Neuronal activity regulates the regional vulnerability to amyloid-β deposition

Bero, Adam W; Yan, Ping; Roh, Jee Hoon; Cirrito, John R; Stewart, Floy R; Raichle, Marcus E; Lee, Jin-Moo; Holtzman, David M

doi:10.1038/nn.2801

Cited by 880Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

Neuronal activity regulates the regional vulnerability to amyloid-β deposition

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Bero, Adam W, Yan, Ping, Roh, Jee Hoon, Cirrito, John R, Stewart, Floy R, Raichle, Marcus E, Lee, Jin-Moo, Holtzman, David M·2011·Nature Neuroscience

DOI 10.1038/nn.2801PMC PMC3102784

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Abstract

Amyloid-β (Aβ) plaque deposition in specific brain regions is a pathological hallmark of Alzheimer's disease. However, the mechanism underlying the regional vulnerability to Aβ deposition in Alzheimer's disease is unknown. Herein, we provide evidence that endogenous neuronal activity regulates the regional concentration of interstitial fluid (ISF) Aβ, which drives local Aβ aggregation. Using in vivo microdialysis, we show that ISF Aβ concentrations in several brain regions of APP transgenic mice before plaque deposition were commensurate with the degree of subsequent plaque deposition and with the concentration of lactate, a marker of neuronal activity. Furthermore, unilateral vibrissal stimulation increased ISF Aβ, and unilateral vibrissal deprivation decreased ISF Aβ and lactate, in contralateral barrel cortex. Long-term unilateral vibrissal deprivation decreased amyloid plaque formation and growth. Our results suggest a mechanism to account for the vulnerability of specific brain regions to Aβ deposition in Alzheimer's disease.

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APP and Aβ homeostasis are exquisitely regulated processes, and bioenergetic metabolism regulates these processes.
“Overall, we feel we can confidently state APP and Aβ homeostasis are exquisitely regulated processes, and bioenergetic metabolism regulates these processes.”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [182]

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Authors: Bero, A. W., Yan, P., Roh, J. H., Cirrito, J. R., Stewart, F. R., Raichle, M. E., Lee, J.-M., & Holtzman, D. M.
Affiliations: Washington University in St. Louis (US)
Corresponding author: Holtzman, David M
ORCID: Yan, Ping
Roh, Jee Hoon
Cirrito, John R
Raichle, Marcus E
Lee, Jin-Moo
Holtzman, David M
Venue: Nature Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2011-05-01
Volume: 14
Issue: 6
Pages: 750-756
ISSN: 1097-6256 (ISSN-L)
1546-1726
DOI: 10.1038/nn.2801
PMC: PMC3102784
OpenAlex: W2124443688
Cited by: 880
References: 51
Citations by year: 2026: 31 · 2025: 57 · 2024: 64 · 2023: 51 · 2022: 53 · 2021: 66 · 2020: 65 · 2019: 63 · 2018: 54 · 2017: 72 · 2016: 57 · 2015: 49 · 2014: 67 · 2013: 56 · 2012: 52
FWCI: 43.22
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Neuroscience (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Israel Science Foundation
National Institutes of Health
National Institute on Aging (R01AG013956, AG033452, AG568127, K01AG029524, R37AG013956, AG13956, AG029524, F31AG033452)
National Institute of Neurological Disorders and Stroke (NS32636, P30NS057105, R01NS067905, NS67905, P01NS032636, P50NS006833, NS 06833)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: amyloid-beta deposition, Alzheimer's disease, regional vulnerability, neuronal activity, lactate, barrel cortex, APP transgenic mice, amyloid plaque formation, amyloid-beta aggregation
MeSH terms: Alzheimer Disease, Animals, Cerebral Cortex, Disease Models, Animal, Female, Male, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Sensory Deprivation, Somatosensory Cortex, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microdialysis, Lactic Acid, Extracellular Fluid, Mice, Plaque, Amyloid

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Neuronal activity regulates the regional vulnerability to amyloid-β deposition

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