The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Defective insulin signaling pathway and increased glycogen synthase kinase‐3 activity in the brain of diabetic mice: Parallels with Alzheimer's disease and correction by insulin
Open accessAbstract
We have evaluated the effect of peripheral insulin deficiency on brain insulin pathway activity in a mouse model of type 1 diabetes, the parallels with Alzheimer's disease (AD), and the effect of treatment with insulin. Nine weeks of insulin‐deficient diabetes significantly impaired the learning capacity of mice, significantly reduced insulin‐degrading enzyme protein expression, and significantly reduced phosphorylation of the insulin‐receptor and AKT. Phosphorylation of glycogen synthase kinase‐3 (GSK3) was also significantly decreased, indicating increased GSK3 activity. This evidence of reduced insulin signaling was associated with a concomitant increase in tau phosphorylation and amyloid β protein levels. Changes in phosphorylation levels of insulin receptor, GSK3, and tau were not observed in the brain of db/db mice, a model of type 2 diabetes, after a similar duration (8 weeks) of diabetes. Treatment with insulin from onset of diabetes partially restored the phosphorylation of insulin receptor and of GSK3, partially reduced the level of phosphorylated tau in the brain, and partially improved learning ability in insulin‐deficient diabetic mice. Our data indicate that mice with systemic insulin deficiency display evidence of reduced insulin signaling pathway activity in the brain that is associated with biochemical and behavioral features of AD and that it can be corrected by insulin treatment. © 2008 Wiley‐Liss, Inc.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B
Cross, D. A. E., Alessi, D. R., Cohen, P., Andjelkovich, M., & Hemmings, B. A. (1995) · Nature · doi:10.1038/378785a0 · Cited by 5,244
Memory deficits associated with senescence: A neurophysiological and behavioral study in the rat.
Barnes, C. A. (1979) · Journal of Comparative and Physiological Psychology · doi:10.1037/h0077579 · Cited by 2,088
Steen, E., Terry, B. M., J. Rivera, E., Cannon, J. L., Neely, T. R., Tavares, R., Xu, X. J., Wands, J. R., & de la Monte, S. M. (2005) · Journal of Alzheimer's Disease · doi:10.3233/jad-2005-7107 · Cited by 1,703
Type 2 Diabetes, APOE Gene, and the Risk for Dementia and Related Pathologies
Peila, R., Rodriguez, B. L., & Launer, L. J. (2002) · Diabetes · doi:10.2337/diabetes.51.4.1256 · Cited by 1,207
Cognitive decline and dementia in diabetes—systematic overview of prospective observational studies
Cukierman, T., Gerstein, H. C., & Williamson, J. D. (2005) · Diabetologia · doi:10.1007/s00125-005-0023-4 · Cited by 1,049 · cited 2×
“There is increasing awareness that diabetes has an impact on the central nervous system, with reports of impaired learning, memory, mental flexibility, and problem solving being more common in both type 1 and type 2 diabetic subjects than in the general population (Ryan et al., 1985; Reaven et al., 1990; Ryan and Will…”
BackgroundSutherland, C., Leighton, I. A., & Cohen, P. (1993) · Biochemical Journal · doi:10.1042/bj2960015 · Cited by 903
Yoshitake, T., Kiyohara, Y., Kato, I., Ohmura, T., Iwamoto, H., Nakayama, K., Ohmori, S., Nomiyama, K., Kawano, H., Ueda, K., et al. (1995) · Neurology · doi:10.1212/wnl.45.6.1161 · Cited by 829
Brain insulin and insulin receptors in aging and sporadic Alzheimer’s disease
Frölich, L., Blum-Degen, D., Bernstein, H.-G., Engelsberger, S., Humrich, J., Laufer, S., Muschner, D., Thalheimer, A., Türk, A., Hoyer, S., et al. (1998) · Journal of Neural Transmission · doi:10.1007/s007020050068 · Cited by 748
Risk of Dementia among Persons with Diabetes Mellitus: A Population-based Cohort Study
Leibson, C. L., Rocca, W. A., Hanson, V. A., Cha, R., Kokmen, E., O'Brien, P. C., & Palumbo, P. J. (1997) · American Journal of Epidemiology · doi:10.1093/oxfordjournals.aje.a009106 · Cited by 700
Cho, J., & Johnson, G. V. W. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2004.02155.x · Cited by 282
Cited by
The Role of Metabolic Disorders in Alzheimer Disease and Vascular Dementia: Two Roads Converged
Craft, S. (2009) · Archives of Neurology · doi:10.1001/archneurol.2009.27 · Cited by 547
Deficient brain insulin signalling pathway in Alzheimer's disease and diabetes
Liu, Y., Liu, F., Grundke‐Iqbal, I., Iqbal, K., & Gong, C. (2011) · The Journal of Pathology · doi:10.1002/path.2912 · Cited by 502
How does diabetes accelerate Alzheimer disease pathology?
Sims-Robinson, C., Kim, B., Rosko, A., & Feldman, E. L. (2010) · Nature Reviews Neurology · doi:10.1038/nrneurol.2010.130 · Cited by 492
Insulin resistance and Parkinson’s disease: A new target for disease modification?
Athauda, D., & Foltynie, T. (2016) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2016.10.001 · Cited by 328
Diabetes mellitus and Alzheimer's disease: GSK-3β as a potential link
Zhang, Y., Huang, N.-Q., Yan, F., Jin, H., Zhou, S.-Y., Shi, J.-S., & Jin, F. (2018) · Behavioural Brain Research · doi:10.1016/j.bbr.2017.11.015 · Cited by 301
Metadata
- Authors
- Jolivalt, C. G., Lee, C. A., Beiswenger, K. K., Smith, J. L., Orlov, M., Torrance, M. A., & Masliah, E.
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2008-07-14
- Volume
- 86
- Issue
- 15
- Pages
- 3265-3274
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- OpenAlex
- W2159406238
- Cited by
- 287
- References
- 13
- FWCI
- 8.65
- Type
- journal article
- Language
- en
- Open access
- green
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 ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Defective insulin signaling pathway and increased glycogen synthase kinase‐3 activity in the brain of diabetic mice: Parallels with Alzheimer's disease and correction by insulin. https://app.cochat.ai/papers/10.1002/jnr.21787
- The paper
- Jolivalt, C. G., Lee, C. A., Beiswenger, K. K., Smith, J. L., Orlov, M., Torrance, M. A., & Masliah, E. (2008). Defective insulin signaling pathway and increased glycogen synthase kinase‐3 activity in the brain of diabetic mice: Parallels with Alzheimer's disease and correction by insulin. Journal of Neuroscience Research. https://doi.org/10.1002/jnr.21787
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
