Two new studies report solanezumab may hold promise for Alzheimer’s patients
The combined results from two studies of solanezumab suggest it might modestly slow mental decline in Alzheimer’s patients, particularly in those with mild disease. The findings were presented on October 8 at the annual American Neurological Association conference, which runs from October 7 through 9 in Boston, Massachusetts.
The findings from each study did not show significant benefit from the experimental medication, which is being developed by Eli Lilly & Co; however, over a period of 18 months, the pooled results found 34% less decline in mild Alzheimer's patients compared to those on a placebo. The researchers caution that the results do not appear strong enough to win FDA approval at present; however, they provide evidence that investigators are on the right track in their quest for medicines that will clear the damaging deposits that clog the brain.
Solanezumab is one of three drugs in late-stage testing that seek to alter the course of Alzheimer's. The two studies each had about 1,000 patients, about two-thirds with mild disease and one-third with moderately severe Alzheimer's, in 16 countries. Their average age was 75.
The main outcome measure of one study was the evaluation of language, memory, and thinking; the other examined the ability to perform daily activities such as eating and grooming. The combined results on the mild disease patients showed a nearly 2-point difference in the roughly 90-point score on thinking abilities. “It's a small difference,” noted Dr. Rachelle Doody of Baylor College of Medicine at the conference. She added, however, “you slow the decline with the drug.” Dr. Doody heads a nationwide research network funded by the National Institute on Aging that did an independent analysis of the pharmaceutical manufacturers results. A Lilly official said the company will discuss further research with the FDA.
Dementia is a loss of brain function that occurs with certain diseases. Alzheimer's disease is one form of dementia that gradually worsens over time. It affects memory, thinking, and behavior. Memory impairment, as well as problems with language, decision-making ability, judgment, and personality, are necessary features for the diagnosis. Age and family history are risk factors for Alzheimer’s disease. The risk rises with age; however, developing Alzheimer's disease is not a part of normal aging. Having a close blood relative, such as a brother, sister, or parent who developed the disease increases one’s risk. Having certain combination of genes for proteins that appear to be abnormal in Alzheimer's disease also increases your risk.
Other risk factors that are not as well proven include:
- Longstanding high blood pressure
- History of head trauma
- Female gender
There are two types of AD: early onset and late onset. In early onset AD, symptoms first appear before age 60. Early onset Alzheimer’s is much less common than late onset. However, it tends to progress rapidly. Early onset disease can run in families. Several genes have been identified. Late onset Alzheimer’s, the most common form of the disease, develops in individuals age 60 and older. Late onset Alzheimer’s may run in some families, but the role of genes is less clear.
The cause of the disease is not entirely known; however, it is thought to include both genetic and environmental factors. A diagnosis of AD is made when certain symptoms are present, and by making sure other causes of dementia are not present. The only way to know for certain that someone has Alzheimer’s is to examine a sample of their brain tissue after death. The following changes are more common in the brain tissue of individuals with the disease:
- Neurofibrillary tangles: twisted fragments of protein within nerve cells that clog up the cell.
- Neuritic plaques: abnormal clusters of dead and dying nerve cells, other brain cells, and protein.
- Senile plaques: areas where products of dying nerve cells have accumulated around protein.
When nerve cells (neurons) are destroyed, there is a decrease in the chemicals that help nerve cells send messages to one another (called neurotransmitters). As a result, areas of the brain that normally work together become disconnected. The buildup of aluminum, lead, mercury, and other substances in the brain is no longer believed to be a cause of the disease.
Reference: American Neurological Association