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The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer’s disease
Open accessAbstract
Innate immunity is associated with Alzheimer's disease 1, but the influence of immune activation on the production of amyloid-β is unknown 2,3. Here we identify interferon-induced transmembrane protein 3 (IFITM3) as a γ-secretase modulatory protein, and establish a mechanism by which inflammation affects the generation of amyloid-β. Inflammatory cytokines induce the expression of IFITM3 in neurons and astrocytes, which binds to γ-secretase and upregulates its activity, thereby increasing the production of amyloid-β. The expression of IFITM3 is increased with ageing and in mouse models that express familial Alzheimer's disease genes. Furthermore, knockout of IFITM3 reduces γ-secretase activity and the formation of amyloid plaques in a transgenic mouse model (5xFAD) of early amyloid deposition. IFITM3 protein is upregulated in tissue samples from a subset of patients with late-onset Alzheimer's disease that exhibit higher γ-secretase activity. The amount of IFITM3 in the γ-secretase complex has a strong and positive correlation with γ-secretase activity in samples from patients with late-onset Alzheimer's disease. These findings reveal a mechanism in which γ-secretase is modulated by neuroinflammation via IFITM3 and the risk of Alzheimer's disease is thereby increased.
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“Activated microglia may be involved in the generation of Aβ plaque by increasing the secretion of Aβ fragments; inducing the expression of interferon-induced transmembrane protein 3 (IFITM3), a γ-secretase modulatory protein; or releasing agents such as iron, which enhances the aggregation of soluble β-amyloid.37–39”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [39]
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“Brain inflammation can also trigger deposition of pathological amyloid proteins via upregulation of interferon‐induced transmembrane protein 3 (IFITM3). 104”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [104]
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Metadata
- Authors
- Hur, J.-Y., Frost, G. R., Wu, X., Crump, C., Pan, S. J., Wong, E., Barros, M., Li, T., Nie, P., Zhai, Y., Wang, J. C., TCW, J., Guo, L., McKenzie, A., Ming, C., Zhou, X., Wang, M., Sagi, Y., Renton, A. E., Esposito, B. T., Kim, Y., Sadleir, K. R., Trinh, I., Rissman, R. A., Vassar, R., Zhang, B., Johnson, D. S., Masliah, E., Greengard, P., Goate, A., & Li, Y.-M.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Icahn School of Medicine at Mount Sinai (US)
- Rockefeller University (US)
- Northwestern University (US)
- University of California San Diego (US)
- Pfizer (United States) (US)
- Corresponding author
- Li, Yue-Ming
- ORCID
- Hur, Ji-Yeun
- Frost, Georgia R.
- Wong, Eitan
- Barros, Marilia
- Li, Thomas
- Zhai, Yujia
- TCW, Julia
- Guo, Lei
- McKenzie, Andrew
- Ming, Chen
- Zhou, Xianxiao
- Wang, Minghui
- Sagi, Yotam
- Renton, Alan E.
- Kim, Yong
- Sadleir, Katherine R.
- Trinh, Ivy
- Rissman, Robert A.
- Vassar, Robert
- Zhang, Bin
- Johnson, Douglas S.
- Masliah, Eliezer
- Greengard, Paul
- Goate, Alison
- Li, Yue-Ming
- Venue
- Nature
- Published
- 2020-09-02
- Volume
- 586
- Issue
- 7831
- Pages
- 735-740
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC7919141
- OpenAlex
- W3082942379
- Cited by
- 382
- References
- 64
- Citations by year
- 2026: 53 · 2025: 51 · 2024: 53 · 2023: 68 · 2022: 77 · 2021: 65 · 2020: 15
- FWCI
- 34.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health (1s10od018522-01, 1s10od026880-01)
- National Institute on Aging (R01AG057907, R01AG026660, U01AG046170, R01AG018440, R01AG006170, RF1AG057440, K01AG062683, RF1AG057593, R01AG061350, P30AG062429)
- National Cancer Institute (P30CA008748)
- National Institute of Neurological Disorders and Stroke (R01NS096275)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
- IFITM3, gamma-secretase, Alzheimer's disease, amyloid-beta, innate immunity, neuroinflammation, inflammatory cytokines, presenilin, amyloid plaques, 5xFAD mice, late-onset Alzheimer's disease, aging, familial Alzheimer's disease
- MeSH terms
- Aged, 80 and over, Aging, Alzheimer Disease, Animals, Astrocytes, Disease Models, Animal, Female, Humans, Immunity, Innate, Inflammation, Male, Membrane Proteins, Mice, Inbred C57BL, Mice, Transgenic, Risk, Up-Regulation, Amyloid beta-Protein Precursor, RNA-Binding Proteins, Age of Onset, Catalytic Domain, Mice, Presenilin-1, Amyloid Precursor Protein Secretases, HEK293 Cells
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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