Mechanism of soluble beta-amyloid 25–35 neurotoxicity in primary cultured rat cortical neurons

Content Provider	Semantic Scholar
Author	Wang, Yong Liu, Lili Hu, Weimin Li, Guanglai
Copyright Year	2016
Abstract	This study aimed to determine the effects of different concentrations of soluble beta-amyloid 25-35 (Aβ25-35) on cell viability, calcium overload, and PI3K-p85 expression in cultured cortical rat neurons. Primary cultured cerebral cortical neurons of newborn rats were divided randomly into six groups. Five groups were treated with soluble Aβ25-35 at concentrations of 10nmol/L, 100nmol/L, 1μmol/L, 10μmol/L, or 30μmol/L. Cell Counting Kit-8 staining was used to measure cell viability, laser-scanning confocal imaging was used to detect changes in intracellular free calcium concentration, and western blot assay was used to measure neuronal PI3K-p85 expression. Soluble Aβ25-35 was found to reduce cell viability and induce calcium overload in primary cultured rat cerebral cortical neurons, in a concentration-dependent manner. At certain concentrations, soluble Aβ25-35 also increased neuronal PI3K-p85 expression. These findings reveal that soluble Aβ25-35 reduces the viability of cultured cerebral cortical rat neurons. The neurotoxicity mechanism may involve calcium overload and disruption of insulin signal transduction pathways.
Starting Page	72
Ending Page	76
Page Count	5
File Format	PDF HTM / HTML
DOI	10.1016/j.neulet.2016.02.050
Alternate Webpage(s)	https://api.elsevier.com/content/article/pii/S0304394016301161
Alternate Webpage(s)	https://www.sciencedirect.com/science/article/pii/S0304394016301161?dgcid=api_sd_search-api-endpoint
PubMed reference number	26940239
Alternate Webpage(s)	https://doi.org/10.1016/j.neulet.2016.02.050
Journal	Medline
Volume Number	618
Journal	Neuroscience Letters
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article