Cholinesterase: phenotyping and genotyping

Goodall, Roberta

doi:10.1258/000456304322879971

Cited by 27 publications

(34 citation statements)

References 59 publications

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“…In a multivariate model, plasma cholinesterase activity was correlated with severe cocaine toxicity in ED patients [50]. There are several phenotypes of human butylcholinesterase, and these may vary in their affinity for cocaine [51]. Interestingly, administration of repeated doses of cocaine may increase plasma butylcholinesterase activity [52].…”

Section: Cocaine-protein Bindingmentioning

confidence: 99%

Mechanisms of Acute Cocaine Toxicity

Heard¹,

Palmer²,

Zahniser³

2008

TOPHARMJ

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Abstract:Patients with acute cocaine poisoning present with life-threatening symptoms involving several organ systems. While the effects of cocaine are myriad, they are the result of a limited number of cocaine-protein interactions, including monoamine transporter, neurotransmitter receptor and voltage-gated ion channels. These primary interactions trigger a cascade of events that ultimately produce the clinical effects. The purpose of this article is to review the primary interactions of cocaine and the effects that these interactions trigger. We also describe the progression of symptoms observed in cocaine poisoning as they relate to serum cocaine concentrations.

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Section: Cocaine-protein Bindingmentioning

confidence: 99%

Mechanisms of Acute Cocaine Toxicity

Heard¹,

Palmer²,

Zahniser³

2008

TOPHARMJ

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“…79 BChE is synthesized primarily in the liver and is distributed throughout the intestinal mucosa, plasma and the brain. 80 For these reasons, BChE has been conceptualized as a therapeutic agent for CoD. 53 Researchers hypothesize that polymorphisms in BCHE lead to various enzyme profiles that allow different concentrations of cocaine to reach the reward system in the brain, thereby influencing susceptibility to developing addiction.…”

Section: Discussionmentioning

confidence: 99%

An endophenotype approach to the genetics of alcohol dependence: a genome wide association study of fast beta EEG in families of African ancestry

et al. 2017

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Fast beta (20–28 Hz) electroencephalogram (EEG) oscillatory activity may be a useful endophenotype for studying the genetics of disorders characterized by neural hyperexcitability, including substance use disorders (SUDs). However, the genetic underpinnings of fast beta EEG have not previously been studied in a population of African-American ancestry (AA). In a sample of 2382 AA individuals from 482 families drawn from the Collaborative Study on the Genetics of Alcoholism (COGA), we performed a genome-wide association study (GWAS) on resting-state fast beta EEG power. To further characterize our genetic findings, we examined the functional and clinical/behavioral significance of GWAS variants. Ten correlated single-nucleotide polymorphisms (SNPs) (r2>0.9) located in an intergenic region on chromosome 3q26 were associated with fast beta EEG power at P<5 × 10−8. The most significantly associated SNP, rs11720469 (β: − 0.124; P<4.5 × 10−9), is also an expression quantitative trait locus for BCHE (butyrylcholinesterase), expressed in thalamus tissue. Four of the genome-wide SNPs were also associated with Diagnostic and Statistical Manual of Mental Disorders Alcohol Dependence in COGA AA families, and two (rs13093097, rs7428372) were replicated in an independent AA sample (Gelernter et al.). Analyses in the AA adolescent/young adult (offspring from COGA families) subsample indicated association of rs11720469 with heavy episodic drinking (frequency of consuming 5+ drinks within 24 h). Converging findings presented in this study provide support for the role of genetic variants within 3q26 in neural and behavioral disinhibition. These novel genetic findings highlight the importance of including AA populations in genetics research on SUDs and the utility of the endophenotype approach in enhancing our understanding of mechanisms underlying addiction susceptibility.

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“…Differences in AChE enzyme activity can be explained by genetic causes that could underlie differences in AChE activity according to distinct alleles [35] or single-nucleotide polymorphisms [36]. This has been documented for butylcholinesterase [37], another non-specific cholinesterase found in humans. This may then suggest that genetics underlying AChE activity could play a role in determining whether patients develop the hypoactive or hyperactive subtype of delirium.…”

Section: Discussionmentioning

confidence: 99%

Acetylcholinesterase Activity Measurement and Clinical Features of Delirium

Jackson

Moorey

Sheehan

et al. 2016

Dement Geriatr Cogn Disord

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Aims: Cholinergic deficiency is commonly implicated in the pathophysiology of delirium. We aimed to investigate the relationship between directly measured serum acetylcholinesterase (AChE) activity and (1) clinical features of delirium and (2) outcomes among older hospital patients with delirium. Methods: Hospitalised patients with delirium were recruited, and delirium motor subtype, severity and duration of delirium were measured. Serum AChE activity was measured using a colorimetric assay. Results: The mean AChE activity for the whole sample was 2.46 μmol/μL/min (standard deviation 1.75). Higher AChE activity was associated with increased likelihood of hypoactive delirium rather than the hyperactive or mixed subtype (odds ratio 1.98, 95% confidence interval 1.10-3.59). Conclusion: Higher AChE activity was associated with hypoactive delirium but did not predict outcomes. Simple enhancement of cholinergic neurotransmission may not be sufficient to treat delirium.

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Cholinesterase: phenotyping and genotyping

Cited by 27 publications

References 59 publications

Mechanisms of Acute Cocaine Toxicity

Mechanisms of Acute Cocaine Toxicity

An endophenotype approach to the genetics of alcohol dependence: a genome wide association study of fast beta EEG in families of African ancestry

Acetylcholinesterase Activity Measurement and Clinical Features of Delirium

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