Insulin-like growth factor I protects and rescues hippocampal neurons against β-amyloid- and human amylin-induced toxicity

Doré, Sylvain; Kar, Satyabrata; Quirion, Rémi

doi:10.1073/pnas.94.9.4772

Cited by 311 publications

(213 citation statements)

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“…Insulin-like growth factor stimulates neuronal release and clearance of Aβ and IGF1 levels are altered in AD [6]. The dose of IGF1 which is neuroprotective in hippocampal neurons is 10uM, the dose used in these studies [9]. In the same study, IGF2 was effective but less potent.…”

Section: Discussionmentioning

confidence: 90%

Beta-amyloid toxicity and reversal in embryonic rat septal neurons

Jarvis

Assis-Nascimento

Mudd

et al. 2007

Neuroscience Letters

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Section: Discussionmentioning

confidence: 90%

Beta-amyloid toxicity and reversal in embryonic rat septal neurons

Jarvis

Assis-Nascimento

Mudd

et al. 2007

Neuroscience Letters

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“…IGF-I protection from ceramide has previously been shown in non-neuronal cells [30,36]. IGF-I has been also shown to protect hippocampal neurons from h-amyloid peptide toxicity [16], dorsal root ganglion neurons from Nerve Growth Factor withdrawal [59] and cortical neurons from hypoxia [58].…”

Section: Discussionmentioning

confidence: 95%

IGF-I protects cortical neurons against ceramide-induced apoptosis via activation of the PI-3K/Akt and ERK pathways; is this protection independent of CREB and Bcl-2?

Willaime‐Morawek

Arbez

Mariani

et al. 2005

Molecular Brain Research

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Current understanding of IGF-I-mediated neuroprotection implies the activation of phosphatidylinositol-3-kinase (PI-3K), which leads to the activation of Akt/Protein Kinase B. In non-neuronal cells, Akt phosphorylates and activates the transcription factor CREB, implicated in the transcription of the anti-apoptotic bcl-2 gene. This paper further analyses the anti-apoptotic IGF-I action in neurons. We show that IGF-I protects cortical neurons against ceramide-induced apoptosis. Ceramide decreases Akt phosphorylation during apoptotic process whereas a simultaneous treatment with IGF-I increases Akt phosphorylation. Analysis of the signal transduction pathways revealed that IGF-I induces CREB phosphorylation via PI-3K and ERK, whereas simultaneous ceramide and IGF-I treatment decreases CREB phosphorylation. Although an overexpression of Bcl-2 protects cortical neurons against ceramide-induced apoptosis, our data indicate that the Bcl-2 protein level is not modulated during IGF-I, ceramide and/or LY294002 treatment. In consequence, we demonstrated that IGF protects neurons against ceramide-induced apoptosis and that IGF-I protection involves the PI-3K/Akt and ERK pathways; this protection may be independent of CREB and Bcl-2. D

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“…Indeed, subcutaneous infusion of IGF-I reduces Aβ levels in the brain (Carro et al, 2002) and protects neurons from Aβ-induced cell death (Doré et al, 1997). We have previously shown that SRIF-and SSTR2-immunopositive cells colocalize with TUNEL labeling, which identifies the cell types undergoing apoptosis, in sections of the temporal cortex from Aβ25-35-treated rats (Aguado-Llera et al, 2006).…”

Section: Protective Effects Of Igf-i On the Somatostatinergic System mentioning

confidence: 99%