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Published on: November 27, 2012
by Melissa Healy for Los Angeles 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.
Researchers have sought to suppress IL-12/23 by different means. But among the most successful so far have been the injection of antibodies that shut down P40’s signal. When the authors of the study injected P40 antibodies and an inactive control substance into young mice who were genetically programmed to develop Alzheimer’s disease, they saw a distinct difference: At about middle age, the mice that got the P40 antibodies had 31% less beta-amyloid plaque in their brains than their peers who got the placebo.
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.
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