Alzheimer' s drugs currently on the market can slow the disease, but there is still no cure. Nearly all major pharmaceutical companies in the United States are racing to find one, but since the cause of Alzheimer's is still a mystery, scientists aren't sure where in the brain to aim treatment. In this excerpt from an article in our Health After 50 newsletter, Johns Hopkins discusses therapies in the pipeline that attack amyloid plaques as a way to stall Alzheimer's.
Doctors know that structural changes occur in the brains of Alzheimer 's patients, but researchers are debating a "chicken-or-the-egg" question: Do these neurological abnormalities cause Alzheimer's, or does Alzheimer's cause them?
-
The answer has dramatic implications for treatment: If the neurological markers that researchers have identified cause Alzheimer's, reversing them may stop Alzheimer's. But if they're merely the result of Alzheimer's, then treating them may not address the root of the problem. It's possible that multiple causes are at play in this complex condition, so there may be more than one way to treat Alzheimer's.
One of these neurological changes is the buildup of amyloid plaques, which are clusters of aberrant proteins found in the brains of all Alzheimer's patients. Many scientists believe going after these plaques will stall dementia. For example …
- In 2008, researchers began testing a vaccine, called bapineuzumab. The vaccine did not turn out to be as effective as researchers had hoped, but it was safe and may slow cognitive decline in patients without the APOE ε4 gene (an inherited genetic variant in 30–45% of patients with Alzheimer's disease). Additional trials are under way.
- Another new therapy that goes after amyloid plaque is tramiprosate (Alzhemed). This anti-inflammatory drug binds to amyloid fragments before they stick together to form plaque, but as of yet, clinical trials haven't shown the drug slows Alzheimer's.
- An alternative tactic against amyloid buildup is targeting the enzymes beta-and gamma-secretase. These enzymes "cut" a large protein known as beta-amyloid precursor protein into toxic fragments that accumulate into plaques. An antienzyme drug currently under investigation, called LY450139, reduced the presence of amyloid in the blood of Alzheimer's patients -- but levels rose again after initial doses. More trials are under way, and the results should come out some time in the next two years.
What now? Families who want access to the most cutting-edge therapies often wonder if they should enroll their relatives with Alzheimer's into clinical trials. One study has shown that trial participants with dementia stay out of nursing homes longer than patients receiving standard care, even when the experimental drugs don't work -- possibly because study participants benefit substantially from the frequent, high-quality medical attention. The bottom line: Since there currently is no cure for Alzheimer's, experimental therapies may be a good bet.
For more information on clinical trials and Alzheimer’s treatment options, contact: Johns Hopkins Alzheimer’s Disease Research Center – 410-502-5164 or http:www.alzresearch.org
