2002
DOI: 10.1016/s0091-3057(02)00838-9
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Intracerebroventricular administration of colchicine produces cognitive impairment associated with oxidative stress in rats

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Cited by 66 publications
(19 citation statements)
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“…Central administration of colchicines caused increased in ROS generation, cognitive dysfunction, microtubule dysfunction and loss of cholinergic neurons in brain [316, 317]. In a recent study, the effect of curcumin against colchicines-induced cognitive and oxidative stress was determined in Wistars rats and compared with rivastigmine treatment.…”
Section: Neuroprotective Action Of Curcumin Against Admentioning
confidence: 99%
“…Central administration of colchicines caused increased in ROS generation, cognitive dysfunction, microtubule dysfunction and loss of cholinergic neurons in brain [316, 317]. In a recent study, the effect of curcumin against colchicines-induced cognitive and oxidative stress was determined in Wistars rats and compared with rivastigmine treatment.…”
Section: Neuroprotective Action Of Curcumin Against Admentioning
confidence: 99%
“…Cut-off time was fixed as 300 seconds and in case a rat could not find the closed arm within this period, it was removed from the maze and rejected. Second trial (retention trial) was performed 24 hrs after the acquisition trial and retention transfer latency was noted (Sharma and Gupta, 2002;Veerendra Kumar and Gupta, 2002) similarly. The retention trial latency was expressed as percentage of initial trial latency.…”
Section: Elevated Plus Maze Testmentioning
confidence: 99%
“…Twenty-four hours later, retention trial was performed and retention latency (RL) to step into the dark compartment was noted (post-shock latency). Cut-off time was fixed at 300 seconds (Sharma and Gupta, 2002;Veerendra Kumar and Gupta, 2002). The retention trial latency was expressed as percentage of initial trial latency.…”
Section: Elevated Plus Maze Testmentioning
confidence: 99%
“…(3) The intracerebroventricular administration of colchicine in rats produces cognitive impairment and oxidative stress by disrupting the microtubule assembly and this method can be effectively used as an animal model for AD. (46) The most logical route toward therapeutic intervention for neurodegenerative diseases involves the identification of small molecules that have the ability to provide neuroprotection. For example, acetaminophen protects hippocampal neurons and PC12 cultures from Aβ peptide-induced oxidative stress through reduction of lipid peroxidation and by lowering cytoplasmic levels of peroxides.…”
Section: Introductionmentioning
confidence: 99%