{"id":"W2122743846","doi":"10.1523/jneurosci.0901-04.2004","title":"Absence of C1q Leads to Less Neuropathology in Transgenic Mouse Models of Alzheimer's Disease","year":2004,"lang":"en","type":"article","venue":"Journal of Neuroscience","topic":"Alzheimer's disease research and treatments","field":"Medicine","cited_by":348,"is_retracted":false,"has_abstract":true,"ca_institutions":"","funders":"National Institute on Aging; National Institutes of Health; National Institute of Neurological Disorders and Stroke; York University","keywords":"Presenilin; Genetically modified mouse; Synaptophysin; Hippocampus; Neuropathology; Hippocampal formation; Pathology; Amyloid precursor protein; Immunohistochemistry; Transgene; Western blot; Complement system; Alzheimer's disease; Neuroscience; Biology; Medicine; Disease; Immunology; Antibody","routes":{"ca_aff":false,"ca_fund":true,"ca_venue":false,"about_ca":false,"invisible_to_affiliation_only":true},"retraction":null,"screen":null,"machine_scores":{"provisional":true,"baseline":true,"maturity_gate_passed":false,"score_opus":0.07622252323976868,"score_gpt":0.3445021951644205,"score_spread":0.2682796719246519,"validation_status":"score_only:v0-immature-baseline","note":"Baseline scores from an immature model (maturity gate not passed). Scores rank; they never assert a category."}}