Analysis of association between butyrylcholinesterase K variant and apolipoprotein E genotypes in Alzheimer's disease

Vaisi‐Raygani, Asad; Zahrai, Mahine; Soltanzadeh, Akbar; Doosti, Mahmood; Javadi, E; Pourmotabbed, Tayebeh

doi:10.1016/j.neulet.2004.08.057

Cited by 39 publications

(14 citation statements)

References 32 publications

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“…But differed significantly of studies such as Bizzaro et al [21], which suggest a protective effect of K variant for AD, and differed also of surveys that suggest K variant as a risk factor for AD [22,23]. Podoly et al [24] considered that the controversial results are due to biochemical properties of variant K, which may have ambiguous effect on AD because the same structural features that destabilize BChE variant K are those that make it less effective as a neuroprotector.…”

Section: Discussionmentioning

confidence: 99%

Association analysis between K and −116A variants of butyrylcholinesterase and Alzheimer’s disease in a Brazilian population

Simão-Silva

Bertolucci

Lábio

et al. 2013

Chemico-Biological Interactions

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Section: Discussionmentioning

confidence: 99%

Association analysis between K and −116A variants of butyrylcholinesterase and Alzheimer’s disease in a Brazilian population

Simão-Silva

Bertolucci

Lábio

et al. 2013

Chemico-Biological Interactions

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“…Recent studies have also demonstrated a relationship between BCHE-K and the occurrence of CAD [15,16]. We have recently demonstrated that the BCHE-K variant is a risk factor for AD in Tehran, Iran [17].…”

Section: Introductionmentioning

confidence: 77%

“…The mechanism by which the BCHE-K allele may act as a risk factor for CAD and diabetes is unknown [15][16][17]26,27,31]. The presence of BCHE-K in the vascular lesions and of amyloid plaques in CAD in types 1 and 2 diabetes and AD could indicate an interaction between BCHE-K protein and b-amyloid [32][33][34].…”

Section: Discussionmentioning

confidence: 99%

Butyrylcholinesterase K variants increase the risk of coronary artery disease in the population of western Iran

Vaisi‐Raygani

Rahimi

Entezami³

et al. 2008

Scandinavian Journal of Clinical and Laboratory Investigation

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The conflicting results of several studies suggest that there is an association between the butyrylcholinesterase-K variant (BCHE-K, G1615A/Ala539Thr) and the risk of developing coronary artery disease (CAD) in diabetes and non-diabetic subjects. The objective of this study was to determine whether the presence of the BCHE-K variant exacerbates the risk of CAD in patients from western Iran with and without type 2 diabetes mellitus (T2DM). This case-control study comprised 464 subjects undergoing their first coronary angiography. They were matched and randomly assigned into four groups: CAD+T2DM+ (CAD/T2DM), CAD+DM(-) (CAD/ND), CAD(-)DM+ (T2DM/NCAD) and CAD(-)DM(-)(control). The BCHE-K variant was detected by PCR-RFLP. The BCHE-K allele frequency in CAD patients with and without T2DM [total CAD (TCAD)] and separately for each group (CAD/T2DM and CAD/ND) was significantly higher than in the control group (21.1 % versus 13.3 % (p = 0.001), 22.4 % versus 13.3 % (p = 0.001) and 19.7 % versus 13.3 % (p = 0.015), respectively). The odds ratios (ORs) for the BCHE-K heterozygous and homozygous variants in TCAD subjects were 1.65 (95 % CI 1.17-2.3; p = 0.004) and 4.3 (1.05-19.4; p = 0.048); for CAD/T2DM individuals 1.76 (1.2-2.6; p = 0.004) and 4.73 (0.96-23.3; p = 0.052); and for CAD/ND patients 1.53 (1.05-2.3; p = 0.029) and 3.88 (0.8-19.7; p = 0.7), respectively. The OR of the BCHE-K allele was found to be 1.74 (1.1-2.4; p = 0.001) in TCAD subjects, 1.87 (1.12-1.48; p = 0.001) in the CAD/T2DM group and 1.59 (1.04-1.4; p = 0.016) in CAD/ND subjects. These data suggest that the BCHE-K allele increases the risk of CAD in the population (with and without DM) in western parts of Iran, and its presence intensifies the risk of CAD in T2DM. The fact that the BCHE-K allele, even in the heterozygous form, exacerbates the risk of CAD in this population, suggests that a specific therapeutic intervention should be considered for this particular group of patients.

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“…The debate of the BChE function on AD neuropathology was accompanied by several studies that aimed to verify association between BChE-K and Alzheimer's disease. Some of them found the BCHE-K was associated with AD (Lehmann et al, 1997;McIlroy et al, 2000;Raygani et al, 2004;Tilley et al, 1999;Wiebusch et al, 1999) and others found no association (Alvarez-Arcaya et al, 2000;Ki et al, 1999;Singleton et al, 1998). Bizzarro et al (2010), in turn, suggest a protective effect of K variant, since the authors found it in a lower frequency in AD patients when compared to healthy controls and to fronto-temporal dementia (FTD) patients.…”

Section: Discussionmentioning

confidence: 99%

Butyrylcholinesterase: K variant, plasma activity, molecular forms and rivastigmine treatment in Alzheimer's disease in a Southern Brazilian population

Bono

Simão-Silva

Batistela

et al. 2015

Neurochemistry International

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Alzheimer's disease (AD) is a neurodegenerative disorder in which there is a decline of cholinergic function. The symptomatic AD treatment involves the use of ChEIs (cholinesterase inhibitors) as rivastigimine, a dual inhibitor. The human butyrylcholinesterase (BChE) is an enzyme that has specific roles in cholinergic neurotransmission and it has been associated with AD. In the serum, BChE is found in four main molecular forms: G1 (monomer); G1-ALB (monomer linked to albumin); G2 (dimer); and G4 (tetramer). The interaction between the products of BCHE gene and CHE2 locus results in CHE2 C5+ and CHE2 C5- phenotypes. CHE2 C5+ phenotype and BChE-K are factors that influence on BChE activity. This work aimed to verify the proportions of BChE molecular forms, total and relative activity in 139 AD patients and 139 elderly controls, taking into account K variant, CHE2 locus, rivastigmine treatment and clinical dementia rating (CDR) of AD patients. Phenotypic frequencies of CHE2 C5+ and frequency of the carriers of the K allele were similar between groups. Total BChE activity in plasma was significantly lower in AD patients than in elderly controls. Furthermore, we found that reduction on plasma BChE activity is associated directly with AD progression in AD patients and that rivastigmine treatment has a stronger effect on BChE activity within the CDR2 group. The reduction in BChE activity did not occur proportionally in all molecular forms. Multiple regression analysis results confirmed that AD acts as the main factor in plasma BChE activity reduction and that severe stages are related with an even greater reduction. These findings suggest that the reduction of total plasma BChE and relative BChE molecular forms activity in AD patients is probably associated with a feedback mechanism and provides a future perspective of using this enzyme as a possible plasmatic secondary marker for AD.

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Analysis of association between butyrylcholinesterase K variant and apolipoprotein E genotypes in Alzheimer's disease

Cited by 39 publications

References 32 publications

Association analysis between K and −116A variants of butyrylcholinesterase and Alzheimer’s disease in a Brazilian population

Association analysis between K and −116A variants of butyrylcholinesterase and Alzheimer’s disease in a Brazilian population

Butyrylcholinesterase K variants increase the risk of coronary artery disease in the population of western Iran

Butyrylcholinesterase: K variant, plasma activity, molecular forms and rivastigmine treatment in Alzheimer's disease in a Southern Brazilian population

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