Neuronal activity and secreted amyloid β lead to altered amyloid β precursor protein and presenilin 1 interactions
Open accessAbstract
Deposition of amyloid β (Aβ) containing plaques in the brain is one of the neuropathological hallmarks of Alzheimer's disease (AD). It has been suggested that modulation of neuronal activity may alter Aβ production in the brain. We postulate that these changes in Aβ production are due to changes in the rate-limiting step of Aβ generation, APP cleavage by γ-secretase. By combining biochemical approaches with fluorescence lifetime imaging microscopy, we found that neuronal inhibition decreases endogenous APP and PS1 interactions, which correlates with reduced Aβ production. By contrast, neuronal activation had a two-phase effect: it initially enhanced APP-PS1 interaction leading to increased Aβ production, which followed by a decrease in the APP and PS1 proximity/interaction. Accordingly, treatment of neurons with naturally secreted Aβ isolated from AD brain or with synthetic Aβ resulted in reduced APP and PS1 proximity. Moreover, applying low concentration of Aβ(42) to cultured neurons inhibited de novo Aβ synthesis. These data provide evidence that neuronal activity regulates endogenous APP-PS1 interactions, and suggest a model of a product-enzyme negative feedback. Thus, under normal physiological conditions Aβ may impact its own production by modifying γ-secretase cleavage of APP. Disruption of this negative modulation may cause Aβ overproduction leading to neurotoxicity.
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One explanation for Aβ aggregation within the DMN is that deposition of Aβ fibrils could be caused by high neuronal activity within the DMN, supported by animal studies showing Aβ secretion and deposition is enhanced by neuronal activity.
“One explanation is that the deposition of Aβ fibrils could be caused by the high neuronal activity within the DMN, which is supported by animal studies showing that Aβ secretion and deposition is enhanced by neuronal activity27–29.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [29]
Subjects with a mean/maximum frame-wise displacement exceeding 0.6/3.0 mm were excluded.
“Subjects with a mean/maximum frame-wise displacement29, 69 exceeding 0.6/3.0 mm were excluded.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [29]
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- Authors
- Li, X., Uemura, K., Hashimoto, T., Nasser-Ghodsi, N., Arimon, M., Lill, C. M., Palazzolo, I., Krainc, D., Hyman, B. T., & Berezovska, O.
- Affiliations
- Harvard University (US)
- Kyoto University (JP)
- Johannes Gutenberg University Mainz (DE)
- Corresponding author
- Berezovska, Oksana
- ORCID
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2013-02
- Volume
- 50
- Pages
- 127-134
- ISSN
- 0969-9961 (ISSN-L)
- PMC
- PMC3534898
- OpenAlex
- W2085770106
- Cited by
- 38
- References
- 37
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 7 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 5 · 2016: 2 · 2014: 3
- FWCI
- 0.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (AG015379)
- Deutscher Akademischer Austauschdienst (DAAD)
- 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, amyloid precursor protein, presenilin 1, gamma-secretase, neuronal activity, Alzheimer's disease, negative feedback regulation, amyloid-beta 42, neuronal inhibition, neuronal activation, fluorescence lifetime imaging, neurotoxicity
- MeSH terms
- Alzheimer Disease, Animals, Humans, Immunohistochemistry, Mice, Transgenic, Neurons, Blotting, Western, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Feedback, Physiological, Immunoprecipitation, Mice, Presenilin-1
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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