Breakthriugh in Alzheimer's disease

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uab.edu

Alzheimer’s disease is a neurodegenerative disorder that affects more than 5.3 million families in the United States each year and unleashes a path of emotional and financial heartache for patients and their families.

The disease carries an annual societal price tag of $148 billion, according to the Alzheimer’s Association. It destroys brain cells, which causes memory loss and problems with thinking, and the behavior of patients with the disease can deteriorate to the point that it affects work, lifelong hobbies and social function. Alzheimer’s gets progressively worse, and it is fatal.

But an experimental drug known as bapineuzumab could change all that.

UAB researchers are participating in national and international Phase III Alzheimer’s clinical trials in which they administer the drug to patients every 13 weeks for 18 months, and there is real hope that bapineuzumab will change the underlying pathology of the disease, ultimately eradicating it from the body.

“There has been much effort and money put into this research, and there is real hope for Alzheimer’s patients,” says Cleveland Kinney, M.D., Ph.D., professor of psychiatry and behavioral neurobiology. “What’s so exciting about these new studies and this new drug in particular is the possibility of changing the pathology of the illness. I don’t know if we’ll ever cure it, but I think it will be managed by a cocktail of medicines and patients will be able to live a normal life.”

Bapineuzumab appears to undermine the grip the disease-causing proteins has on the brain, and that is the reason there is promise in the drug’s efficacy.

Current Alzheimer’s medications, including Aricept, Exelon and Razadyne — the three most popular cholinesterase inhibitors used to treat patients — act as managers of the disease. They maximize the remaining brain activity and slow the disease.

Bapineuzumab uses an antibody not commonly found in the patient’s blood to treat Alzheimer’s. It is designed to bind to a particular protein called beta amyloid protein, which accumulates in the brain and forms plaques related to the progression of the disease. It is hoped that bapineuzumab will attach to the beta amyloid protein in the brain and help the body remove it. Researchers also believe the drug will prevent the build up of beta amyloid protein.

“It’s particularly fascinating that as the study progresses and the plaques are dissolved, the brain shrinks because it’s getting rid of space-occupying lesions,” Kinney says. “But the patients theoretically do better over time, which means they are re-establishing connections in the brain they had lost because the plaques were there.

“If you get rid of the plaques the patients do better; the brain shrinks and the connections are re-made,” he says. “If that’s the case, that means the brain is far more plastic than anyone ever thought possible. That’s what we think is going to happen.”

The studies look at two different patient populations — those carrying what is known as apolipoprotein ε4 gene (APO ε4) alleles and those who do not. APOE contains the instructions needed to make a protein that helps carry cholesterol in the bloodstream and comes in several different forms. Three of those alleles occur more frequently than others. Dozens of studies have confirmed that the allele identified as APOE ε4 increases the risk of developing Alzheimer’s, but the way that happens is not yet understood.

Administered through infusions
Patients in the trials undergo....read the rest tomorrow