Now showing items 1-11 of 11

    • APOE4-specific Changes in A beta Accumulation in a New Transgenic Mouse Model of Alzheimer Disease 

      Youmans, Katherine L.; Tai, Leon M.; Nwabuisi-Heath, Evelyn; Jungbauer, Lisa; Kanekiyo, Takahisa; Gan, Ming; Kim, Jungsu; Eimer, William A.; Estus, Steve; Rebeck, G. William; Weeber, Edwin J; Bu, Guojun; Yu, Chunjiang; LaDu, Mary Jo (American Society for Biochemistry and Molecular Biology, 2012-12)
      APOE4 is the greatest risk factor for Alzheimer disease (AD) and synergistic effects with amyloid-beta peptide (A beta) suggest interactions among apoE isoforms and different forms of A beta accumulation. However, it remains ...
    • Apolipoprotein E as a β-amyloid-independent factor in Alzheimer's disease 

      Wolf, Andrew B.; Valla, Jon; Bu, Guojun; Kim, Jungsu; LaDu, Mary Jo; Reiman, Eric M.; Caselli, Richard J. (BioMed Central, 2013)
      APOE, which encodes apolipoprotein E, is the most prevalent and best established genetic risk factor for late-onset Alzheimer’s disease. Current understanding of Alzheimer’s disease pathophysiology posits an important role ...
    • Differential Regulation of Amyloid-β Endocytic Trafficking and Lysosomal Degradation by Apolipoprotein E Isoforms 

      Li, Jie; Kanekiyo, Takahisa; Shinohara, Mitsuru; Zhang, Yunwu; LaDu, Mary Jo; Xu, Huaxi; Bu, Guojun (American Society for Biochemistry and Molecular Biology, 2012-12)
      Aggregation of amyloid-beta (A beta) peptides leads to synaptic disruption and neurodegeneration in Alzheimer disease (AD). A major A beta clearance pathway in the brain is cellular uptake and degradation. However, how A ...
    • Endocytic pathways mediating oligomeric Aβ42 neurotoxicity 

      Yu, Chunjiang; Nwabuisi-Heath, Evelyn; Laxton, Kevin; LaDu, Mary Jo (BioMed Central, 2010-05-17)
      Background: One pathological hallmark of Alzheimer’s disease (AD) is amyloid plaques, composed primarily of amyloid-β peptide (Aβ). Over-production or diminished clearance of the 42 amino acid form of Aβ (Aβ42) in the ...
    • Endocytic pathways mediating oligomeric Aβ42 neurotoxicity 

      Yu, Chunjiang; Health, Evelyn; Laxton, Kevin; LaDu, Mary Jo (BioMed Central, 2010-05-17)
      Background One pathological hallmark of Alzheimer’s disease (AD) is amyloid plaques, composed primarily of amyloid-β peptide (Aβ). Over-production or diminished clearance of the 42 amino acid form of Aβ (Aβ42) in the brain ...
    • Intraneuronal Aβ detection in 5xFAD mice by a new Aβ-specific antibody 

      Youmans, Katherine L.; Tai, Leon M.; Kanekiyo, Takahisa; Stine Jr, W Blaine; Michon, Sara-Claude; Nwabuisi-Heath, Evelyn; Manelli, Arlene M.; Fu, Yifan; Riordan, Sean; Eimer, William A; Binder, Lester; Bu, Guojun; Yu, Chunjiang; Hartley, Dean M.; LaDu, Mary Jo (BioMed Central, 2012)
      Background: The form(s) of amyloid-b peptide (Ab) associated with the pathology characteristic of Alzheimer’s disease (AD) remains unclear. In particular, the neurotoxicity of intraneuronal Ab accumulation is an issue ...
    • Introducing Human APOE into Aβ Transgenic Mouse Models 

      Tai, Leon M.; Youmans, Katherine L.; Jungbauer, Lisa; Yu, Chunjiang; LaDu, Mary Jo (SAGE-Hindawi Access to Research, 2011)
      Apolipoprotein E (apoE) and apoE/amyloid-β (Aβ) transgenic (Tg) mouse models are critical to understanding apoE-isoform effects on Alzheimer’s disease risk. Compared to wild type, apoE−/− mice exhibit neuronal deficits, ...
    • Levels of soluble apolipoprotein E/amyloid-β complex are reduced and oligomeric Aβ increased with APOE4 and Alzheimer disease in a transgenic mouse model and human samples 

      Tai, Leon M.; Bilousova, Tina; Jungbauer, Lisa; Roeske, Stephen K.; Youmans, Katherine L.; Yu, Chunjiang; Poon, Wayne W.; Cornwell, Lindsey B.; Miller, Carol A.; Vinters, Harry V.; Van Eldik, Linda J.; Fardo, David W.; Estus, Steve; Bu, Guojun; Gylys, Karen Hoppens; LaDu, Mary Jo (Journal of Biological Chemistry, 2013-02-22)
      Human apolipoprotein E (apoE) isoforms may differentially modulate amyloid-β (Aβ) levels. Evidence suggests physical interactions between apoE and Aβ are partially responsible for these functional effects. However, the ...
    • Levels of soluble apolipoprotein E/amyloid-β complex are reduced and oligomeric Aβ increased with APOE4 and Alzheimer disease in a transgenic mouse model and human samples 

      Tai, Leon M.; Bilousova, Tina; Jungbauer, Lisa; Roeske, Stephen K.; Youmans, Katherine L.; Yu, Chunjiang; Poon, Wayne W.; Cornwell, Lindsey B.; Miller, Carol A.; Vinters, Harry V.; Van Eldik, Linda J.; Fardo, David W.; Estus, Steve; Bu, Guojun; Gylys, Karen Hoppens; LaDu, Mary Jo (American Society for Biochemistry and Molecular Biology, 2013-02)
      Human apolipoprotein E (apoE) isoforms may differentially modulate amyloid-β (Aβ) levels. Evidence suggests physical interactions between apoE and Aβ are partially responsible for these functional effects. However, the ...
    • Mechanisms of ApoEIsoform Effects in Alzheimer’s Disease 

      Nwabuisi, Evelyn I. (2013-02-21)
      Alzheimer’s disease (AD) is the primary cause of dementia in the elderly. Mutations that increase the 42 amino acid form of the peptide amyloid-beta (Aβ42) is the only known cause of AD, but accounts for less than 5% of ...
    • Preferential interactions between ApoE-containing lipoproteins and Aβ revealed by a detection method that combines size exclusion chromatography with non-reducing gel-shift 

      LaDu, Mary Jo; Munson, Gregory W.; Jungbauer, Lisa; Getz, Godfrey S.; Reardon, Catherine A.; Tai, Leon M.; Yu, Chunjiang (Elsevier, 2012-02)
      The association between apolipoprotein E (apoE) and amyloid-β peptide (Aβ) may significantly impact the function of both proteins, thus affecting the etiology of Alzheimer's disease (AD). However, apoE/Aβ interactions ...