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IC‐P‐044: Longitudinal Imaging Changes and Vascular Risk Factors: A 10‐1Year Study
Author(s) -
Knopman David S.,
Penman Alan D.,
Coker Laura H.,
Catellier Diane J.,
Shibata Dean,
Mosley Thomas H.
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.058
Subject(s) - medicine , hyperintensity , diabetes mellitus , cardiology , atherosclerosis risk in communities , logistic regression , dementia , odds ratio , ordered logit , magnetic resonance imaging , prospective cohort study , disease , endocrinology , radiology , machine learning , computer science
(M.W. 1500, DD.90%) against Cu(II)-induced neurotoxicity in primary cultured rat cortical neurons. Methods: Cortical neurons were cultured at 37 C for 7days then incubated more for 12 hours in culture medium without or with 0.4, 0.2, and 0.1mg/ml COSs, respectively. After removed the culture medium and the cultured cortical neurons were added fresh culture medium containing 50mM CuCl2, incubated for 48 hours at 37 C in a humidified incubator. Cell viability were assayed by MTT, Hoechst 33342 assay and lactate dehydrogenase (LDH) assay, and the reactive oxygen species(ROS) levels were detected byROS assay based on the ROS-mediated conversion of nonfluorescent 2’,7’-DCFH-DA into fluorescent DCFH. Results: The toxicity of Cu(II) to cortical neurons was obviously attenuated in a concentration-dependent manner by COSs. The data derived from the LDH and Hoechst 33342 assay support the results from MTT assay well. The following ROS assay indicated that COSs prevent Cu(II)-induced the elevation of intracellular ROS. Conclusions: These findings suggest that COSs protect against Cu(II) induced neurotoxicity in primary cortical neurons by interfering with an increase in intracellular ROS. It will be helpful to further develop the usages of COSs in AD treatment.