Source:http://linkedlifedata.com/resource/pubmed/id/19737553
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-3
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pubmed:dateCreated |
2009-10-5
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pubmed:abstractText |
Alzheimer's disease is the most common form of dementia. Amyloid-beta protein is considered as a key factor of pathogenesis of Alzheimer's disease. l-3-n-butylphthalide (L-NBP), an anti-cerebral ischemia drug, has been shown to have therapeutic effects in vascular dementia animal models. In the present study, we investigated the potential of L-NBP to protect against cognitive impairment, oxidative damage and neuropathological changes induced by intracerebroventricular infusion of amyloid-beta peptide in rats. Daily treatments of 10 and 30 mg/kg L-NBP significantly improved spatial learning deficits and attenuated working memory deficits in Morris water maze task. L-NBP partially reversed the reduction of glutathione peroxidase activities and decreased malondialdehyde levels in the cortex and hippocampus. Furthermore, L-NBP markedly inhibited amyloid-beta-induced neuronal apoptosis, possibly by blocking caspase-3 activation. In addition, L-NBP reduced activation of glycogen synthase kinase-3beta and tau protein phosphorylation. Our results demonstrate that L-NBP protects against amyloid-beta-induced neurodegeneration and cognitive decline in a rat model, suggesting that it may have potential as a therapy for Alzheimer's disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/3-n-butylphthalide,
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Benzofurans,
http://linkedlifedata.com/resource/pubmed/chemical/Neuroprotective Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (1-40),
http://linkedlifedata.com/resource/pubmed/chemical/tau Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1879-0712
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
25
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pubmed:volume |
621
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
38-45
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:19737553-Amyloid beta-Peptides,
pubmed-meshheading:19737553-Animals,
pubmed-meshheading:19737553-Apoptosis,
pubmed-meshheading:19737553-Benzofurans,
pubmed-meshheading:19737553-Cerebral Ventricles,
pubmed-meshheading:19737553-Cognition Disorders,
pubmed-meshheading:19737553-Infusion Pumps,
pubmed-meshheading:19737553-Learning,
pubmed-meshheading:19737553-Male,
pubmed-meshheading:19737553-Memory,
pubmed-meshheading:19737553-Neurons,
pubmed-meshheading:19737553-Neuroprotective Agents,
pubmed-meshheading:19737553-Oxidative Stress,
pubmed-meshheading:19737553-Peptide Fragments,
pubmed-meshheading:19737553-Phosphorylation,
pubmed-meshheading:19737553-Rats,
pubmed-meshheading:19737553-Rats, Wistar,
pubmed-meshheading:19737553-tau Proteins
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pubmed:year |
2009
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pubmed:articleTitle |
L-3-n-butylphthalide improves cognitive impairment induced by intracerebroventricular infusion of amyloid-beta peptide in rats.
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pubmed:affiliation |
Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Xuanwu District, Beijing, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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