Reduced β-amyloid pathology in an APP transgenic mouse model of Alzheimer’s disease lacking functional B and T cells
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INTRODUCTION: In Alzheimer's disease, accumulation and pathological aggregation of amyloid β-peptide is accompanied by the induction of complex immune responses, which have been attributed both beneficial and detrimental properties. Such responses implicate various cell types of the innate and adaptive arm of the immunesystem, both inside the central nervous system, and in the periphery. To investigate the role of the adaptive immune system in brain β-amyloidosis, PSAPP transgenic mice, an established mouse model of Alzheimer's disease, were crossbred with the recombination activating gene-2 knockout (Rag2 ko) mice lacking functional B and T cells. In a second experimental paradigm, aged PSAPP mice were reconstituted with bone marrow cells from either Rag2 ko or wildtype control mice. RESULTS: Analyses from both experimental approaches revealed reduced β-amyloid pathology and decreased brain amyloid β-peptide levels in PSAPP mice lacking functional adaptive immune cells. The decrease in brain β-amyloid pathology was associated with enhanced microgliosis and increased phagocytosis of amyloid β-peptide aggregates. CONCLUSION: The results of this study demonstrate an impact of the adaptive immunity on cerebral β-amyloid pathology in vivo and suggest an influence on microglia-mediated amyloid β-peptide clearance as a possible underlying mechanism.
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Depletion of T cells, B cells, and natural killer (NK) cells contributes to an increase in Aβ deposition.
“It has previously been shown that the depletion of T cells, B cells, and natural killer (NK) cells contributes to an increase in Aβ deposition [4–6].”
From Control of the temporal development of Alzheimer’s disease pathology by the MR1/MAIT cell axis (2023) · cites this paper as [5]
The Discussion (page unavailable) reports reduced brain Aβ and β-amyloid pathology in PSAPP mice lacking functional T and B cells—the opposite of the claimed increase. The study does not establish an effect of NK-cell depletion. (LLM, conf=0.91)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredAPP/PS1 mice on a Rag2-deficient background demonstrated improved disease progression.
“APP/PS1 mice on a Rag2 -deficient background (which lack functional T and B cells) demonstrated improved disease progression [110].”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [110]
The Results section on congenital adaptive-immune deficiency reports 25–30% less amyloid plaque pathology in eight-month-old PSAPP/Rag2-deficient mice than in PSAPP controls. But the Results section on cognitive behavior reports impaired memory performance in both groups, so the broader claim of improved disease progression is not established beyond reduced amyloid pathology. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGenetic and antibody-based B cell inactivation strategies in AD mouse models have yielded conflicting results.
“researchers have employed both genetic and antibody-based B cell inactivation strategies, though these approaches have yielded conflicting results.”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [110]
The Introduction and Conclusions describe genetic ablation of both B and T cells in AD mouse models and reduced amyloid pathology. The Discussion contrasts that result with evidence suggesting that loss of Aβ-reactive B cells might instead worsen amyloid pathology. Our copy does not describe antibody-based B-cell inactivation or conflicting results from genetic versus antibody-based strategies. (LLM, conf=0.83)
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- Authors
- Späni, C., Suter, T., Derungs, R., Ferretti, M. T., Welt, T., Wirth, F., Gericke, C., Nitsch, R. M., & Kulic, L.
- Affiliations
- University of Zurich (CH)
- University Hospital Zurich (CH)
- Corresponding author
- Kulic, Luka
- ORCID
- Venue
- Acta Neuropathologica Communications
- Published
- 2015-11-11
- Volume
- 3
- Issue
- 1
- Pages
- 71-71
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC4642668
- OpenAlex
- W2130834754
- Cited by
- 88
- References
- 76
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 15 · 2023: 9 · 2022: 14 · 2021: 8 · 2020: 8 · 2019: 3 · 2018: 5 · 2017: 4 · 2016: 4
- FWCI
- 3.19
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Forschungskredit grant University of Zurich (K-82031-02-01)
- 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 pathology, APP transgenic mice, Rag2 knockout mice, adaptive immunity, B cells, T cells, bone marrow reconstitution, microglial activation, microglial phagocytosis, amyloid clearance, innate immunity
- MeSH terms
- Alzheimer Disease, Animals, B-Lymphocytes, Disease Models, Animal, DNA-Binding Proteins, Exploratory Behavior, Female, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Peptide Fragments, T-Lymphocytes, Cytokines, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Maze Learning, Adoptive Transfer, Recognition, Psychology, Mice
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