The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
Stimulation of β-Amyloid Precursor Protein Trafficking by Insulin Reduces Intraneuronal β-Amyloid and Requires Mitogen-Activated Protein Kinase Signaling
Open accessAbstract
Alzheimer's Disease (AD) is characterized by cerebral accumulation of β-amyloid peptides (Aβ), which are proteolytically derived from β-amyloid precursor protein (βAPP). βAPP metabolism is highly regulated via various signal transduction systems, e.g., several serine/threonine kinases and phosphatases. Several growth factors known to act via receptor tyrosine kinases also have been demonstrated to regulate sβAPP secretion. Among these receptors, insulin and insulin-like growth factor-1 receptors are highly expressed in brain, especially in hippocampus and cortex. Emerging evidence indicates that insulin has important functions in brain regions involved in learning and memory. Here we present evidence that insulin significantly reduces intracellular accumulation of Aβ and that it does so by accelerating βAPP/Aβ trafficking from the trans-Golgi network, a major cellular site for Aβ generation, to the plasma membrane. Furthermore, insulin increases the extracellular level of Aβ both by promoting its secretion and by inhibiting its degradation via insulin-degrading enzyme. The action of insulin on βAPP metabolism is mediated via a receptor tyrosine kinase/mitogen-activated protein (MAP) kinase kinase pathway. The results suggest cell biological and signal transduction mechanisms by which insulin modulates βAPP and Aβ trafficking in neuronal cultures.
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Cites
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Intraneuronal Aβ42 Accumulation in Human Brain
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Insulin-degrading Enzyme Regulates Extracellular Levels of Amyloid β-Protein by Degradation
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Cited by
Intracellular amyloid-β in Alzheimer's disease
LaFerla, F. M., Green, K. N., & Oddo, S. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2168 · Cited by 1,942
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The Gut Microbiota and Alzheimer’s Disease
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Insulin and neurodegenerative disease: shared and specific mechanisms
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A systemic view of Alzheimer disease — insights from amyloid-β metabolism beyond the brain
Wang, J., Gu, B. J., Masters, C. L., & Wang, Y.-J. (2017) · Nature Reviews Neurology · doi:10.1038/nrneurol.2017.111 · Cited by 808
Metadata
- Authors
- Gasparini, L., Gouras, G. K., Wang, R., Gross, R. S., Beal, M. F., Greengard, P., & Xu, H.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2001-04-15
- Volume
- 21
- Issue
- 8
- Pages
- 2561-2570
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1953255974
- Cited by
- 492
- References
- 55
- FWCI
- 8.47
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Stimulation of β-Amyloid Precursor Protein Trafficking by Insulin Reduces Intraneuronal β-Amyloid and Requires Mitogen-Activated Protein Kinase Signaling. https://app.cochat.ai/papers/10.1523/jneurosci.21-08-02561.2001
- The paper
- Gasparini, L., Gouras, G. K., Wang, R., Gross, R. S., Beal, M. F., Greengard, P., & Xu, H. (2001). Stimulation of β-Amyloid Precursor Protein Trafficking by Insulin Reduces Intraneuronal β-Amyloid and Requires Mitogen-Activated Protein Kinase Signaling. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.21-08-02561.2001
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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