Learning performances and vulnerability to amyloid toxicity in the butyrylcholinesterase knockout mouse
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- 作者：Tangui Mauricea ; b ; c ; d ; maurice@univ-montp2.fr" class="auth_mail" title="E-mail the corresponding author ; Manon Strehaianoa ; b ; c ; Nathalie Simé ; ond ; Christelle Bertranda ; e ; Arnaud Chatonneta ; e
- 关键词：ACh ; acetylcholine ; AChE ; acetylcholinesterase ; AD ; Alzheimer&rsquo ; s disease ; Aβ ; amyloid-β ; Aβ25&ndash ; 35 ; amyloid-β[25&ndash ; 35] peptide ; BChE ; butyrylcholinesterase ; ChE ; cholinesterase ; CHP ; cumene hydroperoxide ; HPLC ; high-performance liquid chromatography ; ICV ; intracerebroventricular ; KO ; knockout ; O ; other quadrants ; ScAβ ; scrambled amyloid-β[25&ndash ; 35] peptide ; STL ; step-through latency ; T ; training quadrant ; Wt ; wild-type
- 刊名：Behavioural Brain Research
- 出版年：2016
- 出版时间：1 January 2016
- 年：2016
- 卷：296
- 期：Complete
- 页码：351-360
- 全文大小：2074 K
文摘
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Butyrylcholinesterase knockout (BChE KO) mice showed enhanced learning ability in spatial and non-spatial memory tests.
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In BChE KO mice, the amyloid β25–35 peptide-induced deficit in place learning was attenuated in males and blocked in females.
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No change in oxidative stress or ACh levels was observed after Aβ25–35 in BChE KO mice.
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Genetic invalidation of BChE in mice augmented learning capacities and lowered the vulnerability to Aβ toxicity.
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