Evidence map›Paper›PMID 23930233›Full record

ArticleThe primary care companion for CNS disorders2013

A review of butyrylcholinesterase as a therapeutic target in the treatment of Alzheimer's disease.

Agneta Nordberg, Clive Ballard, Roger Bullock, Taher Darreh-Shori, Monique Somogyi

Abstract read
In one paragraph

Article in The primary care companion for CNS disorders, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
–field-weighted citation impact
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

120 citing papers in PubMed.

  1. A phase 1, safety, tolerability, and pharmacokinetics study of bisnorcymserine, a highly selective inhibitor of butyrylcholinesterase.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  9. Alkaloids from In Vitro CulturedPlants (Basel, Switzerland) · 2026
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  16. Plants (Basel, Switzerland) · 2025
    Review
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  18. Article
  19. Review
  20. Article

60 more citing papers are in PubMed but not listed here.

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

5 authors.

Agneta NordbergAlzheimer Neurobiology Center, Karolinska Institute, Stockholm, Sweden (Drs Nordberg and Darreh-Shori); Wolfson Centre for Age-Related Diseases, King's College, London, United Kingdom (Dr Ballard); Kingshill Research Centre, Victoria Hospital, Swindon, United Kingdom (Dr Bullock); and Novartis Pharmaceuticals Corporation, East Hanover, New Jersey (Dr Somogyi).
Clive Ballard
Roger Bullock
Taher Darreh-Shori
Monique Somogyi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo examine the role of butyrylcholinesterase (BuChE) in cholinergic signaling and neurologic conditions, such as Alzheimer's disease (AD). The rationale for inhibiting cholinesterases in the management of AD, including clinical evidence supporting use of the dual acetylcholinesterase (AChE) and BuChE inhibitor rivastigmine, is discussed. DATA SOURCES: PubMed searches were performed using butyrylcholinesterase as a keyword. English-language articles referenced in PubMed as of September 2011 were included. Study Selection and Data Synthesis: English-language articles related to BuChE considered to be of clinical relevance to physicians were included. English-language articles specifically related to AChE were not included, as the role of AChE in cholinergic signaling and the underlying pathology of AD is well documented. Reference lists of included publications were used to supplement the search.

resultsAChE and BuChE play a role in cholinergic signaling; BuChE can hydrolyze acetylcholine and compensate for AChE when levels are depleted. In the AD brain, AChE levels decrease, while BuChE levels are reportedly increased or unchanged, with changes becoming more pronounced during the disease course. Furthermore, BuChE genotype may influence AD risk and rate of disease progression. Strategies that increase acetylcholine levels (eg, cholinesterase inhibitors) demonstrate symptomatic efficacy in AD. Rivastigmine has proven cognitive efficacy in clinical trials, and data suggest that its action is mediated, in part, by inhibition of BuChE. Retrospective analyses of clinical trials provide evidence that BuChE genotype may also influence treatment response.

conclusionsAChE-selective inhibitors and a dual AChE and BuChE inhibitor demonstrate symptomatic efficacy in AD. Mounting preclinical and clinical evidence for a role of BuChE in maintaining normal cholinergic function and the pathology of AD provides a rationale for further studies investigating use of rivastigmine in AD and the influence of BuChE genotype on observed efficacy.

Identifiers

PMID23930233
PMCPMC3733526

What OpenQuestion holds

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Registered trials

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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.