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BACE inhibition-dependent repair of Alzheimer’s pathophysiology
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Significance The accumulation of amyloid-β (Aβ) proteins in the brain contributes to Alzheimer´s disease (AD). Reducing Aβ by inhibiting its production with a β-secretase (BACE) inhibitor represents a novel mechanism for treating AD; however, whether this therapeutic strategy is capable of repairing impaired brain circuits associated with AD is unknown. Here we demonstrate that BACE inhibition is beneficial to all levels of impairment in an AD mouse model: cellular, long-range circuitry, and memory. We provide evidence that the rescue is dependent on the reduction of soluble forms of Aβ surrounding amyloid plaques. These results have mechanistic and therapeutic implications for AD, including Aβ-related memory defects.
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“which has been shown to be dependent on soluble Aβ [38–40]”
From Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease (2024) · cites this paper as [38]
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Metadata
- Authors
- Keskin, A. D., Kekuš, M., Adelsberger, H., Neumann, U., Shimshek, D. R., Song, B., Zott, B., Peng, T., Förstl, H., Staufenbiel, M., Nelken, I., Sakmann, B., Konnerth, A., & Busche, M. A.
- Affiliations
- Technical University of Munich (DE)
- Novartis (Switzerland) (CH)
- Helmholtz Munich (DE)
- Hertie Institute for Clinical Brain Research (DE)
- Hebrew University of Jerusalem (IL)
- Munich Cluster for Systems Neurology (DE)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2017-07-24
- Volume
- 114
- Issue
- 32
- Pages
- 8631-8636
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC5559049
- OpenAlex
- W2738200982
- Cited by
- 125
- References
- 44
- Citations by year
- 2026: 2 · 2025: 10 · 2024: 19 · 2023: 11 · 2022: 10 · 2021: 19 · 2020: 13 · 2019: 28 · 2018: 13
- FWCI
- 10.93
- 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)
- mediaTUM (Technical University of Munich) (submittedVersion)
- Site cant be reached (submittedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- Funders
- EC | FP7 | FP7 Ideas: European Research Council (Advanced Grant)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
- Alzheimer's disease, beta-secretase inhibitors, amyloid-beta, amyloid plaques, soluble amyloid-beta, memory impairment, AD mouse model
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Humans, Mice, Transgenic, Neurons, Protease Inhibitors, Amyloid beta-Peptides, Mice, Amyloid Precursor Protein Secretases
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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.
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