New study offers hope for Alzheimer’s treatment

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Early treatment of brain lesions associated with Alzheimer’s disease can halt and even reverse the course of the mind-erasing ailment, according to authors of an animal study published on Thursday.

The study provided the best evidence so far that early treatment which target lesions called beta-amyloid plaques could actually stop the disease’s progression, researchers said. 

"I think the results of this study indicate we are on the right track,” said Frank LaFerla, associate professor of neurobiology and behavior at the University of California, Irvine and head of the research team.

“These results offer hope that in five to 10 years there will be therapies available to target beta amyloid plaques and have an effect on treating this disease,” he said. The study was published in the Aug. 5 issue of Neuron.

Alzheimer’s, which affects some 4.5 million Americans, is marked by the presence of two distinct types of brain lesions: beta-amyloid plaques and neurofibrillary tangles. Both accumulate in brain areas critical to learning and memory.

Many neuroscientists believe that the accumulation of amyloid plaques triggers the progression of the disease in a “cascade” process that leads to the tangles.

Earlier clinical trials had indicated that treating beta amyloid lesions could be effective in treating Alzheimer’s. But LaFerla said the UCI study found that treating the beta amyloid lesions could halt the “cascade” effect.

“We found that when we cleared amyloid plaques from the brains of mice, the downstream consequences of the disease were lessened and even removed, provided the disease had not progressed to a certain advanced state,” LaFerla said.

Researchers used transgenic mice that LaFerla’s lab had previously developed. Because mice normally don’t get Alzheimer’s, human genes were inserted into their genome, allowing the mice to develop the ailment.

The researchers then injected anti-beta-amyloid antibodies into the hippocampus—one of most critical brain structures involved in learning and memory—of the mice and found that the amyloid plaques were cleared by three days.

The lesions caused by neurofibrillary tangles disappeared two days later. Thirty days later, the researchers found amyloid plaques re-emerged but the tangle lesions did not.

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