Substantial Neuroprotection Against K(+) Deprivation-Induced Apoptosis in Primary Cerebellar Granule Neurons by Novel Dimer Bis(propyl)-Cognitin Via the Activation of VEGFR-2 Signaling Pathway.

CONCLUSIONS: Our results demonstrate that B3C blocks K(+) deprivation-induced apoptosis in CGNs through regulating VEGFR-2/Akt/GSK3β and VEGFR-2/ERK signaling pathways, providing a molecular insight into the therapeutic potential of B3C for the treatment of neurodegenerative diseases. PMID: 23826635 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/23826635?dopt=Abstract

Source: CNS Neuroscience and Therapeutics - July 4, 2013 Category: Neuroscience Authors: Hu SQ, Cui W, Xu DP, Mak SH, Tang J, Choi CL, Pang YP, Han YF Tags: CNS Neurosci Ther Source Type: research

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