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