Reduced IGF-1 signaling delays age-associated proteotoxicity in mice
Open accessAbstract
The insulin/insulin growth factor (IGF) signaling (IIS) pathway is a key regulator of aging of worms, flies, mice, and likely humans. Delayed aging by IIS reduction protects the nematode C. elegans from toxicity associated with the aggregation of the Alzheimer's disease-linked human peptide, Abeta. We reduced IGF signaling in Alzheimer's model mice and discovered that these animals are protected from Alzheimer's-like disease symptoms, including reduced behavioral impairment, neuroinflammation, and neuronal loss. This protection is correlated with the hyperaggregation of Abeta leading to tightly packed, ordered plaques, suggesting that one aspect of the protection conferred by reduced IGF signaling is the sequestration of soluble Abeta oligomers into dense aggregates of lower toxicity. These findings indicate that the IGF signaling-regulated mechanism that protects from Abeta toxicity is conserved from worms to mammals and point to the modulation of this signaling pathway as a promising strategy for the development of Alzheimer's disease therapy.
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In neurodegenerative disease, soluble oligomers are considered the main toxic species, and depositing them into insoluble aggregates lowers toxicity.
“This conclusion is consistent with the view that soluble oligomers are the major proteotoxic species in neurodegenerative diseases and that their sequestration into insoluble aggregates reduces proteotoxicity (Arrasate et al., 2004; Cohen et al., 2006; Cohen et al., 2009).”
From Widespread Proteome Remodeling and Aggregation in Aging C. elegans (2015) · cites this paper as Cohen et al., 2009
Knockout of Irs2 or the IGF-1 receptor can reduce cognitive impairment, neurodegeneration and premature mortality in mouse models of Alzheimer's disease.
“Similarly, knockout of Irs2 or the IGF-1 receptor can reduce cognitive impairment, neurodegeneration and premature mortality in mouse models of Alzheimer’s disease (71,72).”
From Neural mechanisms of ageing and cognitive decline (2010) · cites this paper as [72]
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Beneficial effects of dietary restriction in aging brain
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- Authors
- Cohen, E., Paulsson, J. F., Blinder, P., Burstyn-Cohen, T., Du, D., Estepa, G., Adame, A., Pham, H. M., Holzenberger, M., Kelly, J. W., Masliah, E., & Dillin, A.
- Affiliations
- Salk Institute for Biological Studies (US)
- Scripps Research Institute (US)
- University of California San Diego (US)
- Inserm (FR)
- Corresponding author
- Dillin, Andrew
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 139
- Issue
- 6
- Pages
- 1157-1169
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3017511
- OpenAlex
- W2050068554
- Cited by
- 488
- References
- 61
- Citations by year
- 2026: 12 · 2025: 17 · 2024: 19 · 2023: 22 · 2022: 16 · 2021: 24 · 2020: 22 · 2019: 21 · 2018: 20 · 2017: 27 · 2016: 36 · 2015: 38 · 2014: 37 · 2013: 42 · 2012: 43
- FWCI
- 29.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- McKnight Foundation
- National Institute on Aging (P01AG031097)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Antioxidants, Aging, Portulaca oleracea
- Keywords
- IGF-1 signaling, aging, Alzheimer's disease, amyloid-beta, proteotoxicity, neuroinflammation, neuronal loss, behavioral impairment, amyloid plaques, Alzheimer's disease treatment
- MeSH terms
- Alzheimer Disease, Animals, Humans, Insulin-Like Growth Factor I, Longevity, Male, Mice, Transgenic, Signal Transduction, Amyloid beta-Peptides, Receptor, IGF Type 1, Mice, Presenilin-1
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.
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