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The neurotoxic effects of aluminum (Al) are associated with the impairment of synaptic plasticity, the biological basis of learning and memory, the major form of which is long-term potentiation (LTP). The canonical glycogen synthase kinase-3β (GSK-3β)/β-catenin signaling-mediated brain-derived neurotrophic factor (BDNF) pathway has been suggested to play important roles in memory. Thus, Al may affect LTP through this pathway. In this study, a Sprague-Dawley rat model of neurotoxicity was established through intracerebroventricular (i.c.