A medication used to treat the symptoms of mild-to-moderate Alzheimer disease may actually do more – it may be able to delay progression of the disorder, according to a study conducted at the Indiana University School of Medicine. The study, which appears in the June issue of Archives of Neurology, enabled researchers to evaluate a change in cognition observed in patients who prematurely discontinued treatment with placebo or Exelon ? (rivastigmine tartrate), a medication prescribed for many patients.
From Indiana University:Medication may slow progression of Alzheimer disease
A medication used to treat the symptoms of mild-to-moderate Alzheimer disease may actually do more – it may be able to delay progression of the disorder, according to a study conducted at the Indiana University School of Medicine.
The study, which appears in the June issue of Archives of Neurology, enabled researchers to evaluate a change in cognition observed in patients who prematurely discontinued treatment with placebo or Exelon ? (rivastigmine tartrate), a medication prescribed for many patients.
“If Exelon only had an effect on the symptoms of the disease, we would have expected rapid deterioration in patients’ cognition to the level observed in the placebo group after treatment withdrawal, but that was not the case with this study,” notes Martin Farlow, M.D., professor of medicine at the IU School of Medicine and director of the Alzheimer Clinic at Indiana University Hospital.
So what did Dr. Farlow, principal investigator and lead author of the study, and his colleagues discover?
“We found that patients who received Exelon before withdrawing from the study showed significantly less cognitive decline than placebo-treated patients, suggesting a possible effect in delaying the biological progression of Alzheimer’s.”
At 26 weeks after discontinuing treatment, the patients who initially had used the medication showed less cognitive decline than patients who had stopped taking the dummy medication.
Exelon is a cholinesterase inhibitor, a laboratory-produced agent designed to enhance memory and other cognitive functions by influencing certain chemical activities in the brain. One particular chemical – acetylcholine – is released by one brain cell to transmit a message to another cell. Once a message is received, enzymes are broken down for reuse.
In the Alzheimer-afflicted brain, the cells using acetylcholine are damaged or destroyed, resulting in lower levels of the chemical messenger.
“Cholinesterase inhibition is the most extensively researched and best therapeutic approach for the symptomatic treatment of Alzheimer disease, providing clinical benefits presumably through an increase of acetylcholine levels and enhancing neurotransmission,” Dr. Farlow said.
Alzheimer disease is a neurodegenerative disorder – and the most common form of dementia – mainly characterized by the progressive and irreversible loss of nerve cells located in specific brain areas. It attacks the brain and results in impaired memory, thinking and behavior. There is no known cure for this disease, which affects four million in the United States and more than 10 million worldwide.
