ArticleThe Journal of experimental medicine2016
Rapid in vivo measurement of β-amyloid reveals biphasic clearance kinetics in an Alzheimer's mouse model.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Preclinical and clinical biomarker studies of CT1812: A novel approach to Alzheimer's disease modification.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Trial
- Passive amyloid-β immunotherapy in Alzheimer's disease: a multicellular clearance system beyond plaque removal.Molecular neurodegeneration · 2026Review
- Age-related macular degeneration and cerebral amyloid angiopathy have similar pathologies from cholesterol-APOE-amyloid-β-complement mediated inflammation.Progress in retinal and eye research · 2026Review
- LRP1 at the crossroads of Aβ clearance and therapeutic targeting in Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- Association of dementia with impaired kidney function and plasma biomarkers: A population-based study.European journal of neurology · 2024Article
- The role of macrophage plasticity in neurodegenerative diseases.Biomarker research · 2024Review
- Cerebral amyloid angiopathy and the immune system.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Monocytes release cystatin F dimer to associate with Aβ and aggravate amyloid pathology and cognitive deficits in Alzheimer's disease.Journal of neuroinflammation · 2024Article
- Serum amyloid beta 42 levels correlated with metabolic syndrome and its components.Frontiers in endocrinology · 2024Article
- The oral-brain axis: can periodontal pathogens trigger the onset and progression of Alzheimer's disease?Frontiers in microbiology · 2024Review
- Improving Blood Monocyte Energy Metabolism Enhances Its Ability to Phagocytose Amyloid-β and Prevents Alzheimer's Disease-Type Pathology and Cognitive Deficits.Neuroscience bulletin · 2023Article
- Proteasome inhibition protects blood-brain barrier P-glycoprotein and lowers Aβ brain levels in an Alzheimer's disease model.Fluids and barriers of the CNS · 2023Article
- Associations of Blood and Cerebrospinal Fluid Aβ and tau Levels with Renal Function.Molecular neurobiology · 2023Article
- Advances in Amyloid-β Clearance in the Brain and Periphery: Implications for Neurodegenerative Diseases.Experimental neurobiology · 2023Review
- Rapid Direct Detection of SARS-CoV-2 Aerosols in Exhaled Breath at the Point of Care.ACS sensors · 2023Article
- Real-time environmental surveillance of SARS-CoV-2 aerosols.Nature communications · 2023Article
- Ergothioneine, a dietary antioxidant improves amyloid beta clearance in the neuroretina of a mouse model of Alzheimer's disease.Frontiers in neuroscience · 2023Article
- Polysaccharide Krestin Prevents Alzheimer's Disease-type Pathology and Cognitive Deficits by Enhancing Monocyte Amyloid-β Processing.Neuroscience bulletin · 2022Article
- Physiological clearance of Aβ by spleen and splenectomy aggravates Alzheimer-type pathogenesis.Aging cell · 2022Article
- Physiological clearance of amyloid-beta by the kidney and its therapeutic potential for Alzheimer's disease.Molecular psychiatry · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Findings from genetic, animal model, and human studies support the observation that accumulation of the β-amyloid (Aβ) peptide in the brain plays a central role in the pathogenic cascade of Alzheimer's disease (AD). Human studies suggest that one key factor leading to accumulation is a defect in brain Aβ clearance. We have developed a novel microimmunoelectrode (MIE) to study the kinetics of Aβ clearance using an electrochemical approach. This is the first study using MIEs in vivo to measure rapid changes in Aβ levels in the brains of living mice. Extracellular, interstitial fluid (ISF) Aβ levels were measured in the hippocampus of APP/PS1 mice. Baseline levels of Aβ40 in the ISF are relatively stable and begin to decline within minutes of blocking Aβ production with a γ-secretase inhibitor. Pretreatment with a P-glycoprotein inhibitor, which blocks blood-brain barrier transport of Aβ, resulted in significant prolongation of Aβ40 half-life, but only in the latter phase of Aβ clearance from the ISF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.