@article{bastiani_transcriptomic_nodate,
	title = {Transcriptomic similarities and differences between mouse models and human},
	abstract = {Alzheimer's disease (AD) is a multifactorial pathology with most cases having a sporadic presentation. Yet, preclinical research studies relied for decades on transgenic models overexpressing human genes found in AD autosomal dominant patients. Recently, knock-in (KI) models, such as the novel hAβ-KI mouse, were introduced; however, its translational potential is still being addressed. To unveil core molecular programs in AD, we compared hippocampal transcriptomic profiles of transgenic (5xFAD and APP/PS1) and KI (hAβ-KI) mouse models with early- (EOAD) and late- (LOAD) onset AD patients. Comparison of differential expression analyses showed seven genes (S100A6, C1QB, CD33, CD14, SLC11A1, KCNK1 and SST) consistently already among models and human AD. Experimental validation of these genes revealed four altered in mice (SLC11A1, S100A6, CD14, CD33, C1QB) and three in humans (S100A6, SLC11A1, KCNK). Our analysis revealed that all three mouse models presented more Gene Ontology biological processes (GOBP) terms and enriched signaling pathways in common with LOAD than with EOAD subjects. Furthermore, semantic similarity of enriched GOBP terms highlighted model-specific biological alterations that might be further explored. Finally, we identified 17 transcription factors potentially acting as master regulators of AD in all models. Our cross-species exploratory analyses evidenced that the three mouse models presented a remarkable specificity of GOBP to LOAD, but the representation of processes in each model may differ. Thus, the molecular and cellular mechanisms under study should be a factor during mouse model selection in AD.},
	language = {en},
	author = {Bastiani, Marco Antônio De and Bellaver, Bruna and Carello-Collar, Giovanna and Kunach, Peter and Lima-Filho, Ricardo A S and Forner, Stefania and Martini, Cadete and Pascoal, Tharick A and Lourenco, Mychael V and Rosa-Neto, Pedro},
}

{"_id":"cc7DddYqq2YjKciET","bibbaseid":"bastiani-bellaver-carellocollar-kunach-limafilho-forner-martini-pascoal-etal-transcriptomicsimilaritiesanddifferencesbetweenmousemodelsandhuman","author_short":["Bastiani, M. A. D.","Bellaver, B.","Carello-Collar, G.","Kunach, P.","Lima-Filho, R. A S","Forner, S.","Martini, C.","Pascoal, T. A","Lourenco, M. V","Rosa-Neto, P."],"bibdata":{"bibtype":"article","type":"article","title":"Transcriptomic similarities and differences between mouse models and human","abstract":"Alzheimer's disease (AD) is a multifactorial pathology with most cases having a sporadic presentation. Yet, preclinical research studies relied for decades on transgenic models overexpressing human genes found in AD autosomal dominant patients. Recently, knock-in (KI) models, such as the novel hAβ-KI mouse, were introduced; however, its translational potential is still being addressed. To unveil core molecular programs in AD, we compared hippocampal transcriptomic profiles of transgenic (5xFAD and APP/PS1) and KI (hAβ-KI) mouse models with early- (EOAD) and late- (LOAD) onset AD patients. Comparison of differential expression analyses showed seven genes (S100A6, C1QB, CD33, CD14, SLC11A1, KCNK1 and SST) consistently already among models and human AD. Experimental validation of these genes revealed four altered in mice (SLC11A1, S100A6, CD14, CD33, C1QB) and three in humans (S100A6, SLC11A1, KCNK). Our analysis revealed that all three mouse models presented more Gene Ontology biological processes (GOBP) terms and enriched signaling pathways in common with LOAD than with EOAD subjects. Furthermore, semantic similarity of enriched GOBP terms highlighted model-specific biological alterations that might be further explored. Finally, we identified 17 transcription factors potentially acting as master regulators of AD in all models. Our cross-species exploratory analyses evidenced that the three mouse models presented a remarkable specificity of GOBP to LOAD, but the representation of processes in each model may differ. Thus, the molecular and cellular mechanisms under study should be a factor during mouse model selection in AD.","language":"en","author":[{"propositions":[],"lastnames":["Bastiani"],"firstnames":["Marco","Antônio","De"],"suffixes":[]},{"propositions":[],"lastnames":["Bellaver"],"firstnames":["Bruna"],"suffixes":[]},{"propositions":[],"lastnames":["Carello-Collar"],"firstnames":["Giovanna"],"suffixes":[]},{"propositions":[],"lastnames":["Kunach"],"firstnames":["Peter"],"suffixes":[]},{"propositions":[],"lastnames":["Lima-Filho"],"firstnames":["Ricardo","A","S"],"suffixes":[]},{"propositions":[],"lastnames":["Forner"],"firstnames":["Stefania"],"suffixes":[]},{"propositions":[],"lastnames":["Martini"],"firstnames":["Cadete"],"suffixes":[]},{"propositions":[],"lastnames":["Pascoal"],"firstnames":["Tharick","A"],"suffixes":[]},{"propositions":[],"lastnames":["Lourenco"],"firstnames":["Mychael","V"],"suffixes":[]},{"propositions":[],"lastnames":["Rosa-Neto"],"firstnames":["Pedro"],"suffixes":[]}],"bibtex":"@article{bastiani_transcriptomic_nodate,\n\ttitle = {Transcriptomic similarities and differences between mouse models and human},\n\tabstract = {Alzheimer's disease (AD) is a multifactorial pathology with most cases having a sporadic presentation. Yet, preclinical research studies relied for decades on transgenic models overexpressing human genes found in AD autosomal dominant patients. Recently, knock-in (KI) models, such as the novel hAβ-KI mouse, were introduced; however, its translational potential is still being addressed. To unveil core molecular programs in AD, we compared hippocampal transcriptomic profiles of transgenic (5xFAD and APP/PS1) and KI (hAβ-KI) mouse models with early- (EOAD) and late- (LOAD) onset AD patients. Comparison of differential expression analyses showed seven genes (S100A6, C1QB, CD33, CD14, SLC11A1, KCNK1 and SST) consistently already among models and human AD. Experimental validation of these genes revealed four altered in mice (SLC11A1, S100A6, CD14, CD33, C1QB) and three in humans (S100A6, SLC11A1, KCNK). Our analysis revealed that all three mouse models presented more Gene Ontology biological processes (GOBP) terms and enriched signaling pathways in common with LOAD than with EOAD subjects. Furthermore, semantic similarity of enriched GOBP terms highlighted model-specific biological alterations that might be further explored. Finally, we identified 17 transcription factors potentially acting as master regulators of AD in all models. Our cross-species exploratory analyses evidenced that the three mouse models presented a remarkable specificity of GOBP to LOAD, but the representation of processes in each model may differ. Thus, the molecular and cellular mechanisms under study should be a factor during mouse model selection in AD.},\n\tlanguage = {en},\n\tauthor = {Bastiani, Marco Antônio De and Bellaver, Bruna and Carello-Collar, Giovanna and Kunach, Peter and Lima-Filho, Ricardo A S and Forner, Stefania and Martini, Cadete and Pascoal, Tharick A and Lourenco, Mychael V and Rosa-Neto, Pedro},\n}\n\n","author_short":["Bastiani, M. A. D.","Bellaver, B.","Carello-Collar, G.","Kunach, P.","Lima-Filho, R. A S","Forner, S.","Martini, C.","Pascoal, T. A","Lourenco, M. V","Rosa-Neto, P."],"key":"bastiani_transcriptomic_nodate","id":"bastiani_transcriptomic_nodate","bibbaseid":"bastiani-bellaver-carellocollar-kunach-limafilho-forner-martini-pascoal-etal-transcriptomicsimilaritiesanddifferencesbetweenmousemodelsandhuman","role":"author","urls":{},"metadata":{"authorlinks":{}},"html":""},"bibtype":"article","biburl":"https://bibbase.org/zotero/qingyuhms","dataSources":["uJZG8wcPfTAfBw67Z"],"keywords":[],"search_terms":["transcriptomic","similarities","differences","between","mouse","models","human","bastiani","bellaver","carello-collar","kunach","lima-filho","forner","martini","pascoal","lourenco","rosa-neto"],"title":"Transcriptomic similarities and differences between mouse models and human","year":null}