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Novel Antisense Compound Reverses Alzheimer's Disease Symptoms in Mouse Models

By BiotechDaily International staff writers
Posted on 02 Jun 2014
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An antisense oligonucleotide, which suppresses the mRNA required for synthesis of amyloid-beta protein precursor (AbetaPP), decreased AbetaPP expression and amyloid-beta protein (Abeta) production, and reversed Alzheimer's disease symptoms in mouse models.

Investigators at Saint Louis University (MO, USA) had shown previously that their OL-1 antisense compound rapidly crossed the blood-brain barrier, reversed learning and memory impairments, reduced oxidative stress, and restored brain-to-blood efflux of Abeta in the SAMP8 mouse model. These animals carry a natural mutation causing them to overproduce mouse amyloid beta.

In the current study, the investigators tested OL-1 in the Tg2576 Alzheimer's disease mouse model, which comprises animals that had been genetically engineered to overexpress a mutant form of the human amyloid beta precursor gene.

Results published in the May 2014 issue of the Journal of Alzheimer's Disease revealed that treatment of the Tg2576 mice with OL-1 produced the same reversal of Alzheimer's disease symptoms as had been observed earlier in the SAMP8 mice. Biochemical analyses of brain tissue taken from the treated animals showed significant reduction of AbetaPP signaling and a reduction of indicators of neuroinflammation.

"Our findings reinforced the importance of amyloid beta protein in the Alzheimer's disease process. They suggest that an antisense that targets the precursor to amyloid beta protein is a potential therapy to explore to reversing symptoms of Alzheimer's disease," said senior author Dr. Susan Farr, professor of geriatrics at Saint Louis University. "It reversed learning and memory deficits and brain inflammation in mice that are genetically engineered to model Alzheimer's disease. Our current findings suggest that the compound, which is called antisense oligonucleotide (OL-1), is a potential treatment for Alzheimer's disease."

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