PMC:6582309 / 29098-30351 JSONTXT

{"project":"2_test","denotations":[{"id":"31249505-16170565-38601624","span":{"begin":380,"end":384},"obj":"16170565"},{"id":"31249505-30333009-38601625","span":{"begin":591,"end":595},"obj":"30333009"},{"id":"31249505-18184371-38601626","span":{"begin":752,"end":756},"obj":"18184371"},{"id":"31249505-10332828-38601627","span":{"begin":867,"end":871},"obj":"10332828"},{"id":"31249505-12146803-38601628","span":{"begin":1247,"end":1251},"obj":"12146803"}],"text":"In patients with AD, accumulation of Aβ is often observed in the walls of blood vessels in the brain. This is called CAA and is caused by pathological deposits of Aβ and other proteins in the cerebral arterioles and capillaries of the leptomeninges and cortex. It is considered as an early and integral part of AD pathogenesis and the prevalence of CAA in AD is over 70% (Attems, 2005). CAA is a risk factor for hemorrhagic stroke and contributes to AD dementia. Atherosclerosis may also cause cerebrovascular dysfunction that may lead to cognitive decline as well as stroke (Shabir et al., 2018). The accumulation of amyloid in the walls of blood vessels is common in elderly people, patients with CAA and in almost all patients with AD (Kumar-Singh, 2008). The most CAA affected brain regions are the leptomeninges and frontal and temporal cortices (Borràs et al., 1999) with Aβ deposits in arteries, arterioles, capillaries, venules, and veins. The CAA disease progresses from mild, to moderate to severe stage, this is from almost intact blood vessels with minor Aβ deposits to extensive vascular Aβ load, which disrupts vessel architecture and exacerbates microangiopathies, microaneurysmal dilatation, and fibrinoid necrosis (Revesz et al., 2002)."}

{"project":"0_colil","denotations":[{"id":"31249505-16170565-737049","span":{"begin":380,"end":384},"obj":"16170565"},{"id":"31249505-30333009-737050","span":{"begin":591,"end":595},"obj":"30333009"},{"id":"31249505-18184371-737051","span":{"begin":752,"end":756},"obj":"18184371"},{"id":"31249505-10332828-737052","span":{"begin":867,"end":871},"obj":"10332828"},{"id":"31249505-12146803-737053","span":{"begin":1247,"end":1251},"obj":"12146803"}],"text":"In patients with AD, accumulation of Aβ is often observed in the walls of blood vessels in the brain. This is called CAA and is caused by pathological deposits of Aβ and other proteins in the cerebral arterioles and capillaries of the leptomeninges and cortex. It is considered as an early and integral part of AD pathogenesis and the prevalence of CAA in AD is over 70% (Attems, 2005). CAA is a risk factor for hemorrhagic stroke and contributes to AD dementia. Atherosclerosis may also cause cerebrovascular dysfunction that may lead to cognitive decline as well as stroke (Shabir et al., 2018). The accumulation of amyloid in the walls of blood vessels is common in elderly people, patients with CAA and in almost all patients with AD (Kumar-Singh, 2008). The most CAA affected brain regions are the leptomeninges and frontal and temporal cortices (Borràs et al., 1999) with Aβ deposits in arteries, arterioles, capillaries, venules, and veins. The CAA disease progresses from mild, to moderate to severe stage, this is from almost intact blood vessels with minor Aβ deposits to extensive vascular Aβ load, which disrupts vessel architecture and exacerbates microangiopathies, microaneurysmal dilatation, and fibrinoid necrosis (Revesz et al., 2002)."}