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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Acetamides, Alzheimer Disease, Amyloid beta-Peptides, Animals, CHO Cells, Cricetulus, Drosophila melanogaster, HEK293 Cells, Humans, Mice, Mice, Transgenic, Neuroprotective Agents, Nootropic Agents, Plaque, Amyloid, Streptozocin, Sulfonamides.
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Does small molecule LX2343 ameliorate cognitive deficits in AD model mice by targeting both amyloid β production and clearance? Context: Streptozotocin (STZ) is widely used to induce oxidative damage and to impair glucose metabolism, apoptosis, and tau/Aβ pathology, eventually leading to cognitive deficits in both in vitro and in vivo models of Alzheimer's disease (AD). In this study, we constructed a cell-based platform using STZ to induce stress conditions mimicking the complicated pathologies of AD in vitro, and evaluated the anti-amyloid effects of a small molecule, N-(1,3-benzodioxol-5-yl)-2-[5-chloro-2-methoxy(phenylsulfonyl)anilino]acetamide (LX2343) in the amelioration of cognitive deficits in AD model mice. Cell-based assays for screening anti-amyloid compounds were established by assessing Aβ accumulation in HEK293-APP LX2343 (5-20 μmol/L) dose-dependently decreased Aβ accumulation in HEK293-APP
assistant
LX2343 ameliorates cognitive dysfunction in APP/PS1 transgenic mice via both Aβ production inhibition and clearance promotion, which highlights the potential of LX2343 in the treatment of AD. Final Decision: yes