Alzheimer's disease is a notoriously difficult cognitive disorder to deal with. For people in the advanced stages of the disease, little other than providing supportive care and memory care can be done — there is no known cure and, to date, no known medicine that could be given to reliably slow its advance.
Nearly 5 million American seniors have Alzheimer's today, and as the Baby Boom generation reaches retirement, that number is expected to grow.
By 2025, according to the Alzheimer's Association, over 13 million Americans will be living with the disease, unless an effective treatment or preventative measure can be found. But there is some hope: human trials for a preventative medication are now underway.
Amyloid plaques and their relationship to advanced dementia.
Although the cause of Alzheimer's disease isn't understood, researchers have noted that patients with advanced disease exhibit collections of amyloid plaques, a type of misfolded protein molecule, in their brains.
Again, scientists have few clues why amyloids develop— random byproducts of a relatively chaotic system, genetics, cell damaged from infection by disease pathogens or exposure to radiation, harmful chemicals and other environmental stimuli.
Like bad cholesterol in the cardiovascular system, amyloids do not dissolve in water, as they tend to stick together when they come into contact with one another. There are many types of amyloids, but beta amyloids are associated with Alzheimer's.
As the beta amyloid proteins aggregate into larger and larger particles, they can form big clumps, called "plaques" along interior surfaces of the brain. This changes the structure of the tissue and disrupts the normal function of the brain.
The question science has not yet been able to answer is a chicken-and-egg scenario: does the presence of beta amyloid plaques in the brain cause Alzheimer's disease or are beta amyloid plaques a byproduct of a disease process that also causes Alzheimer's?
Indeed, not everyone who develops beta amyloid plaques in the brain will exhibit dementia symptoms. But they are certainly present in all Alzheimer's patients.
A new drug may help the body to clear amyloids before they can form plaques.
If you have high cholesterol, your doctor may have prescribed a type of medication called a "statin," such as Crestor or Lipitor, to help your body to clear LDL ("bad" cholesterol) from your blood. A new drug now in human trials may yield a similar benefit for people with elevated beta amyloid levels.
Developed by Eli Lily, solanezumab showed little benefit for patients with severely advanced Alzheimer's disease in a study published in 2012. But clinical researchers did note that patients with only early signs of Alzheimer's who participated in the trial did seem to do better, with a reported 30% decline in their rate of memory loss.
That surprising result was enough to get researchers thinking: what if solanezumab could be used not to treat, but to prevent Alzheimer's by inhibiting the formation of amyloid plaques altogether?
If beta amyloid plaques are in fact the cause of Alzheimer's, then a drug that would prevent them from doing so may prevent the disease. In a sense, researchers may be able to begin answering the Alzheimer's cause question by seeing if they can prevent plaques from forming.
Volunteer participants are now being screened.
Researchers at 61 medical centers in the United States, Canada and Australia— including locally at the University of Kentucky in Lexington, Case Western Reserve in Cleveland and Indiana University— are now in the process of indentifying and screening potential study participants in a new trial of solanezumab called the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s study, or simply "A4."
Approximately 1,000 people aged 65-84, with normal memory and no unstable disease, will be registered for a double-blind trial that will attempt to determine whether solanezumab can prevent beta amyloid plaque formation in the brain. Volunteers are needed for screening, but seniors who are already in skilled nursing care are not eligible.
Researchers hope that the drug will prove to be an effective preventative measure that healthy seniors could take, like anti-cholesterol statins, to prevent the development of later disease. With no known way to reverse structural brain damage caused by Alzheimer's, "our best chance of really changing the disease is to start treatment before people have symptoms,” according to A4 lead researcher Reisa Sperling, a professor of neurology at Harvard Medical School.
If the drug is effective in preventing beta amyloid plaque formation, it will be truly interesting to see whether or not study participants develop Alzheimer's disease anyway— this would answer the question of whether or not amyloid plaques are to blame for the disease or are merely a byproduct of it.
Either way, the trial has exciting potential to make a significant impact on senior health and dementia research.
