{"id":"27b94e56-f1e3-57d0-ad7f-8b2d99e57c04","stable_key":"a8baf7e9-80e4-5d8c-adec-9a63e84d2f21:l-cysteine-nac-neuronal-rescue","predicate":"restores_in_transport_deficient_model","statement":"N-acetylcysteine treatment reversed reduced neuronal glutathione and oxidant-related abnormalities in EAAC1-deficient mice.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"a30cdf23-8f1c-57ec-8be3-791853e39070","mechanism_event_label":"A different precursor bypassed part of the uptake limitation in this animal model.","subject":{"id":"b5fa7a22-e5a7-58d9-9e39-91a611aa431e","slug":"n-acetylcysteine","display_name":"N-Acetyl-L-cysteine","entity_type_key":"small_molecule"},"object":{"id":"5120ca34-ff36-5a46-b764-500163dad284","slug":"mouse-neuronal-gsh-pool","display_name":"Mouse neuronal glutathione pool","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"a30cdf23-8f1c-57ec-8be3-791853e39070","stable_key":"a8baf7e9-80e4-5d8c-adec-9a63e84d2f21:l-cysteine-nac-neuronal-rescue-event","event_type":"observed_relationship","label":"A different precursor bypassed part of the uptake limitation in this animal model.","description":"N-acetylcysteine treatment reversed reduced neuronal glutathione and oxidant-related abnormalities in EAAC1-deficient mice.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"b5fa7a22-e5a7-58d9-9e39-91a611aa431e","slug":"n-acetylcysteine","display_name":"N-Acetyl-L-cysteine","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"5120ca34-ff36-5a46-b764-500163dad284","slug":"mouse-neuronal-gsh-pool","display_name":"Mouse neuronal glutathione pool","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"ca899f13-50ad-55e5-ab99-329ae0038c74","slug":"l-cysteine","display_name":"L-Cysteine","entity_type_key":"small_molecule"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"f5b92207-a3ca-5e80-8240-bd00c6036474","slug":"mouse-slc1a1","display_name":"Mouse EAAT3 / Slc1a1","entity_type_key":"protein"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""},{"entity":{"id":"b44c9e27-4bbb-52d3-a022-14cddded5073","slug":"glutathione","display_name":"GSH","entity_type_key":"small_molecule"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":4,"notes":""}]},"contexts":[{"dimension":"availability_state","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null},{"dimension":"evidence_access","value_text":"Primary abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Mouse Slc1a1 deletion with NAC treatment.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"NAC is the tested intervention, not free L-cysteine; no human cognitive benefit is established.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit.","comparator":null,"unit":null,"notes":"","entity":{"slug":"l-cysteine","display_name":"L-Cysteine","entity_type_key":"small_molecule"}},{"dimension":"plain_language","value_text":"A different precursor bypassed part of the uptake limitation in this animal model.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"Neuronal glutathione deficiency and age-dependent neurodegeneration in the EAAC1 deficient mouse. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16311588/ · DOI 10.1038/nn1609","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"15dadd8f-f5e0-52c7-b6e2-2c5636a8c5b5","evidence_kind":"source_excerpt","locator":"Lines 108-114","start_line":108,"end_line":114,"excerpt":"## l-cysteine-nac-neuronal-rescue\nA different precursor bypassed part of the uptake limitation in this animal model.\nN-acetylcysteine treatment reversed reduced neuronal glutathione and oxidant-related abnormalities in EAAC1-deficient mice.\nModel: Mouse Slc1a1 deletion with NAC treatment.\nLimitations: NAC is the tested intervention, not free L-cysteine; no human cognitive benefit is established.\nEvidence access: Primary abstract\nNeuronal glutathione deficiency and age-dependent neurodegeneration in the EAAC1 deficient mouse. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16311588/ · DOI 10.1038/nn1609","model_system":"Mouse Slc1a1 deletion with NAC treatment.","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Original curation paraphrase; evidence access and experimental limitations specified.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"654560f6-8d7f-596b-8722-48d94053cfe3","stable_key":"import-a8baf7e9-80e4-5d8c-adec-9a63e84d2f21","title":"L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19)","document_type":"imported_text","citation_label":"AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text.","file_path":"","sha256":"f722669e54eab08ffe7289f9d79ddfc443014ed8c4bc5ba10ce2635470d22498","revision_id":"8ae25609-a031-5782-9c62-6cad8767ea46","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}