The Role of Apolipoprotein E in Guillain-Barré Syndrome and Experimental Autoimmune Neuritis

Zhang, Hong‐Liang; Wu, Jing; Zhu, Jie

doi:10.1155/2010/357412

Cited by 41 publications

(26 citation statements)

References 166 publications

(149 reference statements)

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“…7 Potential interactions between 25(OH)D and APOE genotype on memory function might also be explained via their proposed influences on immunological processes, which in turn could influence cognitive function. [30][31][32] The observed interaction between APOE ε4 and 25(OH)D complements findings from previous work, showing an association between APOE ε4 alleles with both lower cognitive function and higher 25(OH)D. 5,7 Although our study shows effect estimates in the consistent direction, no significant associations were observed between APOE ε4 alleles and 25(OH)D or memory function.…”

Section: Discussionsupporting

confidence: 87%

25-Hydroxyvitamin D, APOE ɛ4 genotype and cognitive function: findings from the 1958 British birth cohort

Maddock¹,

Cavadino²,

Power³

et al. 2014

Eur J Clin Nutr

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Both high and low vitamin D statuses have been associated with lower memory function. Apolipoprotein E (APOE) ɛ4 alleles have been associated with reduced memory function, and separately with higher vitamin D concentrations. This report aims to examine if the presence of APOE ɛ4 alleles contributes to the relationship between vitamin D and memory function. A total of 4848 (46% female) participants from the 1958 British birth cohort had information on APOE genotypes and completed memory tests at 50 years, where 4644 also had 25-hydroxyvitamin D (25(OH)D) concentrations measured at 45 years. Both low and high 25(OH)D concentrations were associated with lower memory function after adjustment for number of APOE ɛ4 alleles (P curvature=0.02). There was evidence of interaction between APOE ɛ4 and 25(OH)D, suggesting the association between 25(OH)D concentrations and memory function is different for those with two APOE ɛ4 alleles compared with those with zero or one APOE ɛ4 alleles (recessive model P interaction=0.01). Among participants with two APOE ɛ4 alleles, higher 25(OH)D concentrations were associated with higher memory function, whereas in others, memory scores were slightly lower for individuals with higher versus lower concentrations. Further studies are required to replicate these findings.

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Section: Discussionsupporting

confidence: 87%

25-Hydroxyvitamin D, APOE ɛ4 genotype and cognitive function: findings from the 1958 British birth cohort

Maddock¹,

Cavadino²,

Power³

et al. 2014

Eur J Clin Nutr

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“…For example, apolipoprotein E (ApoE) is a protein produced by macrophages known to act as an immunomodulator. ApoE is thought to interact with many immunological processes including suppression of T cell proliferation, macrophage function regulation and activation of natural killer T cells [24]. One study investigated the expression levels of the ApoE receptor, ApoER2, in lymphocytes of patients with MDD and healthy controls [25], demonstrating that patients with MDD had a significantly lower expression of ApoER2 compared with controls.…”

Section: Alterations In the Expression Of Genes Involved In Inflammationmentioning

confidence: 99%

Depression pathogenesis and treatment: what can we learn from blood mRNA expression?

Hepgul

Cattaneo

Zunszain

et al. 2013

BMC Med

115

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Alterations in several biological systems, including the neuroendocrine and immune systems, have been consistently demonstrated in patients with major depressive disorder. These alterations have been predominantly studied using easily accessible systems such as blood and saliva. In recent years there has been an increasing body of evidence supporting the use of peripheral blood gene expression to investigate the pathogenesis of depression, and to identify relevant biomarkers. In this paper we review the current literature on gene expression alterations in depression, focusing in particular on three important and interlinked biological domains: inflammation, glucocorticoid receptor functionality and neuroplasticity. We also briefly review the few existing transcriptomics studies. Our review summarizes data showing that patients with major depressive disorder exhibit an altered pattern of expression in several genes belonging to these three biological domains when compared with healthy controls. In particular, we show evidence for a pattern of 'state-related' gene expression changes that are normalized either by remission or by antidepressant treatment. Taken together, these findings highlight the use of peripheral blood gene expression as a clinically relevant biomarker approach.

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“…In metaanalysis, the -ε2 allele has also been demonstrated to be associated with a lower risk for depression compared to the ε3 allele (Lopez-Leon et al, 2008) (Table 1). There is growing evidence for the interaction of ApoE with immunological processes, including macrophage and T-cell functioning (Zhang et al, 2010a).…”

Section: Mouse Models Informed By the Human Evidence For Polymorphismmentioning

confidence: 99%

Translating the evidence for gene association with depression into mouse models of depression-relevant behaviour: Current limitations and future potential

Pryce¹,

Klaus

2013

Neuroscience & Biobehavioral Reviews

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Depression is characterised by high prevalence and complex, heterogeneous psychopathology. At the level of aetio-pathology, considerable research effort has been invested to identify specific gene polymorphisms associated with increased depression prevalence. Genome-wide association studies have not identified any risk polymorphisms, and candidate gene case-control studies have identified a small number of risk polymorphisms. It is increasingly recognised that interaction between genotype and environmental factors (G×E), notably stressful life events, is the more realistic unit of depression aetiopathology, with G×E evidence described for a small number of risk polymorphisms. An important complementary approach has been to describe genes exhibiting brain region-specific expression changes in depression. Mouse models of depression informed by the human evidence allow for the study of causality, but to-date have also yielded limited insights into depression aetio-pathology. This review of the translational evidence integrates human and mouse research approaches and evidence. It also makes specific recommendations in terms of how future research in human and mouse should be designed in order to deliver evidence for depression aetio-pathology and thereby to inform the development of novel and improved antidepressant treatments. AbstractDepression is characterised by high prevalence and complex, heterogeneous psychopathology. At the level of aetio-pathology, considerable research effort has been invested to identify specific gene polymorphisms associated with increased depression prevalence. Genome-wide association studies have not identified any risk polymorphisms, and candidate gene case-control studies have identified a small number of risk polymorphisms. It is increasingly recognised that interaction between genotype and environmental factors (GxE), notably stressful life events, is the more realistic unit of depression aetio-pathology, with GxE evidence described for a small number of risk polymorphisms.An important complementary approach has been to describe genes exhibiting brain region-specific expression changes in depression. Mouse models of depression informed by the human evidence allow for the study of causality, but to-date have also yielded limited insights into depression aetiopathology. This review of the translational evidence integrates human and mouse research approaches and evidence. It also makes specific recommendations in terms of how future research in human and mouse should be designed in order to deliver evidence for depression aetio-pathology and thereby to inform the development of novel and improved antidepressant treatments.

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The Role of Apolipoprotein E in Guillain-Barré Syndrome and Experimental Autoimmune Neuritis

Cited by 41 publications

References 166 publications

25-Hydroxyvitamin D, APOE ɛ4 genotype and cognitive function: findings from the 1958 British birth cohort

25-Hydroxyvitamin D, APOE ɛ4 genotype and cognitive function: findings from the 1958 British birth cohort

Depression pathogenesis and treatment: what can we learn from blood mRNA expression?

Translating the evidence for gene association with depression into mouse models of depression-relevant behaviour: Current limitations and future potential

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