Plaque‐associated disruption of CSF and plasma amyloid‐β (Aβ) equilibrium in a mouse model of Alzheimer's disease
Explore this paper's citation graph
Summary
Findings suggest that there is a dynamic equilibrium between CNS and plasma Aβ, and that plaques create a new equilibrium because soluble CNS Aβ not only enters the plasma but also deposits onto amyloid plaques in the CNS.
- Type
- article
- Published
- 2002-04-01
- Cited by
- 279
- References
- 37
- OpenAlex
- https://openalex.org/W1817515827
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:83594259
Keywords
Genetically modified mouse, Amyloid (mycology), Alzheimer's disease, In vivo, Endocrinology
References
- Deposition of monomeric, not oligomeric, Abeta mediates growth of Alzheimer's disease amyloid plaques in human brain preparations.
- Amyloid β40/42 clearance across the blood-brain barrier following intra-ventricular injections in wild-type, apoE knock-out and human apoE3 or E4 expressing transgenic mice
- Imaging of amyloid-β deposits in brains of living mice permits direct observation of clearance of plaques with immunotherapy
- Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease
- Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of Alzheimer disease.
- Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease
- Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.
- Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease
- Peripheral anti-Aβ antibody alters CNS and plasma Aβ clearance and decreases brain Aβ burden in a mouse model of Alzheimer's disease
- β-sheet breaker peptides inhibit fibrillogenesis in a rat brain model of amyloidosis: Implications for Alzheimer's therapy
- Reversible in vitro growth of Alzheimer disease beta-amyloid plaques by deposition of labeled amyloid peptide.
- Receptor-mediated transport of human amyloid beta-protein 1-40 and 1-42 at the blood-brain barrier.
- Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid.
- Brain uptake of circulating apolipoproteins J and E complexed to Alzheimer's amyloid beta.
- Nasal administration of amyloid‐β peptide decreases cerebral amyloid burden in a mouse model of Alzheimer's disease
- Immunization with a nontoxic/nonfibrillar amyloid-beta homologous peptide reduces Alzheimer's disease-associated pathology in transgenic mice.
- Prominent cerebral amyloid angiopathy in transgenic mice overexpressing the london mutant of human APP in neurons.
- Clearance of Alzheimer's amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier.
- Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline.
- Apolipoprotein E and Alzheimer's Disease
Cited by
- The value and limitations of transgenic mouse models used in drug discovery for Alzheimer's disease: an update
- Elevation of Plasma Amyloid-β Level is More Significant in Early Stage of Cognitive Impairment: A Population-Based Cross-Sectional Study
- Therapeutic Albumin Binding to Remove Amyloid-β
- Biomarkers in patients with idiopathic normal pressure hydrocephalus
- Meta-Analysis of Plasma Amyloid-β levels in Alzheimer’s Disease
- Pathogenesis of Alzheimer’s disease
- Alzheimer's disease biomarkers in animal models: closing the translational gap.
- Validity of Cerebrospinal Fluid Biomarkers as Endpoints in Early-Phase Clinical Trials for Alzheimer's Disease
- Animal models of amyloid‐β‐related pathologies in Alzheimer’s disease
- Amyloid-β protofibril levels correlate with spatial learning in Arctic Alzheimer’s disease transgenic mice
- Identification of Novel Fluid Biomarkers for Alzheimer's Disease
- Specific reactivity of mild/severe Alzheimer’s disease patient’s sera to antibody against Aβ1–40 epitope 17–21
- A Critique of the Drug Discovery and Phase 3 Clinical Programs Targeting the Amyloid Hypothesis for Alzheimer Disease
- GENOME-WIDE ASSOCIATION STUDIES AT THE INTERFACE OF ALZHEIMER'S DISEASE AND EPIDEMIOLOGICALLY RELATED DISORDERS
- Trace copper levels in the drinking water, but not zinc or aluminum influence CNS Alzheimer-like pathology.
- Magnetic Resonance Imaging Improves Cerebrospinal Fluid Biomarkers in the Early Detection of Alzheimer’s Disease
- Immunomodulation As A Potential Therapeutic Approach For Alzheimer’s Disease
- Inhibition of amyloid-β plaque formation by α-synuclein
- Anti-Aβ single-chain antibody brain delivery via AAV reduces amyloid load but may increase cerebral hemorrhages in an Alzheimer mouse model
- Amyloid-associated depression and ApoE4 allele: longitudinal follow-up for the development of Alzheimer’s disease
Related papers
- Early Changes in Behavior Deficits, Amyloid β-42 Deposits and MAPK Activation in Doubly Transgenic Mice Co-expressing NSE-Controlled Human Mutant PS2 and APPsw
- Development and Characterization of Thy*IκBα-SI Transgenic Mice
- SIRT1 transgenic mice show phenotypes resembling calorie restriction
- Transgenic mice: beyond the knockout.
- [Transgenic mice in basic research].
- Transgenic mice models in autoimmunity--discussion.
- In vivo expression of a conditional TGF-beta1 transgene: no evidence for TGF-beta1 transgene expression in SM22alpha-tTA transgenic mice.
- Endothelium‐specific Cre recombinase activity in flk‐1‐Cre transgenic mice
- Gene expression profile in liver of hB1F transgenic mice.
- Principles for the use of in vivo transgene techniques: overview and an introductory practical guide for the selection of tetracycline-controlled transgenic mice.