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作 者:Raghuraman Vasantharaja Ajeet Kumar Ashok Kumar Jamuna R. Subramaniam Raghuraman Vasantharaja;Ajeet Kumar;Ashok Kumar;Jamuna R. Subramaniam(Department of Biological Sciences and Bioengineering, Indian Institute of Technology, Kanpur, India;Center for Preclinical and Translational Medicine Research, Central Research Facility, Sri Ramachandra University, Chennai, India)
机构地区:[1]Department of Biological Sciences and Bioengineering, Indian Institute of Technology, Kanpur, India [2]Center for Preclinical and Translational Medicine Research, Central Research Facility, Sri Ramachandra University, Chennai, India
出 处:《Journal of Behavioral and Brain Science》2016年第3期107-112,共6页行为与脑科学期刊(英文)
摘 要:Despite exhaustive search, no drug is in sight for AD. Earlier, we reported that reserpine, an antihypertensive and antipsychotic drug, ameliorates Amyloid beta (Aβ-AD causing peptide) toxicity and confers several positive enhancements in the C. elegans model system. Here, we evaluate whether reserpine can provide protection against working memory and against AD in the mouse model. Reserpine (0.08 mg) was administered orally on alternate days to the non-Tg and accelerated Aβ deposition (at 2 months of age)and cognitive deficit (4 months of age) developing 5XFAD AD Tg mouse model expressing mutant human APP (3 familial mutations) and human Presenilin1(2 familial mutations) in the neurons, and follow their working memory for 2 months using the spontaneous Y-maze alteration behavioral paradigm. Reserpine enhanced working memory in non-Tg mice and improved the cognitive deficit in the 5XFAD AD Tg mice. Hence, reserpine can be considered for a detailed evaluation in the 3X Tg AD mouse model and a pilot study in AD patients.Despite exhaustive search, no drug is in sight for AD. Earlier, we reported that reserpine, an antihypertensive and antipsychotic drug, ameliorates Amyloid beta (Aβ-AD causing peptide) toxicity and confers several positive enhancements in the C. elegans model system. Here, we evaluate whether reserpine can provide protection against working memory and against AD in the mouse model. Reserpine (0.08 mg) was administered orally on alternate days to the non-Tg and accelerated Aβ deposition (at 2 months of age)and cognitive deficit (4 months of age) developing 5XFAD AD Tg mouse model expressing mutant human APP (3 familial mutations) and human Presenilin1(2 familial mutations) in the neurons, and follow their working memory for 2 months using the spontaneous Y-maze alteration behavioral paradigm. Reserpine enhanced working memory in non-Tg mice and improved the cognitive deficit in the 5XFAD AD Tg mice. Hence, reserpine can be considered for a detailed evaluation in the 3X Tg AD mouse model and a pilot study in AD patients.
关 键 词:Alzheimer’s Disease Amyloid-β-Aβ RESERPINE Cognitive Deficits Transgenic Mice Working Memory
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