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Experiment #00000016

Analyze the potential for zinc-binding competition between synaptic transporters (e.g., SLC39A8, ZnT3) and ALS-associated proteins (RGNEF, TDP-43) in the RGC-thalamic axis. Can this competition explain the coexistence of RGC excitotoxicity and STMN2 depletion in clinical samples?

TAR DNA-Binding Protein 43 _gates_from_tar_dna_binding_protein_43 Stathmin 2 _gates_to_stathmin_2 SLC39A8 protein, human _gates_from_slc39a8_protein__human Zinc _gates_to_zinc Excitotoxicity _gates_from_excitotoxicity
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Experiment #00000015

Given that schizophrenia is characterized by a deficit in the attenuation of sensory input via corollary discharge, how might pathologically elevated RGC signaling—potentially caused by synaptic glutamate overflow without zinc modulation—interfere with the thalamic integration of extra-retinal CD signals to effectively reverse the predictive timing of visual stability?

SLC39A8 Protein _gates_from_slc39a8_protein Zinc Deficiency _gates_to_zinc_deficiency _gates_from_zinc_deficiency Glutamic Acid _gates_to_glutamic_acid _gates_from_glutamic_acid Thalamus _gates_to_thalamus
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