PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35570231-3	2022	Naturally-occurring antibodies against Bim (NAbs-Bim) exist in human blood, with their levels and functions unknown in AD.	nabs	44-48	BCL2-like 11 (apoptosis facilitator)	Mus musculus	39-42	
35570231-3	2022	Naturally-occurring antibodies against Bim (NAbs-Bim) exist in human blood, with their levels and functions unknown in AD.	nabs	44-48	BCL2-like 11 (apoptosis facilitator)	Mus musculus	49-52	
35570231-4	2022	In this study, we found that circulating NAbs-Bim were decreased in AD patients.	nabs	41-45	BCL2-like 11 (apoptosis facilitator)	Mus musculus	46-49	
35570231-5	2022	Plasma levels of NAbs-Bim were negatively associated with brain amyloid burden and positively associated with cognitive functions.	nabs	17-21	BCL2-like 11 (apoptosis facilitator)	Mus musculus	22-25	
35570231-6	2022	Furthermore, NAbs-Bim purified from intravenous immunoglobulin rescued the behavioral deficits and ameliorated Abeta deposition, tau hyperphosphorylation, microgliosis, and neuronal apoptosis in APP/PS1 mice.	nabs	13-17	BCL2-like 11 (apoptosis facilitator)	Mus musculus	18-21	
35570231-7	2022	In vitro investigations demonstrated that NAbs-Bim were neuroprotective against AD through neutralizing Bim-directed neuronal apoptosis and the amyloidogenic processing of amyloid precursor protein.	nabs	42-46	BCL2-like 11 (apoptosis facilitator)	Mus musculus	47-50	
35570231-7	2022	In vitro investigations demonstrated that NAbs-Bim were neuroprotective against AD through neutralizing Bim-directed neuronal apoptosis and the amyloidogenic processing of amyloid precursor protein.	nabs	42-46	BCL2-like 11 (apoptosis facilitator)	Mus musculus	104-107	
35570231-8	2022	These findings indicate that the decrease of NAbs-Bim might contribute to the pathogenesis of AD and immunotherapies targeting Bim hold promise for the treatment of AD.	nabs	45-49	BCL2-like 11 (apoptosis facilitator)	Mus musculus	50-53	
35570231-8	2022	These findings indicate that the decrease of NAbs-Bim might contribute to the pathogenesis of AD and immunotherapies targeting Bim hold promise for the treatment of AD.	nabs	45-49	BCL2-like 11 (apoptosis facilitator)	Mus musculus	127-130