Cited by 563Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Brain to Plasma Amyloid-β Efflux: a Measure of Brain Amyloid Burden in a Mouse Model of Alzheimer's Disease

DeMattos, Ronald B., Bales, Kelly R., Cummins, David J., Paul, Steven M., Holtzman, David M.·2002·Science

Abstract

The deposition of amyloid-beta (Abeta) peptides into amyloid plaques precedes the cognitive dysfunction of Alzheimer's disease (AD) by years. Biomarkers indicative of brain amyloid burden could be useful for identifying individuals at high risk for developing AD. As in AD in humans, baseline plasma Abeta levels in a transgenic mouse model of AD did not correlate with brain amyloid burden. However, after peripheral administration of a monoclonal antibody to Abeta (m266), we observed a rapid increase in plasma Abeta and the magnitude of this increase was highly correlated with amyloid burden in the hippocampus and cortex. This method may be useful for quantifying brain amyloid burden in patients at risk for or those who have been diagnosed with AD.

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Crossref · 10.1126/science.1067568

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  • For certain Aβ antibodies such as m266, increases of peripheral Aβ have been observed because antibody prevented Aβ from being degraded via binding to it and potentially increasing net Aβ efflux out of the brain.

    “For certain A␤ antibodies, such as m266, increases of peripheral A␤ has been observed because antibody prevented A␤ from being degraded via binding to it and potentially increasing net A␤ efflux out of the brain (DeMattos et al., 2002;Yamada et al., 2009).”
  • Unbound Aβ42 was rapidly cleared possibly through the blood brain barrier.

    “However, non-plaque areas immediately adjacent demonstrated very low fluorescence levels (Figure 3A) suggesting that unbound Aβ42 was rapidly cleared possibly through the blood brain barrier (DeMattos et al., 2002).”

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Authors
DeMattos, R. B., Bales, K. R., Cummins, D. J., Paul, S. M., & Holtzman, D. M.
Affiliations
  • Center for the Study of Nervous System Injury,
  • Eli Lilly (United States) (US)
  • Washington University in St. Louis (US)
Corresponding author
  • DeMattos, Ronald B.
  • Bales, Kelly R.
  • Paul, Steven M.
  • Holtzman, David M.
Venue
Science
Published
2002-03-22
Volume
295
Issue
5563
Pages
2264-2267
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2058614488
Cited by
563
References
5
Citations by year
2026: 2 · 2025: 13 · 2024: 14 · 2023: 12 · 2022: 13 · 2021: 19 · 2020: 16 · 2019: 6 · 2018: 18 · 2017: 15 · 2016: 15 · 2015: 17 · 2014: 32 · 2013: 21 · 2012: 28
FWCI
26.82
Type
journal article
Language
en
Open access
closed
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute on Aging (AG20222, R01AG020222)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
amyloid-beta, Alzheimer's disease, brain amyloid burden, plasma amyloid-beta, biomarkers, transgenic mouse model, amyloid plaques, hippocampus, cortex, amyloid-beta clearance
MeSH terms
Alzheimer Disease, Amyloidosis, Animals, Antibodies, Monoclonal, Brain, Cerebral Cortex, Disease Models, Animal, Hippocampus, Humans, Solubility, Time Factors, Amyloid beta-Peptides, Amino Acid Substitution, Protein Transport, Mice

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