Cited by 218Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Neuronal IGF‐1 resistance reduces Aβ accumulation and protects against premature death in a model of Alzheimer's disease

Freude, Susanna, Hettich, Moritz M., Schumann, Christina, Stöhr, Oliver, Koch, Linda, Köhler, Christoph, Udelhoven, Michael, Leeser, Uschi, Müller, Marita, Kubota, Naoto, Kadowaki, Takashi, Krone, Wilhelm, Schroder, Hannsjörg, Brüning, Jens C., Schubert, Markus·2009·The FASEB Journal

DOI 10.1096/fj.09-132043

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Abstract

Alzheimer's disease (AD) is characterized by progressive neurodegeneration leading to loss of cognitive abilities and ultimately to death. Postmortem investigations revealed decreased expression of cerebral insulin‐like growth factor (IGF)‐1 receptor (IGF‐1R) and insulin receptor substrate (IRS) proteins in patients with AD. To elucidate the role of insulin/IGF‐1 signaling in AD, we crossed mice expressing the Swedish mutation of amyloid precursor protein (APP SW , Tg2576 mice) as a model for AD with mice deficient for either IRS‐2, neuronal IGF‐1R (nIGF‐1R −/− ), or neuronal insulin receptor (nIR −/− ), and analyzed survival, glucose, and APP metabolism. In the present study, we show that IRS‐2 deficiency in Tg2576 mice completely reverses premature mortality in Tg2576 females and delays β‐amyloid (Aβ) accumulation. Analysis of APP metabolism suggested that delayed Aβ accumulation resulted from decreased APP processing. To delineate the upstream signal responsible for IRS‐2‐mediated disease protection, we analyzed mice with nIGF‐1R or nIR deficiency predominantly in the hippocampus. Interestingly, both male and female nIGF‐1R −/− Tg2576 mice were protected from premature death in the presence of decreased Aβ accumulation specifically in the hippocampus formation. However, neuronal IR deletion had no influence on lethality of Tg2576 mice. Thus, impaired IGF‐1/IRS‐2 signaling prevents premature death and delays amyloid accumulation in a model of AD.—Freude, S., Hettich, M. M., Schumann, C., Stohr, O., Koch, L., Kohler, C., Udelhoven, M., Leeser, U., Müller, M., Kubota, N., Kadowaki, T., Krone, W., Schroder, H., Bruning, J. C., Schubert, M. Neuronal IGF‐1 resistance reduces Aβ accumulation and protects against premature death in a model of Alzheimer's disease. FASEB J . 23, 3315–3324 (2009). www.fasebj.org

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Authors: Freude, S., Hettich, M. M., Schumann, C., Stöhr, O., Koch, L., Köhler, C., Udelhoven, M., Leeser, U., Müller, M., Kubota, N., Kadowaki, T., Krone, W., Schroder, H., Brüning, J. C., & Schubert, M.
Affiliations: University of Cologne (DE)
The University of Tokyo (JP)
Department II of Anatomy University of Cologne Cologne Germany
Corresponding author: Schubert, Markus
ORCID: Hettich, Moritz M.
Schumann, Christina
Koch, Linda
Köhler, Christoph
Kubota, Naoto
Kadowaki, Takashi
Brüning, Jens C.
Schubert, Markus
Venue: The FASEB Journal
Publisher: Wiley
Published: 2009-06
Volume: 23
Issue: 10
Pages: 3315-3324
ISSN: 0892-6638 (ISSN-L)
1530-6860
DOI: 10.1096/fj.09-132043
OpenAlex: W2134406000
Cited by: 218
References: 61
Citations by year: 2026: 3 · 2025: 5 · 2024: 12 · 2023: 16 · 2022: 13 · 2021: 8 · 2020: 9 · 2019: 10 · 2018: 11 · 2017: 7 · 2016: 16 · 2015: 10 · 2014: 26 · 2013: 15 · 2012: 21
FWCI: 12.63
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: The FASEB Journal (publishedVersion)
PubMed (publishedVersion)
OPUS (Augsburg University) (submittedVersion)
Funders: Fritz Thyssen Stiftung (AZ 10.06.2.209)
Deutsche Forschungsgemeinschaft (Br-1492-7)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: Alzheimer's disease, IGF-1 resistance, IGF-1 receptor, insulin receptor substrate 2, insulin/IGF-1 signaling, amyloid-beta deposition, amyloid precursor protein, Tg2576 mice, premature mortality, hippocampus, APP processing, neuroprotection
MeSH terms: Alzheimer Disease, Animals, Disease Models, Animal, Female, Insulin-Like Growth Factor I, Male, Mice, Mutant Strains, Neurons, Amyloid beta-Peptides, Receptor, IGF Type 1, Mice, Insulin Receptor Substrate Proteins

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Neuronal IGF‐1 resistance reduces Aβ accumulation and protects against premature death in a model of Alzheimer's disease

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