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Psoriasis drug may halt or reverse Alzheimer's disease

Posted Dec 04 2012 12:00am

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LA Times

A biological medication already widely used to treat plaque psoriasis  may be able to slow the accumulation of amyloid plaques in  the brain  that are the hallmark of  Alzheimer's disease , a new study has found. The same study found that in older mice with established Alzheimer's, this treatment approach, which suppresses the brain's immune reaction to beta amyloid, brought a marked improvement in cognitive function and may even halt or reverse early signs of Alzheimer's.
The new study was published this week in the journal Nature Medicine.
Conducted by researchers in Switzerland and Germany, the study offers a glimmer of hope in the thus-far discouraging search for a therapy that could halt or reverse the inexorable process of neuronal loss and mental decline that affects some 35-million people worldwide. It also strengthens evidence for the long-suspected role of  inflammation  in the development of Alzheimer's disease.
The authors of the study suggest that researchers should immediately launch clinical trials of ustekinumab — a biologic drug already approved by the Food & Drug Administration for the treatment of plaque psoriasis (and marketed as  Stelara ) — on patients with mild cognitive impairment or very early Alzheimer's disease. They called agents that shut down specific immune responses — medications tested in auto-immune disorders such as psoriasis,  Crohn's disease  and  multiple sclerosis  — "the ideal candidate for the initiation of clinical trials" for Alzheimer's. "This kind of research is a step forward in identifying potential human targets for drug action," said Dr. Lon Schneider, director of pharmacological research at USC's Alzheimer's Disease Research Center, who was not involved with the current study.
At the same time, Schneider cautioned against drawing too much hope from the latest research. In animal models of Alzheimer's disease, he said, interventions that seem to work for mice "have not translated to humans," he said. And even when an existing drug appears promising, he added, researchers are far from knowing what dose or form of administration will be safe and effective for humans. "Using the drug off the shelf may not be either" safe or effective, he warned. The latest research focuses on the role of the  immune system  in the degenerative process at the heart of Alzheimer's. Looking at the cerebrospinal fluid of 39 human subjects with established Alzheimer's disease and 20 healthy control subjects, the researchers showed that the accumulation of beta-amyloid in the brain may set off an immune reaction — including the release of two proteins known as interleukin-12 and interleukin-23. These two chemicals, collectively called IL-12/23, send forth a signaling molecule called P40 that increases inflammation across the brain. Past research suggests that in brains where P40 is in plentiful supply, beta-amyloid particles that are circulating form plaques. Those plaques, in turn, disrupt signaling throughout the brain and appear to  cause the decline in memory and mental function so familiar to the loved ones of those with the devastating disease. The researchers also sought to test the effect of suppressing P40 in rats with established Alzheimer's disease. They implanted mini-pumps that for 60 days infused P40 antibodies directly into the brains of older rats with full-blown Alzheimer's. Another group of such rats got a placebo infusion. The treated mice performed far better than those who got the placebo in tests of memory and cognitive function. And while the treated mice still had amyloid plaques, there was far less beta-amyloid in their brains available to form new ones. See recent reports of other drugs that have generated hope for Alzheimer's disease: A hint of success in treating Alzheimer's raises ethical quandary ; and New Alzheimer's pill more likely to cause misery, medical experts sa y
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