Cognitive decline due to excess synaptic Zn(2+) signaling in the hippocampus
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Pharmacology of cognitive enhancers for exposure-based therapy of fear, anxiety and trauma-related disordersYXQN Reduces Alzheimer's Disease-Like Pathology and Cognitive Decline in APPswePS1dE9 Transgenic Mice.Amyloid β-mediated Zn2+ influx into dentate granule cells transiently induces a short-term cognitive deficit.Chelation of hippocampal zinc enhances long-term potentiation and synaptic tagging/capture in CA1 pyramidal neurons of aged rats: implications to aging and memory.The role of intracellular zinc release in aging, oxidative stress, and Alzheimer's disease.Preliminary Data on the Interaction between Some Biometals and Oxidative Stress Status in Mild Cognitive Impairment and Alzheimer's Disease Patients.Supplementation with zinc in rats enhances memory and reverses an age-dependent increase in plasma copper.Editorial: The molecular pathology of cognitive decline: focus on metals.Intracellular Zn(2+) signaling in the dentate gyrus is required for object recognition memory.The Zinc Ion Chelating Agent TPEN Attenuates Neuronal Death/apoptosis Caused by Hypoxia/ischemia Via Mediating the Pathophysiological Cascade Including Excitotoxicity, Oxidative Stress, and Inflammation.Structural determinants of specificity and regulation of activity in the allosteric loop network of human KLK8/neuropsin.
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Cognitive decline due to excess synaptic Zn(2+) signaling in the hippocampus
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article científic
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Cognitive decline due to excess synaptic Zn(2+) signaling in the hippocampus
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Cognitive decline due to excess synaptic Zn(2+) signaling in the hippocampus
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Cognitive decline due to excess synaptic Zn(2+) signaling in the hippocampus
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P2860
P356
P1476
Cognitive decline due to excess synaptic Zn(2+) signaling in the hippocampus
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P2093
Atsushi Takeda
Haruna Tamano
P2860
P356
10.3389/FNAGI.2014.00026
P577
2014-02-27T00:00:00Z