scholarly journals Elevated Aβ and Apolipoprotein E in AβPP Transgenic Mice and Its Relationship to Amyloid Accumulation in Alzheimer’s Disease

2000 ◽  
Vol 6 (5) ◽  
pp. 430-439 ◽  
Author(s):  
Yu-Min Kuo ◽  
Fiona Crawford ◽  
Michael Mullan ◽  
Tyler A. Kokjohn ◽  
Mark R. Emmerling ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Apolipoprotein E ◽  
Amyloid Accumulation

scholarly journals Treatment with a Copper-Zinc Chelator Markedly and Rapidly Inhibits β-Amyloid Accumulation in Alzheimer's Disease Transgenic Mice

Neuron ◽  
2001 ◽  
Vol 30 (3) ◽  
pp. 665-676 ◽  
Author(s):  
Robert A Cherny ◽  
Craig S Atwood ◽  
Michel E Xilinas ◽  
Danielle N Gray ◽  
Walton D Jones ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Accumulation ◽  
Zinc Chelator ◽  
Copper Zinc ◽  
Β Amyloid

scholarly journals Blocking the apolipoprotein E/Amyloid β interaction in triple transgenic mice ameliorates Alzheimer's disease related amyloid β and tau pathology

2013 ◽  
Vol 128 (4) ◽  
pp. 577-591 ◽  
Author(s):  
Shan Liu ◽  
Ariel Breitbart ◽  
Yanjie Sun ◽  
Pankaj D. Mehta ◽  
Allal Boutajangout ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Apolipoprotein E ◽  
Amyloid Β ◽  
Tau Pathology

scholarly journals Multi-method investigation of factors influencing amyloid onset and impairment in three cohorts

2021 ◽  
Author(s):  
Tobey J. Betthauser ◽  
Murat Bilgel ◽  
Rebecca L. Koscik ◽  
Bruno M. Jedynak ◽  
Yang An ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Cox Regression ◽  
Amyloid Pet ◽  
Onset Age ◽  
Longitudinal Course ◽  
Modeling Methods ◽  
Amyloid Accumulation ◽  
Apolipoprotein E Genotype

AbstractAlzheimer’s disease biomarkers are becoming increasingly important for characterizing the longitudinal course of disease, predicting the timing of clinical and cognitive symptoms, and for recruitment and treatment monitoring in clinical trials. In this work, we develop and evaluate three methods for modeling the longitudinal course of amyloid accumulation in three cohorts using amyloid PET imaging. We then use these novel approaches to investigate factors that influence the timing of amyloid onset and the timing from amyloid onset to impairment onset in the Alzheimer’s disease continuum.Data were acquired from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), the Baltimore Longitudinal Study of Aging (BLSA) and the Wisconsin Registry for Alzheimer’s Prevention (WRAP). Amyloid PET was used to assess global amyloid burden. Three methods were evaluated for modeling amyloid accumulation using 10-fold cross-validation and hold-out validation where applicable. Estimated amyloid onset age was compared across all three modeling methods and cohorts. Cox regression and accelerated failure time models were used to investigate whether sex, apolipoprotein E genotype and e4 carriage were associated with amyloid onset age in all cohorts. Cox regression was used to investigate whether apolipoprotein E (e4 carriage and e3e3, e3e4, e4e4 genotypes), sex or age of amyloid onset were associated with the time from amyloid onset to impairment onset (global Clinical Dementia Rating ≥1) in a subset of 595 ADNI participants that were not impaired prior to amyloid onset.Model prediction and estimated amyloid onset age were similar across all three amyloid modeling methods. Sex and apolipoprotein E-e4 carriage were not associated with PET-measured amyloid accumulation rates. Apolipoprotein E genotype and e4 carriage, but not sex, were associated with amyloid onset age such that e4 carriers became amyloid positive at an earlier age compared to non-carriers, and greater e4 dosage was associated with an earlier amyloid onset age. In the ADNI, e4 carriage, being female and a later amyloid onset age were all associated with a shorter time from amyloid onset to impairment onset. The risk of impairment onset due to age of amyloid onset was nonlinear and accelerated for amyloid onset age >65. These findings demonstrate the feasibility of modeling longitudinal amyloid accumulation to enable individualized estimates of amyloid onset age from amyloid PET imaging. These estimates provide a more direct way to investigate the role of amyloid and other factors that influence the timing of clinical impairment in Alzheimer’s disease.

Intraneuronal β-Amyloid Accumulation in the Amygdala Enhances Fear and Anxiety in Alzheimer's Disease Transgenic Mice

2010 ◽  
Vol 67 (6) ◽  
pp. 513-521 ◽  
Author(s):  
Judit España ◽  
Lydia Giménez-Llort ◽  
Jorge Valero ◽  
Alfredo Miñano ◽  
Alberto Rábano ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Accumulation ◽  
Β Amyloid ◽  
Fear And Anxiety

scholarly journals Rapamycin rescues vascular, metabolic and learning deficits in apolipoprotein E4 transgenic mice with pre-symptomatic Alzheimer’s disease

2016 ◽  
Vol 37 (1) ◽  
pp. 217-226 ◽  
Author(s):  
Ai-Ling Lin ◽  
Jordan B Jahrling ◽  
Wei Zhang ◽  
Nicholas DeRosa ◽  
Vikas Bakshi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Apolipoprotein E ◽  
Late Onset ◽  
Human Subjects ◽  
Susceptibility Gene ◽  
Learning Deficits ◽  
Cerebrovascular Function

Apolipoprotein E ɛ4 allele is a common susceptibility gene for late-onset Alzheimer's disease. Brain vascular and metabolic deficits can occur in cognitively normal apolipoprotein E ɛ4 carriers decades before the onset of Alzheimer's disease. The goal of this study was to determine whether early intervention using rapamycin could restore neurovascular and neurometabolic functions, and thus impede pathological progression of Alzheimer's disease-like symptoms in pre-symptomatic Apolipoprotein E ɛ4 transgenic mice. Using in vivo, multimodal neuroimaging, we found that apolipoprotein E ɛ4 mice treated with rapamycin had restored cerebral blood flow, blood–brain barrier integrity and glucose metabolism, compared to age- and gender-matched wild-type controls. The preserved vasculature and metabolism were associated with amelioration of incipient learning deficits. We also found that rapamycin restored the levels of the proinflammatory cyclophilin A in vasculature, which may contribute to the preservation of cerebrovascular function in the apolipoprotein E ɛ4 transgenics. Our results show that rapamycin improves functional outcomes in this mouse model and may have potential as an effective intervention to block progression of vascular, metabolic and early cognitive deficits in human Apolipoprotein E ɛ4 carriers. As rapamycin is FDA-approved and neuroimaging is readily used in humans, the results of the present study may provide the basis for future Alzheimer's disease intervention studies in human subjects.

P4-381 Reduction of β-amyloid load in Alzheimer's disease transgenic mice by competitive blocking of β-amyloid binding to apolipoprotein E

2004 ◽  
Vol 25 ◽  
pp. S583
Author(s):  
Thomas Wisniewski ◽  
Joanna Pankiewicz ◽  
Henrieta Scholtzova ◽  
Stephen D. Schmidt ◽  
Paul M. Mathews ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Apolipoprotein E ◽  
Amyloid Load ◽  
Β Amyloid

Relationship between apolipoprotein E and the amyloid deposits and dystrophic neurites of Alzheimer's disease

1997 ◽  
Vol 23 (6) ◽  
pp. 483-491 ◽  
Author(s):  
T. C. Dickson ◽  
H. L. Saunders ◽  
J. C. Vickers
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Dystrophic Neurites ◽  
Amyloid Deposits

Age Modifies the Association Between Apolipoprotein E Genotype and Alzheimer's Disease: A CSF Biomarker-Based Multicentric Case-Control Study

2019 ◽  
Author(s):  
Hana Sadikki ◽  
Aurore Fayosse ◽  
Emmanuel Cognat ◽  
Séverine Sabia ◽  
Sebastiaan Engelborghs ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Case Control Study ◽  
Case Control ◽  
Csf Biomarker ◽  
Control Study ◽  
Apolipoprotein E Genotype
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