2018
DOI: 10.1016/j.neuro.2018.07.008
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Neuroprotective effects of cordycepin inhibit Aβ-induced apoptosis in hippocampal neurons

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Cited by 33 publications
(29 citation statements)
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“…In this study, the BBB was significantly damaged after CCH with decreased tight junction proteins including ZO-1 and Occludin. Aβ toxicity increases the formation of reactive oxygen species (ROS) and intracellular calcium levels, resulting in neuron death (Song et al, 2018). Considering Aβ plaque deposition is the remarkable pathological feature of AD, the pathogenesis and neuropathological changes caused by VD and AD are still different.…”
Section: Discussionmentioning
confidence: 99%
“…In this study, the BBB was significantly damaged after CCH with decreased tight junction proteins including ZO-1 and Occludin. Aβ toxicity increases the formation of reactive oxygen species (ROS) and intracellular calcium levels, resulting in neuron death (Song et al, 2018). Considering Aβ plaque deposition is the remarkable pathological feature of AD, the pathogenesis and neuropathological changes caused by VD and AD are still different.…”
Section: Discussionmentioning
confidence: 99%
“…The structure of cordycepin comprises a purine (adenine) nucleoside molecule attached to a ribose sugar (ribofuranose) moiety via a β-N9-glycosidic bond. These characteristics indicate that the protective effect of cordycepin on the CNS may be closely associated with A 1 R. A recent study has confirmed the speculation that cordycepin exerts neuroprotective effects by inhibiting Aβ-induced hippocampal neuronal apoptosis via activating A 1 R [22].…”
Section: Introductionmentioning
confidence: 83%
“…Among the different kinds of Aβ generated during AD pathogenesis, Aβ1–42 is the most toxic, while Aβ1–40 has the largest amount [20]. Aβ25–35, a synthetic peptide based on Aβ1–40 and Aβ1–42, was reported to have the physical and biological properties of Aβ without the need of aging before usage [28]. Our previous research demonstrated that Aβ25–35 was capable of inducing autophagy in HT22 hippocampus cells, which involved the PI3K/AKT/mTOR/p70S6K pathway [29].…”
Section: Discussionmentioning
confidence: 99%