g(HBP:"APOE e4")

Entity

Name

APOE e4

Namespace

HBP

Namespace Version

20190307

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/209a3048003c8d92394e6b64778447bd996a21e6/export/hbp-names.belns

By up-regulating endocytosis, high dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels and increase delivery of Ab1–42 to lysosomes in cellular model systems (Ji et al. 2006; Cossec et al. 2010). PubMed:22908190

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

High dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels (Ji et al. 2006; Cossec et al. 2010), and these levels are also elevated in NPC, DS, and AD, particularly in early-onset forms of AD caused by certain mutations of APP. PubMed:22908190

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

By up-regulating endocytosis, high dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels and increase delivery of Ab1–42 to lysosomes in cellular model systems (Ji et al. 2006; Cossec et al. 2010). PubMed:22908190

Acceleration of endosome pathology is also seen in individuals who inherit the 14 allele of APOE, a key mediator of neuronal cholesterol transport and the major genetic risk factor for late-onset AD (Cataldo et al. 2000). PubMed:22908190

Genetics have a role to play within AD; patients with a mutation in Amyloid Precursor Protein (APP), which results in overproduction of Aβ, will experience early onset AD. 36 Patients with a mutation in Apolipoprotein E4 (APOE4), which affects the clearance of Aβ, will experience late onset AD. PubMed:30444369

Genetics have a role to play within AD; patients with a mutation in Amyloid Precursor Protein (APP), which results in overproduction of Aβ, will experience early onset AD. 36 Patients with a mutation in Apolipoprotein E4 (APOE4), which affects the clearance of Aβ, will experience late onset AD. PubMed:30444369

For instance, ApoE4–an important determinant of cholesterol metabolism and the strongest genetic risk factor for sporadic AD – regulates Aβ degradation [77]. PubMed:29758300

For instance, ApoE4–an important determinant of cholesterol metabolism and the strongest genetic risk factor for sporadic AD – regulates Aβ degradation [77]. PubMed:29758300

For instance, ApoE4–an important determinant of cholesterol metabolism and the strongest genetic risk factor for sporadic AD – regulates Aβ degradation [77]. PubMed:29758300

Acceleration of endosome pathology is also seen in individuals who inherit the 14 allele of APOE, a key mediator of neuronal cholesterol transport and the major genetic risk factor for late-onset AD (Cataldo et al. 2000). PubMed:22908190

Acceleration of endosome pathology is also seen in individuals who inherit the 14 allele of APOE, a key mediator of neuronal cholesterol transport and the major genetic risk factor for late-onset AD (Cataldo et al. 2000). PubMed:22908190

High dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels (Ji et al. 2006; Cossec et al. 2010), and these levels are also elevated in NPC, DS, and AD, particularly in early-onset forms of AD caused by certain mutations of APP. PubMed:22908190

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

By up-regulating endocytosis, high dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels and increase delivery of Ab1–42 to lysosomes in cellular model systems (Ji et al. 2006; Cossec et al. 2010). PubMed:22908190

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

By up-regulating endocytosis, high dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels and increase delivery of Ab1–42 to lysosomes in cellular model systems (Ji et al. 2006; Cossec et al. 2010). PubMed:22908190

Expression of the ApoE epsilon 4 allele, but not ApoE epsilon 3, in mice administered a neprilysin inhibitor increases Ab immunoreactivity in lysosomes and causes neurodegeneration of hippocampal CA1, entorhinal,and septal neurons (Belinson et al. 2008). PubMed:22908190

Expression of the ApoE epsilon 4 allele, but not ApoE epsilon 3, in mice administered a neprilysin inhibitor increases Ab immunoreactivity in lysosomes and causes neurodegeneration of hippocampal CA1, entorhinal,and septal neurons (Belinson et al. 2008). PubMed:22908190

ApoE epsilon4 that trafficks to lysosomes more readily than ApoE epsilon3, promotes leakage of acid hydrolases, and induces apoptosis in cultured neuronal cells by forming membrane-damaging intermediates in the low-pHenvironment (Ji et al. 2002). PubMed:22908190