Colchicine lesions in the rat hippocampus mimic the alterations of several markers in Alzheimer's disease

Nakagawa, Yuzo; Nakamura, Shizuo; Kasé, Yoshitoshi; Noguchi, Teruhisa; Ishihara, Takafumi

doi:10.1016/0006-8993(87)90358-1

Cited by 53 publications

(28 citation statements)

References 23 publications

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“…However, there have been a number of shortcomings with these animal models, which provide important clues to understanding the underlying pathophysiology of neurodegeneration in humans. Centrally administered colchicine-induced cognitive dysfunction is a well-known model of AD that involves preferential destruction of den-tate gyrus granule cells and mossy fibres of the hippocampus as well as a direct cholinotoxic effect leading to marked destruction of the septohippocampal pathway that plays a central role in mediation and coordination of memory processes [4,5] . Colchicine binds irreversibly to tubulin dimers and prevents addition of tubulin molecules to the fast growing and thereby inhibiting microtubule assembly [6] .…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Resveratrol against Intracerebroventricular Colchicine-Induced Cognitive Impairment and Oxidative Stress in Rats

et al. 2006

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Alzheimer’s disease is a complex and multifactorial neurodegenerative disease. Central administration of colchicine, a microtubule-disrupting agent, causes loss of cholinergic neurons and cognitive dysfunction that is associated with excessive free radical generation. The present study was aimed at evaluating the effects of trans-resveratrol in the prevention of colchicine-induced cognitive impairment and oxidative stress in rats. Intracerebroventricular administration of colchicine (15 µg/5 µl) induced impaired cognitive functions in both the Morris water maze task and the elevated plus-maze task. Chronic treatment with resveratrol (10 and 20 mg/kg, p.o.) for a period of 25 days, beginning 4 days prior to colchicine injection, significantly improved the colchicine-induced cognitive impairment. Intracerebroventricular colchicine injection resulted in free radical generation characterized by alterations in oxidative stress markers with a significant increase in malondialdehyde (MDA) and nitrite levels and depletion of reduced glutathione (GSH) activity in the rat brains. It also showed a significant decrease in acetylcholinesterase activity. Besides improving cognitive dysfunction, chronic administration of resveratrol significantly reduced the elevated MDA and nitrite levels and restored the depleted GSH and acetylcholinesterase activity. Results of the present study indicated that trans-resveratrol has a neuroprotective role against colchicine-induced cognitive impairment and associated oxidative stress.

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Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Resveratrol against Intracerebroventricular Colchicine-Induced Cognitive Impairment and Oxidative Stress in Rats

et al. 2006

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“…H 2 O 2 and methylmercury(MeHg) were used to induce oxidative stress, which is known to be involved in age-related disorders and the pathogenesis of a variety of neurological and neurodegenerative conditions, such as Alzheimer's disease (17), Parkinson's disease (18) and amyotrophic lateral sclerosis (19). The microtubule disrupting agent colchicine, mimicking the cytoskeletal damage that occurs in Alzheimer's disease (20), but not causing oxidative stress, also was tested. Because mitochondria play a key role in many models of apoptosis (21,22) the mitochodrial function also was investigated.…”

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confidence: 99%

Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death

Ahlbom

Gogvadze

Chen

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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There is growing concern that prenatal exposure to excessive glucocorticoids may have deleterious effects on the development of various organs, including the nervous system. This study aimed at evaluating whether prenatal exposure to high levels of glucocorticoids might produce long-term effects on neuronal cell survival. Pregnant rats were injected i.p. with 0.1 mg͞kg dexamethasone (DEX) from day 14 postconception, and cerebellar granule cells (CGC) were prepared from 1-week-old rats from DEX-treated and control dams. After 7 days in culture, cells were exposed to H 2O2, methylmercury, or colchicine at concentrations known to induce apoptotic cell death. After exposure to H 2O2 or methylmercury, both inducing oxidative stress, the number of apoptotic cells was significantly higher in DEX-than in control-CGC. Because mitochondria play a key role in apoptosis, mitochondrial function was investigated, and a decrease in the threshold level of Ca 2؉ necessary for induction of mitochondrial permeability transition, in Ca 2؉ accumulation rate, and in oxygen consumption was detected in DEX-CGC. Moreover, the activity of the antioxidant enzyme catalase was significantly decreased in DEX-CGC. A similar decrease in catalase activity was observed in cerebellar homogenate from newborn and 40-day-old DEX-rats. In conclusion, these results indicate that prenatal exposure to high levels of glucocorticoids induces long-lasting changes in CGC rendering them more sensitive to oxidative stress. With the increasing use of multiple doses of glucocorticoids in preterm infants, the possibility that prenatal exposure to excess glucocorticoids may lead to long-term neurological consequences becomes a relevant issue.

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“…Scopolamine administration is characterized by progressive deterioration of learning and memory, oxidative stress, and decrease in acetylcholine turnover. 17,18 CA leaf extract has been reported to improve spatial learning performance and enhance memory retention in neonatal rats during growth spurt period and also found efficient in enhancing hippocampal CA3 neuronal dendritic arborization in mice. 22,23 In our study, CA showed Neuroprotective activity with 150 and 300 mg/kg but it was significant in 300 mg/kg group when compared to control group.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Neuroprotective Effects of Centella asiatica Against Scopolamine Induced Cognitive Impairment in Mice

Bpv¹,

Latha²,

Rammohan³

et al. 2014

IJPER

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Objective: This study was conducted to show Neuroprotective effect of aqueous extract of Centella asiatica in scopolamine induced cognitive impairment in mice. The improvement of cognitive impairment with Centella asiatica was compared against standard drug (Donepezil 50 µg/kg). Methods: Swiss albino mice (20-25 g) of either sex were randomly divided into 5 groups of 6 animals each. All the animals except the control group, received scopolamine (0.05 mg/kg) for 14 days.

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Colchicine lesions in the rat hippocampus mimic the alterations of several markers in Alzheimer's disease

Cited by 53 publications

References 23 publications

Neuroprotective Effects of Resveratrol against Intracerebroventricular Colchicine-Induced Cognitive Impairment and Oxidative Stress in Rats

Neuroprotective Effects of Resveratrol against Intracerebroventricular Colchicine-Induced Cognitive Impairment and Oxidative Stress in Rats

Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death

Evaluation of the Neuroprotective Effects of Centella asiatica Against Scopolamine Induced Cognitive Impairment in Mice

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