Several drugs are currently FDA-approved to treat Alzheimer's disease. At best, these drugs lead to only modest improvements in the cognitive functions of patients; none can stop the destruction of brain cells that underlies the illness.
Michele Norris surveys the current treatment landscape with Jerry Yesavage of Stanford University's Alzheimer's Disease Center.
Facts about Alzheimer's Disease
Alzheimer's disease gradually destroys brain cells, extinguishing a person's memory and ability to learn, reason, communicate and care for themselves. The disease advances at different rates, lasting from three to 20 years.
The first symptoms people notice are often forgetfulness and confusion, progressing to profound memory loss, language problems and difficulty performing everyday tasks.
Scientists believe that by the time symptoms emerge, brain damage has already begun. As Alzheimer's progresses, sufferers may exhibit changes in their personality, such as anxiety, suspiciousness or agitation, delusions or hallucinations.
Eventually, the loss of brain function will kill an Alzheimer's patient, even if that person isn't otherwise seriously ill.
There's no single cause of Alzheimer's disease. The most common form of the illness is late-onset Alzheimer's, which mainly affects people over age 65. The risk of developing the late-onset disease increases with age and family history of the disease. Scientists have also discovered one gene that boosts the risk.
Rare types of Alzheimer's linked to specific genes have been found in a few hundred families around the world. Individuals who inherit the genes are almost certain to develop the disease, sometimes as early as their 30s.
Alzheimer's has no known cure, but preliminary evidence suggests that controlling blood pressure, weight and cholesterol levels, keeping mentally and physically fit and staying socially active may help reduce the risk of developing the disease.
Scientists regard two different brain abnormalities as hallmarks of Alzheimer's disease — "plaques" and "tangles." Plaques are protein deposits on the outside of brain cells that result from a protein called beta-amyloid. Tangles are deadly, twisted strands of another protein (called tau) that form inside brain cells.
Alzheimer's researchers disagree on whether plaques or tangles are the primary cause of the disease. However, research over the past couple of years has suggested that plaques outside of brain cells may trigger an enzyme inside the cells that in turn causes tau proteins to form tangles.
There is no cure for Alzheimer's disease. Today's treatments can at best slow the progress of the disease and help stabilize symptoms temporarily. None of the drugs currently FDA-approved to treat Alzheimer's can prevent the deterioration of brain cells, nor can they stop the downhill decline of the illness over time. Prescription medications to treat Alzheimer's include:
— Cholinesterase Inhibitors: Cholinesterase inhibitors are designed to prevent the breakdown of acetylcholine, a chemical messenger important for memory and other cognitive functions, and keep levels high even when the cells that produce it degenerate or die.
Of this class of drugs, the most commonly prescribed are donepezil (Aricept); rivastigmine (Exelon) and galantamine (Reminyl). About half the people taking these drugs experience a modest improvement in memory and other thinking skills.
— Memantine: Approved for the treatment of moderate to severe Alzheimer's in late 2003, Memantine (trade name Namenda) appears to work by regulating glutamate, a specialized messenger chemical in the brain that plays an essential role in memory, learning, and the processing, storage and retrieval of information.
Memantine is classified as an "uncompetitive low-to-moderate affinity N-methyl-D-aspartate" (NMDA) receptor antagonist. Too much glutamate overstimulates NMDA receptors, allowing too much calcium into nerve cells and leading to cell death. Memantine may protect cells against excess glutamate by partially blocking NMDA receptors.
Several clinical trials are investigating treatment strategies for Alzheimer's disease. Results of a small but promising study released Monday suggest that antibodies derived from human blood can halt or even reverse Alzheimer's disease.
The findings are the result of a phase I trial, which assesses a treatment's safety. In the study, patients received immunoglobulin, a product of human blood derived from plasma and containing antibodies — the proteins that protect the body against disease.
Eight study patients were administered immunoglobulin by infusion through a vein, a process that takes several hours. Researchers found that the antibodies in the immunoglobulin can trap beta-amyloid proteins and help improve patients' thinking abilities. Beta-amyloid proteins cause the telltale plaques in the brains of Alzheimer's patients that are believed to be a prime cause of the disease.
So far, seven of the patients in the study have undergone cognitive testing after six months of therapy. Cognitive function stopped declining in all seven patients and actually improved in six of them.
Still, the researchers — from New York-Presbyterian Hospital and Weill Cornell Medical Center — warn that it is much too early to hail intravenous immunoglobin as anything more than promising, though they say the findings do suggest the value of a larger, phase II trial. They do not recommend that doctors begin treating Alzheimer's patients with the technique.
Intravenous immunoglobin is FDA-approved for treating immune disorders in children. It is NOT currently approved to treat Alzheimer's disease.
In 1999, research in mice showed that antibodies could block the plaque-causing effects of the beta-amyloid proteins. The news prompted a flurry of research into a potential Alzheimer's vaccine.
In 2002, researchers halted an Alzheimer's vaccine trial in Europe. The vaccine caused the body to produce its own antibodies to attack the protein, but several patients died from swelling in the brain.
But a year after the trial was stopped, a follow-up study of 30 patients in that trial found that, in patients who developed antibodies against the amyloid deposits, Alzheimer's appeared to have stabilized rather than progressed.