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D. A. Butterfield, A. Castegna, C. M. Lauderback and J. Drake, “Evidence That Amyloid Beta-Peptide-Induced Lipid Peroxidation and Its Sequelae in Alzheimer’s Disease Brain Contribute to Neuronal Death,” Neurobiology of Aging, Vol. 23, No. 5, 2002, pp. 655-664.
http://dx.doi.org/10.1016/S0197-4580(01)00340-2

has been cited by the following article:

• TITLE: Crocetin Prevents Amyloid β1-42-Induced Cell Death in Murine Hippocampal Cells

  AUTHORS: Yuta Yoshino, Mitsue Ishisaka, Naofumi Umigai, Masamitsu Shimazawa, Kazuhiro Tsuruma, Hideaki Hara

  KEYWORDS: Alzheimer’s Disease; Amyloid β1-42; Crocetin; HT22; Oxidative Stress

  JOURNAL NAME: Pharmacology & Pharmacy, Vol.5 No.1, January 13, 2014

  ABSTRACT: Crocetin is an aglycon of carotenoid extracted by saffron stigmas (Crocus sativus L.) and known to have a potent anti-oxidative effect. Amyliod β (Aβ), hallmark of Alzheimer’s disease, is reported to have neurotoxicity partly via oxidative stress. In this study, we investigated the effect of crocetin on hippocampal HT22 cell death induced by Aβ1-42. Furthermore, to clarify the mechanism underlying the protective effects of crocetin against Aβ1-42- induced cell death, we measured reactive oxygen species (ROS) production by CM-H2DCFDA kit assay. Crocetin at 1 -10 μM protected HT22 cells against Aβ1-42-induced neuronal cell death and decreased ROS production increased by Aβ1-42. These results that crocetin has the potent neuroprotective effect against Aβ1-42-induced cytotoxicity in hippocampal cells by attenuating oxidative stress, suggest that crocetin may provide a useful therapeutic strategy against Aβ-related disorders.