Cited by 219Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsStress Responses and Cortisol

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Acute stress increases interstitial fluid amyloid-β via corticotropin-releasing factor and neuronal activity

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Kang, Jae-Eun, Cirrito, John R., Dong, Hongxin, Csernansky, John G., Holtzman, David M.·2007·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0700148104PMC PMC1965571

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Abstract

Aggregation of the amyloid-beta (Abeta) peptide in the extracellular space of the brain is critical in the pathogenesis of Alzheimer's disease. Abeta is produced by neurons and released into the brain interstitial fluid (ISF), a process regulated by synaptic activity. To determine whether behavioral stressors can regulate ISF Abeta levels, we assessed the effects of chronic and acute stress paradigms in amyloid precursor protein transgenic mice. Isolation stress over 3 months increased Abeta levels by 84%. Similarly, acute restraint stress increased Abeta levels over hours. Exogenous corticotropin-releasing factor (CRF) but not corticosterone mimicked the effects of acute restraint stress. Inhibition of endogenous CRF receptors or neuronal activity blocked the effects of acute stress on Abeta. Thus, behavioral stressors can rapidly increase ISF Abeta through neuronal activity in a CRF-dependent manner, and the results suggest a mechanism by which behavioral stress may affect Alzheimer's disease pathogenesis.

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Authors: Kang, J.-E., Cirrito, J. R., Dong, H., Csernansky, J. G., & Holtzman, D. M.
Affiliations: Washington University in St. Louis (US)
Departments of *Neurology,
ORCID: Cirrito, John R.
Dong, Hongxin
Holtzman, David M.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2007-06-19
Volume: 104
Issue: 25
Pages: 10673-10678
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.0700148104
PMC: PMC1965571
OpenAlex: W2031441539
Cited by: 219
References: 44
Citations by year: 2026: 6 · 2025: 8 · 2024: 10 · 2023: 11 · 2022: 7 · 2021: 12 · 2020: 9 · 2019: 12 · 2018: 13 · 2017: 11 · 2016: 5 · 2015: 17 · 2014: 12 · 2013: 14 · 2012: 10
FWCI: 10.24
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Alzheimer's Association (AG13956)
Eli Lilly and Company
Cure Alzheimer's Fund
National Institutes of Health (AG13956)
National Institute on Aging (AG 025824, R01AG013956, R01AG025824, R37AG013956, AG13956)
National Institute on Drug Abuse (DA07261, T32DA007261)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords: amyloid-beta, interstitial fluid, acute stress, restraint stress, isolation stress, corticotropin-releasing factor, CRF receptors, neuronal activity, synaptic activity, amyloid precursor protein transgenic mice, Alzheimer's disease, corticosterone
MeSH terms: Acute Disease, Animals, Corticotropin-Releasing Hormone, Crosses, Genetic, Female, Male, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Stress, Psychological, Amyloid beta-Peptides, Microdialysis, Extracellular Fluid, Mice

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Acute stress increases interstitial fluid amyloid-β via corticotropin-releasing factor and neuronal activity

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