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  1. All, This new study [1] (science press coverage) appears like it might be a significant breakthrough in the treatment of Alzheimer's disease. Researchers appear to have discovered a small molecule that at least in rodents is safe, crosses the blood-brain barrier, and is effective at breaking up beta amyloid plaques, thought to play an important role in the neuronal death associated with Alzheimer's disease. From the article linked above: The Korean scientists, led by YoungSoo Kim of the Brain Science Institute at the Korea Institute of Science and Technology (KIST) in Seoul, investigated the ability of EPPS [4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid] to attach to amyloid-beta clumps and convert them into simpler, smaller molecules. Through a series of experiments, they found that EPPS could break apart plaque in a living mammal. They also found the molecule could be added to drinking water yet still travel in the blood to the brain and cross the blood-brain barrier, which otherwise prevents foreign material from entering the brain. EPPS could penetrate the barrier because it is a relatively small molecule, Kim said. The scientists found that doses between 30 and 100 milligrams per kilogram of body weight per day were effective in breaking up the amyloid beta. Further tests demonstrated that EPPS appears to have no toxic effects in mice up to 2,000 mg/kg per day. From the full text, not only did mice treated with EPPS show a reduction in beta amyloid plaques in their hippocampus and other brain areas in a dose dependent manner, they also showed less cognitive impairment relative to control mice using several measures of cognitive performance. The lead author is quite optimistic about this compound's potential: "I strongly believe these drug candidates [based on EPPS] will halt the neurodegeneration and rescue patients from death," Kim said. Here's hoping human trials prove that he's right! --Dean ------ [1] Nat Commun. 2015 Dec 8;6:8997. doi: 10.1038/ncomms9997. EPPS rescues hippocampus-dependent cognitive deficits in APP/PS1 mice by disaggregation of amyloid-β oligomers and plaques. Kim HY(1,)(2,)(3), Kim HV(1,)(2), Jo S(4), Lee CJ(4), Choi SY(1), Kim DJ(1), Kim Y(1,)(2). Full text: http://www.nature.com.sci-hub.io/ncomms/2015/151208/ncomms9997/abs/ncomms9997.html Alzheimer's disease (AD) is characterized by the transition of amyloid-β (Aβ) monomers into toxic oligomers and plaques. Given that Aβ abnormality typically precedes the development of clinical symptoms, an agent capable of disaggregating existing Aβ aggregates may be advantageous. Here we report that a small molecule, 4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid (EPPS), binds to Aβ aggregates and converts them into monomers. The oral administration of EPPS substantially reduces hippocampus-dependent behavioural deficits, brain Aβ oligomer and plaque deposits, glial γ-aminobutyric acid (GABA) release and brain inflammation in an Aβ-overexpressing, APP/PS1 transgenic mouse model when initiated after the development of severe AD-like phenotypes. The ability of EPPS to rescue Aβ aggregation and behavioural deficits provides strong support for the view that the accumulation of Aβ is an important mechanism underlying AD. PMCID: PMC4686862 PMID: 26646366
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