The alterations of Ca2+/Calmodulin/CaMKII/CaV1.2 signaling in experimental models of Alzheimer's disease and vascular dementia

Dongyu Min, Feng Guo, Shu Zhu, Xiaoxue Xu, Xiaoyuan Mao, Yonggang Cao, Xintong Lv, Qinghua Gao, Lei Wang, Tianbao Chen, Chris Shaw, Liying Hao, Jiqun Cai

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)

Abstract

The two critical forms of dementia are Alzheimer's disease (AD) and vascular dementia (VD).The alterations of Ca2+/calmodulin/CaMKII/CaV1.2 signaling in AD and VD have not been well elucidated. Here we have demonstrated changes in the levels of CaV1.2, calmodulin, p-CaMKII, p-CREB and BDNF proteins by Western blot analysis and the co-localization of p-CaMKII/CaV1.2 by double-labeling immunofluorescence in the hippocampus of APP/PS1 mice and VD gerbils. Additionally, expression of these proteins and intracellular calcium levels were examined in cultured neurons treated with Aß1–42. The expression of CaV1.2 protein was increased in VD gerbils and in cultured neurons but decreased in APP/PS1 mice; the expression of calmodulin protein was increased in APP/PS1 mice and VD gerbils; levels of p-CaMKII, p-CREB and BDNF proteins were decreased in AD and VD models. The number of neurons in which p-CaMKII and CaV1.2 were co-localized, was decreased in the CA1 and CA3 regions in two models. Intracellular calcium was increased in the cultured neurons treated with Aß1–42. Collectively, our results suggest that the alterations in CaV1.2, calmodulin, p-CaMKII, p-CREB and BDNF can be reflective of an involvement in the impairment in memory and cognition in AD and VD models.
Original languageEnglish
Pages (from-to)60-65
Number of pages6
JournalNeuroscience Letters
Volume538
Early online date08 Feb 2013
DOIs
Publication statusPublished - 22 Mar 2013

Keywords

  • Alzheimer's disease; vascular dementia; CaV1.2;CaMKII; calmodulin

ASJC Scopus subject areas

  • Neuroscience(all)

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