Experimental evidence for temporal uncoupling of brain Aβ deposition and neurodegenerative sequelae
Open accessAbstract
Brain Aβ deposition is a key early event in the pathogenesis of Alzheimer´s disease (AD), but the long presymptomatic phase and poor correlation between Aβ deposition and clinical symptoms remain puzzling. To elucidate the dependency of downstream pathologies on Aβ, we analyzed the trajectories of cerebral Aβ accumulation, Aβ seeding activity, and neurofilament light chain (NfL) in the CSF (a biomarker of neurodegeneration) in Aβ-precursor protein transgenic mice. We find that Aβ deposition increases linearly until it reaches an apparent plateau at a late age, while Aβ seeding activity increases more rapidly and reaches a plateau earlier, coinciding with the onset of a robust increase of CSF NfL. Short-term inhibition of Aβ generation in amyloid-laden mice reduced Aβ deposition and associated glial changes, but failed to reduce Aβ seeding activity, and CSF NfL continued to increase although at a slower pace. When short-term or long-term inhibition of Aβ generation was started at pre-amyloid stages, CSF NfL did not increase despite some Aβ deposition, microglial activation, and robust brain Aβ seeding activity. A dissociation of Aβ load and CSF NfL trajectories was also found in familial AD, consistent with the view that Aβ aggregation is not kinetically coupled to neurotoxicity. Rather, neurodegeneration starts when Aβ seeding activity is saturated and before Aβ deposition reaches critical (half-maximal) levels, a phenomenon reminiscent of the two pathogenic phases in prion disease.
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5×FAD models are particularly suitable for dissecting earlier mechanisms, processes, and for testing early therapeutic interventions relevant to prodromal human AD.
“In summary, 5×FAD models are particularly suitable for dissecting earlier mechanisms, processes, and for testing early therapeutic interventions relevant to prodromal human AD, a case recently also made by Jucker and colleagues78,79.”
From Magnetic resonance microscopy maps widespread effects of Alzheimer’s disease on brain structures and behavior in mice (2026) · cites this paper as [78]
The Discussion describes APP-transgenic mice as models of presymptomatic AD and argues for earlier Aβ-targeting intervention. But the Methods (Experimental animals; BACE1 inhibitor treatment) identify APPPS1 and APP23 mice, not 5×FAD mice. The paper supports the broader rationale for studying early disease and interventions in mouse models, but not the claim that 5×FAD is particularly suitable. (LLM, conf=0.88)
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- Authors
- Rother, C., Uhlmann, R. E., Müller, S. A., Schelle, J., Skodras, A., Obermüller, U., Häsler, L. M., Lambert, M., Baumann, F., Xu, Y., Bergmann, C., Salvadori, G., Loos, M., Brzak, I., Shimshek, D., Neumann, U., Dominantly Inherited Alzheimer Network, Walker, L. C., Schultz, S. A., Chhatwal, J. P., Kaeser, S. A., Lichtenthaler, S. F., Staufenbiel, M., & Jucker, M.
- Affiliations
- German Center for Neurodegenerative Diseases (DE)
- Sylics (Netherlands) (NL)
- Novartis (Switzerland) (CH)
- Emory University (US)
- Massachusetts General Hospital (US)
- Corresponding author
- Jucker, Mathias
- ORCID
- Venue
- Nature Communications
- Published
- 2022-11-28
- Volume
- 13
- Issue
- 1
- Pages
- 7333-7333
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC9705543
- OpenAlex
- W4310142253
- Cited by
- 28
- References
- 70
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 12 · 2023: 5
- FWCI
- 3.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DZNE Pub (publishedVersion, other-oa)
- Open access LMU (Ludwid Maxmilian's Universitat Munchen) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Alexander von Humboldt-Stiftung
- EU Joint Programme – Neurodegenerative Disease Research
- European Federation of Pharmaceutical Industries and Associations (116060)
- Deutsche Forschungsgemeinschaft (EXC 2145, EXC 2145SyNergy, 390857198, JU655/4-1)
- Bundesministerium für Bildung und Forschung
- National Institutes of Health (P51OD011132)
- National Institute on Aging (U19AG032438)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, amyloid-beta deposition, neurofilament light chain, cerebrospinal fluid biomarkers, neurodegeneration, familial Alzheimer's disease, microglial activation, prion pathogenesis, presymptomatic phase
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Brain, Inhibition, Psychological, Mice, Transgenic, Disease Progression, Mice, Amyloidogenic Proteins
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