Comparative profiling of cortical gene expression in Alzheimer’s disease patients and mouse models demonstrates a link between amyloidosis and neuroinflammation
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Abstract Alzheimer’s disease (AD) is the most common form of dementia, characterized by accumulation of amyloid β (Aβ) and neurofibrillary tangles. Oxidative stress and inflammation are considered to play an important role in the development and progression of AD. However, the extent to which these events contribute to the Aβ pathologies remains unclear. We performed inter-species comparative gene expression profiling between AD patient brains and theAppNL-G-F/NL-G-Fand 3xTg-AD-H mouse models. Genes commonly altered inAppNL-G-F/NL-G-Fand human AD cortices correlated with the inflammatory response or immunological disease. Among them, expression of AD-related genes (C4a/C4b,Cd74,Ctss,Gfap,Nfe2l2,Phyhd1,S100b,Tf,Tgfbr2, andVim) was increased in theAppNL-G-F/NL-G-Fcortex as Aβ amyloidosis progressed with exacerbated gliosis, while genes commonly altered in the 3xTg-AD-H and human AD cortices correlated with neurological disease. TheAppNL-G-F/NL-G-Fcortex also had altered expression of genes (Abi3,Apoe,Bin2,Cd33,Ctsc,Dock2,Fcer1g,Frmd6,Hck,Inpp5D,Ly86,Plcg2,Trem2,Tyrobp) defined as risk factors for AD by genome-wide association study or identified as genetic nodes in late-onset AD. These results suggest a strong correlation between cortical Aβ amyloidosis and the neuroinflammatory response and provide a better understanding of the involvement of gender effects in the development of AD.
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PLCG2 mRNA upregulation has been reported in transgenic mice carrying early-AD mutations or overexpressing human tau.
“and in transgenic mice carrying mutations associated with early AD (APP KM670/671 NL, PNSEN1 M146V) or overexpressing the human tau-4R/2N isoform (P301L) [34, 35].”
From Alzheimer’s disease phospholipase C-gamma-2 (PLCG2) protective variant is a functional hypermorph (2019) · cites this paper as [34]
The Results report significantly increased Plcg2 expression in the cortex of App NL-G-F/NL-G-F mice carrying pathogenic App mutations. But this is an App knock-in model, not the APP/PSEN1/MAPT transgenic model described in the citing sentence. For that 3xTg-AD-H model, the Results report only Trem2—not Plcg2—as significantly increased. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSome studies have identified selected overlaps in expression changes between AD mouse models and human brains.
“Although some studies have identified selected overlaps in expression changes between AD mouse models and human brains (Bennett et al., 2018; Castillo et al., 2017; Mostafavi et al., 2018; Neuner et al., 2019; Rojo et al., 2017), other studies have questioned the overall degree of conservation (Burns et al., 2015; Galatro et al., 2017; Hargis and Blalock, 2017).”
From Meta-Analysis of the Alzheimer’s Disease Human Brain Transcriptome and Functional Dissection in Mouse Models (2020) · cites this paper as Castillo et al., 2017
Another study found an upregulation of INPP5D RNA expression in both human AD patients and an App knock-in mouse model.
“Another study similarly found an upregulation of INPP5D RNA expression in both human AD patients and an App knock-in mouse model [170].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [170]
Comparative gene expression profiling of known genetic risk factors in AD revealed an increase of PLCG2 gene expression in the cortex of AppNL-G-F/NL-G-F mice.
“Comparative gene expression profiling of known genetic risk factors in AD revealed an increase of PLCG2 gene expression in the cortex of AppNL-G-F/NL-G-F mice (165).”
From The role of PLCγ2 in immunological disorders, cancer, and neurodegeneration (2021) · cites this paper as [165]
LILRB4 orthologues are increased with amyloid deposition and specifically associated with amyloid plaques.
“LILRB4 (leukocyte immunoglobulin-like receptor, subfamily B, member 4), orthologues have also been shown to be increased with amyloid deposition and specifically associated with amyloid plaques (Wirz et al., 2013; Kamphuis et al., 2016; Castillo et al., 2017).”
From Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk (2019) · cites this paper as Castillo et al., 2017
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- Authors
- Castillo, E., Leon, J., Mazzei, G., Abolhassani, N., Haruyama, N., Saito, T., Saido, T., Hokama, M., Iwaki, T., Ohara, T., Ninomiya, T., Kiyohara, Y., Sakumi, K., LaFerla, F. M., & Nakabeppu, Y.
- Affiliations
- Kyushu University (JP)
- RIKEN (JP)
- Hisayama Research Institute For Lifestyle Diseases (JP)
- University of California, Irvine (US)
- Corresponding author
- Nakabeppu, Yusaku
- ORCID
- Venue
- Scientific Reports
- Published
- 2017-12-19
- Volume
- 7
- Issue
- 1
- Pages
- 17762-17762
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5736730
- OpenAlex
- W2771127066
- Cited by
- 158
- References
- 61
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 16 · 2023: 29 · 2022: 21 · 2021: 24 · 2020: 23 · 2019: 18 · 2018: 10
- FWCI
- 10.31
- Type
- journal article
- Language
- en
- Update notices
- correction (2021-09-09)
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Kyushu University Institutional Repository (QIR) (Kyushu University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Japan Agency for Medical Research and Development (H25-ninchisho-ippann-004)
- Ministry of Health, Labour and Welfare (H20-ninchisho-ippan-004)
- Fakultet Medicinskih Nauka, Univerziteta U Kragujevcu
- Japan Society for the Promotion of Science (26290017, 22221004, 15K15085, 17H01391)
- 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, neuroinflammation, cortical gene expression, gliosis, oxidative stress, sex differences
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Amyloidosis, Animals, Brain, Disease Models, Animal, Female, Gliosis, Humans, Inflammation, Male, Middle Aged, Gene Expression, Amyloid beta-Peptides, Gene Expression Profiling, Mice, Genome-Wide Association Study
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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