Progranulin protects against amyloid β deposition and toxicity in Alzheimer's disease mouse models
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Haploinsufficiency of the progranulin (PGRN) gene (GRN) causes familial frontotemporal lobar degeneration (FTLD) and modulates an innate immune response in humans and in mouse models. GRN polymorphism may be linked to late-onset Alzheimer's disease (AD). However, the role of PGRN in AD pathogenesis is unknown. Here we show that PGRN inhibits amyloid β (Aβ) deposition. Selectively reducing microglial expression of PGRN in AD mouse models impaired phagocytosis, increased plaque load threefold and exacerbated cognitive deficits. Lentivirus-mediated PGRN overexpression lowered plaque load in AD mice with aggressive amyloid plaque pathology. Aβ plaque load correlated negatively with levels of hippocampal PGRN, showing the dose-dependent inhibitory effects of PGRN on plaque deposition. PGRN also protected against Aβ toxicity. Lentivirus-mediated PGRN overexpression prevented spatial memory deficits and hippocampal neuronal loss in AD mice. The protective effects of PGRN against Aβ deposition and toxicity have important therapeutic implications. We propose enhancing PGRN as a potential treatment for PGRN-deficient FTLD and AD.
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In Aβ-mice, overexpressing progranulin inhibits Aβ deposition and protects against Aβ toxicity.
“In Aβ-mice, progranulin overexpression inhibits Aβ deposition and protects from Aβ toxicity.”
From Microglia in neurodegeneration (2018) · cites this paper as [144]
Reducing microglial progranulin expression in Aβ-mice impairs phagocytosis, raises plaque load, and worsens cognitive deficits.
“Selective reduction of microglial expression of progranulin in Aβ-mice also impairs phagocytosis, increases plaque load, and exacerbates cognitive deficits.”
From Microglia in neurodegeneration (2018) · cites this paper as [144]
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- Authors
- Minami, S. S., Min, S.-W., Krabbe, G., Wang, C., Zhou, Y., Asgarov, R., Li, Y., Martens, L. H., Elia, L. P., Ward, M. E., Mucke, L., Farese, R. V., & Gan, L.
- Affiliations
- University of California, San Francisco (US)
- Gladstone Institutes (US)
- Stockholm University (SE)
- Corresponding author
- Gan, Li
- ORCID
- Venue
- Nature Medicine
- Published
- 2014-09-28
- Volume
- 20
- Issue
- 10
- Pages
- 1157-1164
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4196723
- OpenAlex
- W1966113514
- Cited by
- 237
- References
- 61
- Citations by year
- 2026: 10 · 2025: 19 · 2024: 23 · 2023: 12 · 2022: 21 · 2021: 19 · 2020: 20 · 2019: 26 · 2018: 35 · 2017: 26 · 2016: 14 · 2015: 10 · 2014: 2
- FWCI
- 11.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute on Aging (F31AG034793, R01AG030207, R01AG036884, P50AG023501)
- National Institute of Neurological Disorders and Stroke (P30NS065780, F32NS076239)
- 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
- progranulin, Alzheimer's disease, amyloid-beta deposition, amyloid plaques, microglia, phagocytosis, spatial memory impairment, hippocampal neuronal loss, familial frontotemporal lobar degeneration, cognitive impairment, therapeutic target
- MeSH terms
- Progranulins, Granulins, Alzheimer Disease, Animals, Brain, Cognition, Disease Models, Animal, Female, Gene Expression Regulation, Humans, Immunity, Innate, Male, Mice, Inbred C57BL, Mice, Transgenic, Phagocytosis, Up-Regulation, Amyloid beta-Peptides, Microglia, Mice, Knockout, Intercellular Signaling Peptides and Proteins, Mice, Rats, Frontotemporal Lobar Degeneration, Plaque, Amyloid
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