Association between the macrophage inflammatory protein-l alpha gene polymorphism and Alzheimer's disease in the Chinese population

Li, Keshen; Dai, Dawei; Yao, Lifen; Gu, Xuefeng; Luan, Kuan; Zhao, Yong; Wang, Binyou

doi:10.1016/j.neulet.2008.01.002

Cited by 17 publications

(12 citation statements)

References 24 publications

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“…MIP‐1α is another cytokine commonly expressed during neuroinflammation. It is able to specifically recruit and activate immune cells, such as T cells …”

Section: Discussionsupporting

confidence: 93%

“…It is able to specifically recruit and activate immune cells, such as T cells. 26 It was reported that the anti-inflammatory effect by IL-4 and IL-13 resulted in a dose-dependent inhibition of Aβ-induced pro-inflammatory IL-6 secretion in glial cells. 27 Nevertheless, as deposition and oligemerization of Aβ increase during progression of AD, overproduction of pro-inflammatory cytokines would reduce production of anti-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

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Peripheral cytokines, C‐X‐C motif ligand10 and interleukin‐13, are associated with Malaysian Alzheimer's disease

Hasni

Lim

Chin

et al. 2016

Geriatrics Gerontology Int

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“…MIP‐1α is another cytokine commonly expressed during neuroinflammation. It is able to specifically recruit and activate immune cells, such as T cells …”

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Peripheral cytokines, C‐X‐C motif ligand10 and interleukin‐13, are associated with Malaysian Alzheimer's disease

Hasni

Lim

Chin

et al. 2016

Geriatrics Gerontology Int

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“…A relationship between CCL3 and Alzheimer’s disease (AD) was previously reported 43. In fact, the peripheral T-cells of individuals with AD demonstrate over expression of CCL3, which promotes T-cell transendothelial migration across the blood-brain barrier via binding to CCR5 on brain endothelial cells 44.…”

Section: Discussionmentioning

confidence: 87%

CCL3 genotype and current depression increase risk of HIV-associated dementia

Levine

Singer²,

Sinsheimer³

et al. 2009

NBHIV

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Background:The prevalence of Human immunodeficiency virus (HIV)-associated dementia (HAD) has continued to rise even as incidence has fallen. Several host genetic variants have been identified that modify risk for HAD. However, the findings have not been replicated consistently and most studies did not consider the multitude of factors that might themselves confer risk for HAD. In the current study, we sought to replicate the findings of previous studies in a neurologically and behaviorally well-characterized cohort. Methods:The sample consisted of 143 HIV+ individuals enrolled in the National NeuroAIDS Tissue Consortium (NNTC). Based on consensus diagnosis, 117 were considered neurologically normal upon study entry, and 26 had HAD. Seven single-nucleotide polymorphisms (SNPs) were genotyped within seven genes (CCL2, CCL3, CCL5, interleukin-1α [IL-1α], IL-10, stromal cell-derived factor 1, and tumor necrosis factor-α). Logistic regression analysis was used to predict group membership (normal vs HAD), with predictor variables including length of infection, age, current drug dependence, current depression, and genotype. Results: The two groups were statistically similar with regards to demographic characteristics, current drug use, and disease factors. The HAD group had significantly greater number of individuals with current depression. Only one SNP, rs1130371 within the gene for CCL3, was entered into the analysis as the others showed symmetric distribution between groups. Logistic regression indicated that current depression and CCL3 genotype were significant predictors of HAD. Depression conferred a fivefold greater risk of HAD, while the TT genotype for CCL3 SNP (rs1130371) was associated with twofold risk for HAD. Conclusion: Depression and CCL3 genotype predicted HAD. The fact that SNPs previously found to be associated with HAD were not in our analysis, and that rs1130371 is in high linkage disequilibrium with neighboring genes indicates that more dense genotyping in significantly larger cohorts is required to further characterize the relationship between genotype and risk for HAD.

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“…Li et al reported that serum CCL3 levels depend on a microsatellite TA repeat polymorphism in the promoter region in Chinese population [96]. They showed that the (TA)(6)/(TA)(6) genotype was associated with higher CCL3 levels than non-(TA)(6)/(TA) (6) genotypes.…”

Section: Alzheimer Diseasementioning

confidence: 99%