Evidence map›Paper›PMID 21820013›Full record

ArticleBehavioural brain research2011

Butyrylcholinesterase inhibitors ameliorate cognitive dysfunction induced by amyloid-β peptide in mice.

Yoko Furukawa-Hibi, Tursun Alkam, Atsumi Nitta, Akihiro Matsuyama, Hiroyuki Mizoguchi, Kazuhiko Suzuki, Saliha Moussaoui, Qian-Sheng Yu, Nigel H Greig, Taku Nagai and 1 more

Abstract read
In one paragraph

Article in Behavioural brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
7.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 142 citations in OpenAlex.

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  18. Structure-activity relationship,Journal of enzyme inhibition and medicinal chemistry · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 3 countries.

Yoko Furukawa-HibiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University, Graduate School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466-8560, Japan.
Tursun Alkam
Atsumi Nitta
Akihiro Matsuyama
Hiroyuki Mizoguchi
Kazuhiko Suzuki
Saliha Moussaoui
Qian-Sheng Yu
Nigel H Greig
Taku Nagai
Kiyofumi Yamada
Nagoya University Hospital · JPNational Institute on Aging · USNagoya University · JPNovartis (Japan) · JPNovartis (Switzerland) · CH

Funding

Design And Development Of Experimental Therapeutics ((Systemic & Neurodegenerative Disorders and Alzheimer's Disease)ZIAAG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$16.0M
Design And Development Of Experimental TherapeuticsZ01AG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2001 to 2008
$1.7M
Intramural NIH HHS Z01 AG000311Intramural NIH HHS ZIA AG000311
6 · The paper itself

Abstract

The cholinesterase inhibitor, rivastigmine, ameliorates cognitive dysfunction and is approved for the treatment of Alzheimer's disease (AD). Rivastigmine is a dual inhibitor of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE); however, the impact of BuChE inhibition on cognitive dysfunction remains to be determined. We compared the effects of a selective BuChE inhibitor, N1-phenethyl-norcymserine (PEC), rivastigmine and donepezil (an AChE-selective inhibitor) on cognitive dysfunction induced by amyloid-β peptide (Aβ(1-40)) in mice. Five-week-old imprinting control region (ICR) mice were injected intracerebroventricularly (i.c.v.) with either Aβ(1-40) or the control peptide Aβ(40-1) on Day 0, and their recognition memory was analyzed by a novel object recognition test. Treatment with donepezil (1.0mg/kg), rivastigmine (0.03, 0.1, 0.3mg/kg) or PEC (1.0, 3.0mg/kg) 20min prior to, or immediately after the acquisition session (Day 4) ameliorated the Aβ(1-40) induced memory impairment, indicating a beneficial effect on memory acquisition and consolidation. In contrast, none of the investigated drugs proved effective when administrated before the retention session (Day 5). Repeated daily administration of donepezil, rivastigmine or PEC, on Days 0-3 inclusively, ameliorated the cognitive dysfunction in Aβ(1-40) challenged mice. Consistent with the reversal of memory impairments, donepezil, rivastigmine or PEC treatment significantly reduced Aβ(1-40) induced tyrosine nitration of hippocampal proteins, a marker of oxidative damage. These results indicate that BuChE inhibition, as well as AChE inhibition, is a viable therapeutic strategy for cognitive dysfunction in AD.

Indexed as

Amyloid beta-PeptidesAnalysis of VarianceAnimalsButyrylcholinesteraseCholinesterase InhibitorsCognition DisordersDisease Models, AnimalDonepezilDose-Response Relationship, DrugIndansMaleMiceMice, Inbred ICRMotor ActivityPeptide FragmentsPhenylcarbamatesAmyloid beta-Peptidesamyloid beta-protein (1-40)ButyrylcholinesteraseCholinesterase InhibitorsDonepezilIndansPeptide FragmentsPhenylcarbamatesPiperidinesRivastigmine

Identifiers

PMID21820013
PMCPMC4979006
OpenAlexW1975976078

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.