{"id":"6f5ff3a5-f194-586c-a1d1-e55f1cabba6c","stable_key":"e3f6ce02-0bd7-5103-acc1-68503ab6751b:ad96-null","predicate":"no_detected_change_in_recorded_comparison","statement":"ALCAR did not slow overall primary cognitive/clinical decline in the 431-participant Alzheimer trial.","claim_class":"observational","status":"source_recorded","evidence_grade":"ungraded","direction":"neutral","is_public":true,"mechanism_event_id":"70e22e92-24a5-57a1-835a-82bcdba3521a","mechanism_event_label":"ALCAR did not slow overall primary cognitive/clinical decline in the 431-participant Alzheimer trial.","subject":{"id":"5ce394a9-6ec6-56dd-866f-37d85c0556e4","slug":"acetylcarnitine","display_name":"Acetyl-L-carnitine","entity_type_key":"small_molecule"},"object":{"id":"4ba056b1-f961-57b4-88b4-129dec760232","slug":"human-ad-cognitive-decline","display_name":"Human Alzheimer trial cognitive and functional decline","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"70e22e92-24a5-57a1-835a-82bcdba3521a","stable_key":"e3f6ce02-0bd7-5103-acc1-68503ab6751b:ad96-null-event","event_type":"experimental_observation","label":"ALCAR did not slow overall primary cognitive/clinical decline in the 431-participant Alzheimer trial.","description":"### ad96-null\n\nALCAR did not slow overall primary cognitive/clinical decline in the 431-participant Alzheimer trial.\nPost hoc age-subgroup trends were exploratory and motivated prospective testing.\nModel and exposure: Mild-to-moderate probable AD; 3 g/day versus placebo, 12 months, 1996.\nLimitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.\nReference: A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease. | 1996 | https://pubmed.ncbi.nlm.nih.gov/8797468/ | https://doi.org/10.1212/wnl.47.3.705 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"5ce394a9-6ec6-56dd-866f-37d85c0556e4","slug":"acetylcarnitine","display_name":"Acetyl-L-carnitine","entity_type_key":"small_molecule"},"role":"tested factor","stoichiometry":null,"state_label":"ALCAR 3 g/day for one year","sequence_order":0,"notes":""},{"entity":{"id":"4ba056b1-f961-57b4-88b4-129dec760232","slug":"human-ad-cognitive-decline","display_name":"Human Alzheimer trial cognitive and functional decline","entity_type_key":"cellular_process"},"role":"measured outcome","stoichiometry":null,"state_label":"no_detected_change","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"evidence_access","value_text":"Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_contrast","value_text":"{\"intervention\": \"ALCAR 3 g/day for one year\", \"comparator\": \"Placebo\", \"endpoint\": \"ALCAR did not slow overall primary cognitive/clinical decline in the 431-participant Alzheimer trial.\", \"effect_direction\": \"no_detected_change\", \"combination\": \"single\", \"conditions\": []}","comparator":null,"unit":null,"notes":"Explicit extracted experimental comparison; source-derived draft.","entity":null},{"dimension":"experimental_model","value_text":"Mild-to-moderate probable AD; 3 g/day versus placebo, 12 months, 1996.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"interpretation_status","value_text":"Source-derived curation with stated access limits; ungraded, not independent replication.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation.","comparator":null,"unit":null,"notes":"","entity":{"slug":"acetylcarnitine","display_name":"Acetyl-L-carnitine","entity_type_key":"small_molecule"}},{"dimension":"plain_language","value_text":"ALCAR did not slow overall primary cognitive/clinical decline in the 431-participant Alzheimer trial.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease. | https://pubmed.ncbi.nlm.nih.gov/8797468/ | https://doi.org/10.1212/wnl.47.3.705","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"source_locator","value_text":"Reviewed reference ad96-null; Post hoc age-subgroup trends were exploratory and motivated prospective testing.","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"0f52c62a-2ee8-563c-8b9f-b3e99404f595","evidence_kind":"source_excerpt","locator":"Lines 595-601","start_line":595,"end_line":601,"excerpt":"### ad96-null\n\nALCAR did not slow overall primary cognitive/clinical decline in the 431-participant Alzheimer trial.\nPost hoc age-subgroup trends were exploratory and motivated prospective testing.\nModel and exposure: Mild-to-moderate probable AD; 3 g/day versus placebo, 12 months, 1996.\nLimitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.\nReference: A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease. | 1996 | https://pubmed.ncbi.nlm.nih.gov/8797468/ | https://doi.org/10.1212/wnl.47.3.705 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.","model_system":"Mild-to-moderate probable AD; 3 g/day versus placebo, 12 months, 1996.","directness":"reported_statement","verification_status":"source_recorded","notes":"Original paraphrase in the retained reviewed reference, not a verbatim primary-paper quotation. Access level is explicit.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"2588f904-245a-597a-8a12-65118013fb90","stable_key":"import-e3f6ce02-0bd7-5103-acc1-68503ab6751b","title":"Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026)","document_type":"imported_text","citation_label":"AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed.","file_path":"","sha256":"84cc82d6fbb0fd5d73c4ce779e9f88e7f0184ba2d29b18ad0f153815380f2975","revision_id":"dac7a950-dbe5-5c7a-9c70-2ea711d5c71a","review_status":"source_recorded","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}