Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease.

By D. Holtzman, K. Bales, T. Tenkova, Anne M. Fagan, Maia Parsadanian, Leah J. Sartorius, Brian Mackey, J. Olney, D. McKeel, D. Wozniak and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2000

927 citations recorded by the source corpus.

Subfields: Pharmacology, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/3ec5074580d8b47a74285adf741e5c8a7894e61c

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Citations in the corpus

Alzheimer's disease. (2011, background): “When these offspring are then crossed with mice expressing human ApoE3 or ApoE4, both resultant genotypes show more Ab deposits than the mice lacking ApoE, but the ApoE4-expressing mice show significantly more than those with ApoE3 (Holtzman et al. 2000).”
Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy (2009, background): “Indeed, several studies using different amyloid mouse models expressing either human APOE3 or human APOE4 demonstrated that APOE3-expressing mice develop fewer amyloid plaques than APOE4-expressing mic”
The Major Risk Factors for Alzheimer’s Disease: Age, Sex, and Genes Modulate the Microglia Response to Aβ Plaques (2019, result): “Lack of Apoe expression did not alter the global amyloid burden (Figures 6B, 6D, and 6E); however, it caused a significant decrease in the amounts of Metoxy-XO4-stained amyloid (Figure 6F), as previously reported for other Apoenull AD mouse models (Holtzman et al., 2000; Irizarry et al., 2000; Krase”
The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics (2011, background): “How the different APOE proteins mediate their effects in AD is not definitively known, but a compelling series of experiments in PDAPP transgenic mice that harboured the human APOE genes indicate that these cognate proteins mediate the clearance of amyloid-”
Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease. (2012, background): “In addition, the anatomical pattern of Ab deposition differs in the absence of apoE (Holtzman et al. 2000a; Irizarry et al. 2000).”
Cell biology of protein misfolding: The examples of Alzheimer's and Parkinson's diseases (2004, background): “The mechanism seems not to involve increased Aβ production but rather stabilization and decreased clearance of fibrillar Aβ deposits, as revealed by expression of human ApoE4 compared with ApoE3 in ApoE-knock-out mic”
Human apoE isoforms differentially regulate brain amyloid-β peptide clearance (2011, positive): “Consistent with this observation, we found that old PDAPP/TRE mice developed Aβ/amyloid deposition in an apoE isoform-dependent pattern, that is, E4> E3> E2, a finding that extends previous reports of apoE isoform-dependent Aβ deposition in various mouse models (10, 11, 13, 14).”
Alzheimer’s disease: experimental models and reality (2017, background): “Expression of mouse ApoE resulted in greater plaque formation than expression of human ApoE, and mouse ApoE preferentially promoted the formation of parenchymal plaques, while human ApoE promoted the formation of CAA [59, 60, 94].”
Alzheimer's disease: the cholesterol connection (2003, background): “The interaction between Alzheimer amyloid beta(1-40) peptide and ganglioside GM1-containing membranes.”
Age-related myelin breakdown: a developmental model of cognitive decline and Alzheimer's disease. (2004, background): “[110] Holtzman DM, Bales KR, Tenkova T, Fagan AM, Parsadanian M, Sartorius LJ, et al.”
The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “How ApoE4 promotes AD: chronically decreased Aß clearance Humans expressing the ApoE4 protein develop more plaque and vascular b-amyloid deposits than those expressing only ApoE3 (Rebeck et al, 1993), and this has been confirmed in genetically engineered mice (Holtzman et al, 2000).”