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- W2020656871 abstract "Novel evidence demonstrates that insulin and its signaling pathway may significantly contribute to the pathogenesis of Alzheimer's disease (AD). Since insulin has generally been thought as a neurotrophic and neuroprotective factor, which can promote synaptic function and memory formation, it is logically considered that insulin administration as an alternative to the potential therapeutic strategies for memory impairment in AD patients. However, the contribution of insulin to AD is riddled with conflicting and unresolved concepts. Substantial evidence has suggested that the cAMP-response element-binding protein (CREB), a ubiquitous transcription factor, is a key molecule for learning and memory and a core component of the molecular switch that converts short-term to long-term memory. Disturbance of CREB function has been shown in AD brain and some mouse models of AD. Aß-derived diffusible ligands (ADDLs), which are the most toxic species of Aß peptide and the key candidates for initiating memory deficits, may also contribute to calcium homeostatic disturbance in AD brains. In addition, calcium homeostatic disturbance may cause dysregulation of CREB by cAMP-dependent protein kinase (PKA) and calpain. In order to assess the effect of insulin on pCREB after treated by ADDLs, we incubated neuronal-like differentiated PC12 cells with insulin and either low or high concentration of ADDLs, comparing them with those treated with insulin or ADDLs alone. The levels of pCREB, activated calpain, total catalytic subunits of PKA (PKA-C), PKA-C in nuclear and cytosolic fraction were determined by western blot. When calpain was not activated by a relatively low concentration of ADDLs (0.5ÂμM), insulin could partially reverse ADDL-induced down-regulation of pCREB. The enhanced nuclear translocation of catalytic subunits of protein kinase A (PKA-C) but not PI3K/Akt pathway might contribute to the reverse. However, when insulin was with a relatively high concentration of ADDLs (2ÂμM) that could activate calpain, it exacerbated the decrease of pCREB by enhancing calpain activation." @default.
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- W2020656871 date "2011-07-01" @default.
- W2020656871 modified "2023-09-27" @default.
- W2020656871 title "P2-263: An investigation into insulin on pCREB after treated by ADDLs" @default.
- W2020656871 doi "https://doi.org/10.1016/j.jalz.2011.05.1143" @default.
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