin to notice deficiencies. Problems with memory or concentration may be measurable in clinical testing or discernible during a detailed medical interview. Common difficulties include:
At this stage, a careful medical interview detects clear-cut deficiencies in the following areas:
Major gaps in memory and deficits in cognitive function emerge. Some assistance with day-to-day activities becomes essential. At this stage, individuals may:
Memory difficulties continue to worsen, significant personality changes may emerge, and affected individuals need extensive help with customary daily activities. At this stage, individuals may:
This is the final stage of the disease when individuals lose the ability to respond to their environment, the ability to speak, and, ultimately, the ability to control movement.
The primary symptoms of Alzheimer’s disease include memory loss, disorientation, confusion, and problems with reasoning and thinking. These symptoms worsen as brain cells die and the connections between cells are lost. Although current drugs cannot alter the progressive loss of cells, they may help minimize or stabilize symptoms. These medications may also delay the need for nursing home care.
The U.S. Food and Drug Administration (FDA) has approved two classes of drugs to treat cognitive symptoms of Alzheimer’s disease. The first Alzheimer medications to be approved were cholinesterase (KOH luh NES ter ays) inhibitors. Three of these drugs are commonly prescribed donepezil (Aricept), approved in 1996; rivastigmine (Exelon), approved in 2000; and galantamine (Reminyl), approved in 2001. Tacrine (Cognex), the first cholinesterase inhibitor, was approved in 1993 but is rarely prescribed today because of associated side effects, including possible liver damage.
All of these drugs are designed to prevent the breakdown of acetylcholine (pronounced a SEA til KOH lean), a chemical messenger in the brain that is important for memory and other thinking skills. The drugs work to keep levels of the chemical messenger high, even while the cells that produce the messenger continue to become damaged or die. About half of the people who take cholinesterase inhibitors experience a modest improvement in cognitive symptoms.
Memantine (Namenda) is a drug approved in October 2003 by the FDA for treatment of moderate to severe Alzheimer’s disease. Memantine is classified as an uncompetitive low-to-moderate affinity N-methyl-D-aspartate (NMDA) receptor antagonist, the first Alzheimer drug of this type approved in the United States. It appears to work by regulating the activity of glutamate, one of the brains specialized messenger chemicals involved in information processing, storage and retrieval.
Glutamate plays an essential role in learning and memory by triggering NMDA receptors to allow a controlled amount of calcium to flow into a nerve cell, creating the chemical environment required for information storage.
Excess glutamate, on the other hand, overstimulates NMDA receptors to allow too much calcium into nerve cells, leading to disruption and death of cells. Memantine may protect cells against excess glutamate by partially blocking NMDA receptors.
Vitamin E supplements are often prescribed as a treatment for Alzheimer’s disease, because they may help brain cells defend themselves from attacks Normal cell functions create a byproduct a called free radical, a kind of oxygen molecule that can damage cell structures and genetic material. This damage, called oxidative stress, may play a role in Alzheimer’s disease.
Cells have natural defenses against this damage, including the antioxidants vitamins C and E, but with age some of these natural defenses decline.
Research has shown that taking vitamin E supplements may offer some benefit to people with Alzheimer’s.
Most people can take vitamin E without side effects. However, any change in medications should first be discussed with a primary care physician because all medication can cause side effects or interactions with other medications. A person taking blood-thinners, for example, may not be able to take Vitamin E or will need to be monitored closely by a physician.