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Figure 10 | Molecular Neurodegeneration

Figure 10

From: Molecular interplay between leptin, insulin-like growth factor-1, and β-amyloid in organotypic slices from rabbit hippocampus

Figure 10

Schematic representation of the interplay between leptin, IGF-1 and Aβ42. Leptin activates JAK2/STAT5 pathway (1), resulting in increased levels of p-Tyr694 STAT5 in the cytosol (2) and its translocation into the nucleus (3). Increased levels of p-Tyr694 STAT5 in the nucleus leads to increased expression of IGF-1 (4), which through an effect on IGF-1R (5), activates the Akt/mTORC1 pathway (6). Activation of mTORC1 results in the increased expression levels of the transcription factor C-EBPα (7) and its translocation to the nucleus (8). Increased nuclear levels of C-EBPα result in its increased binding to the leptin promoter and augmentation in leptin expression (9). Aβ42 inhibits the activation of the JAK2/STAT5 pathway (10) and attenuates the levels of p-Tyr694 STAT5 in the cytosol and the nucleus (11), resulting in reduced IGF-1 expression. Aβ42 also decreases mTORC1 activation and signaling (12) leading to reduction in C-EBPα levels in the cytosol and nucleus (13), effects that reduce leptin expression.

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