ArticleThe Journal of biological chemistry2009
The butyrylcholinesterase K variant confers structurally derived risks for Alzheimer pathology.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Butyrylcholinesterase K variant and Alzheimer's disease risk: a meta-analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015Pooled it
- Synergy between the alteration in the N-terminal region of butyrylcholinesterase K variant and apolipoprotein E4 in late-onset Alzheimer's disease.Scientific reports · 2019Trial
- Pharmacogenomics of Dementia: Personalizing the Treatment of Cognitive and Neuropsychiatric Symptoms.Genes · 2023Review
- Mechanisms and implications in gene polymorphism mediated diverse reponses to sedatives, analgesics and muscle relaxants.Korean journal of anesthesiology · 2023Article
- Elevated Ghrelin Promotes Hippocampal Ghrelin Receptor Defects in Humanized Amyloid-β Knockin Mice During Aging.Journal of Alzheimer's disease : JAD · 2023Article
- Altered levels of variant cholinesterase transcripts contribute to the imbalanced cholinergic signaling in Alzheimer's and Parkinson's disease.Frontiers in molecular neuroscience · 2022Article
- Characterization of four BCHE mutations associated with prolonged effect of suxamethonium.The pharmacogenomics journal · 2021Article
- Interaction between Apolipoprotein E and Butyrylcholinesterase Genes on Risk of Alzheimer's Disease in a Prospective Cohort Study.Journal of Alzheimer's disease : JAD · 2020Article
- Butyrylcholinesterase Protein Ends in the Pathogenesis of Alzheimer's Disease-CouldBiomolecules · 2019Review
- Synthesis and Biological Evaluation of New Cholinesterase Inhibitors for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2018Article
- Strategies for Continued Successful Treatment in Patients with Alzheimer's Disease: An Overview of Switching Between Pharmacological Agents.Current Alzheimer research · 2018Review
- Cholinergic Pathway SNPs and Postural Control in 477 Older Adults.Frontiers in aging neuroscience · 2018Article
- Assessment of Enzyme Inhibition: A Review with Examples from the Development of Monoamine Oxidase and Cholinesterase Inhibitory Drugs.Molecules (Basel, Switzerland) · 2017Review
- Deleterious Effect of Butyrylcholinesterase K-Variant in Donepezil Treatment of Mild Cognitive Impairment.Journal of Alzheimer's disease : JAD · 2017Article
- Rivastigmine: the advantages of dual inhibition of acetylcholinesterase and butyrylcholinesterase and its role in subcortical vascular dementia and Parkinson's disease dementia.Clinical interventions in aging · 2017Review
- Association between butyrylcholinesterase K variant and mild cognitive impairment in the Thai community-dwelling patients.Clinical interventions in aging · 2017Article
- RGS2 expression predicts amyloid-β sensitivity, MCI and Alzheimer's disease: genome-wide transcriptomic profiling and bioinformatics data mining.Translational psychiatry · 2016Article
- Recent development of multifunctional agents as potential drug candidates for the treatment of Alzheimer's disease.Current medicinal chemistry · 2015Review
- Competing targets of microRNA-608 affect anxiety and hypertension.Human molecular genetics · 2014Article
- Cholinesterases as biomarkers for parasympathetic dysfunction and inflammation-related disease.Journal of molecular neuroscience : MN · 2014Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The K variant of butyrylcholinesterase (BChE-K, 20% incidence) is a long debated risk factor for Alzheimer disease (AD). The A539T substitution in BChE-K is located at the C terminus, which is essential both for BChE tetramerization and for its capacity to attenuate beta-amyloid (Abeta) fibril formation. Here, we report that BChE-K is inherently unstable as compared with the "usual" BChE (BChE-U), resulting in reduced hydrolytic activity and predicting prolonged acetylcholine maintenance and protection from AD. A synthetic peptide derived from the C terminus of BChE-K (BSP-K), which displayed impaired intermolecular interactions, was less potent in suppressing Abeta oligomerization than its BSP-U counterpart. Correspondingly, highly purified recombinant human rBChE-U monomers suppressed beta-amyloid fibril formation less effectively than dimers, which also protected cultured neuroblastoma cells from Abeta neurotoxicity. Dual activity structurally derived changes due to the A539T substitution can thus account for both neuroprotective characteristics caused by sustained acetylcholine levels and elevated AD risk due to inefficient interference with amyloidogenic processes.
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Registered trials
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.