PMC:6582309 / 34163-34728 JSONTXT

{"project":"2_test","denotations":[{"id":"31249505-1303239-38601654","span":{"begin":92,"end":96},"obj":"1303239"},{"id":"31249505-11409420-38601655","span":{"begin":116,"end":120},"obj":"11409420"},{"id":"31249505-15365148-38601656","span":{"begin":136,"end":140},"obj":"15365148"},{"id":"31249505-20697050-38601657","span":{"begin":158,"end":162},"obj":"20697050"},{"id":"31249505-27858710-38601658","span":{"begin":179,"end":183},"obj":"27858710"},{"id":"31249505-18184371-38601659","span":{"begin":270,"end":274},"obj":"18184371"},{"id":"31249505-23771217-38601660","span":{"begin":542,"end":546},"obj":"23771217"},{"id":"31249505-26341746-38601661","span":{"begin":559,"end":563},"obj":"26341746"}],"text":"Some presenilin mutations and mutations in APP have been connected to CAA (Hendriks et al., 1992; Grabowski et al., 2001; Rossi et al., 2004; Bugiani et al., 2010; Sellal et al., 2017) and also a polymorphism in the neprilysin gene was associated with CAA (Kumar-Singh, 2008), although the exact connections between these mutations and AD/CAA symptoms and progression are not yet understood. Furthermore, APOEε4 was shown to be a risk factor for CAA and both APOEε2 and ε4 alleles are associated with more severe forms of CAA (Nelson et al., 2013; Yu et al., 2015)."}

{"project":"0_colil","denotations":[{"id":"31249505-1303239-737079","span":{"begin":92,"end":96},"obj":"1303239"},{"id":"31249505-11409420-737080","span":{"begin":116,"end":120},"obj":"11409420"},{"id":"31249505-15365148-737081","span":{"begin":136,"end":140},"obj":"15365148"},{"id":"31249505-20697050-737082","span":{"begin":158,"end":162},"obj":"20697050"},{"id":"31249505-27858710-737083","span":{"begin":179,"end":183},"obj":"27858710"},{"id":"31249505-18184371-737084","span":{"begin":270,"end":274},"obj":"18184371"},{"id":"31249505-23771217-737085","span":{"begin":542,"end":546},"obj":"23771217"},{"id":"31249505-26341746-737086","span":{"begin":559,"end":563},"obj":"26341746"}],"text":"Some presenilin mutations and mutations in APP have been connected to CAA (Hendriks et al., 1992; Grabowski et al., 2001; Rossi et al., 2004; Bugiani et al., 2010; Sellal et al., 2017) and also a polymorphism in the neprilysin gene was associated with CAA (Kumar-Singh, 2008), although the exact connections between these mutations and AD/CAA symptoms and progression are not yet understood. Furthermore, APOEε4 was shown to be a risk factor for CAA and both APOEε2 and ε4 alleles are associated with more severe forms of CAA (Nelson et al., 2013; Yu et al., 2015)."}