Washington state researchers have developed a new Alzheimer's drug that works differently from current treatments. They designed it to actually repair damage that has already occurred to a patient's brain.
Current treatments function in one of two ways, according to Medical News Today. They either retard cell death or act as inhibitors of cholinesterase, an enzyme experts believe breaks down a major neurotransmitter linked to learning and memory. Their objective is slowing the progress of the illness.
The findings on the new drug were published in the Journal of Pharmacology and Experimental Therapeutics. The lead authors were Joe Harding, a medicinal chemist at Washington State University's College of Veterinary Medicine, and Jay Wright, a neuroscientist at the College of Arts and Sciences.
The Alzheimer's Association estimates that Alzheimer's disease -- the most common form of dementia -- will cost American society $200 billion in 2012. Some 5.4 million Americans have this debilitating disorder. By 2050, experts expect the number to soar to 16 million.
The U.S. pharmaceutical industry has tried for years to find an effective treatment. According to the Pharmaceutical Research and Manufacturers of America, between 1998 and 2011, only three of 104 prospective medications were approved to treat Alzheimer's patients.
The drug developed by the Washington researchers, Dihexa, has restored brain function in rats in two distinct environments. It must get the blessing of the U.S. Food and Drug Administration before clinical trials in humans can begin. The cost for just safety testing could exceed $1 million.
Harding and Wright started working on Dihexa's predecessors in 1992. Earlier versions lacked practical application, since there was no way to deliver them across the blood-brain barrier, a cellular wall that prevents drugs from entering the brain. The researchers then created a smaller molecule that should work in pill form.
Scientists have known for some time that the key to creating neuron connections in the human brain is brain-derived neurotrophic factor (BDNF). Autopsies have shown lower-than-normal levels of BDNF in the brains of Alzheimer's patients.
The Washington researchers concluded that it would take 10 million times as much BDNF as Dihexa to create the same amount of new synapses in the brain. They hope that the new drug's high activity level will yield applications for other degenerative neurological diseases or brain trauma damage.
My husband's father developed Alzheimer's disease in his 50s. He often struggled physically with his caregivers. Trying to flee the house in search of some imaginary destination, he fell, broke a hip, and ended up confined to bed. When the house caught fire one night, his wife was unable to get him out of the bedroom. Both perished. In a sense, both were Alzheimer's victims. Having access to an Alzheimer's drug that actually repairs brain damage might have spared the family a great deal of heartache.
Vonda J. Sines has published thousands of print and online health and medical articles. She specializes in diseases and other conditions that affect the quality of life.
