Genetics of methamphetamine use disorder: A systematic review and meta-analyses of gene association studies.
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ABSTRACT:
SUBMITTER: Guerin AA
PROVIDER: S-EPMC7856253 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Autism spectrum disorder (ASD) is a class of neurodevelopmental conditions with a large epidemiological and societal impact worldwide. To date, numerous studies have investigated the associations between genetic variants and ASD risk. To provide a robust synthesis of published evidence of candidate gene studies for ASD, we performed an umbrella review (UR) of meta-analyses of genetic studies for ASD (PROSPERO registration number: CRD42021221868). We systematically searched eight English and Chinese databases from inception to March 31, 2022. Reviewing of eligibility, data extraction, and quality assessment were performed by two authors. In total, 28 of 5062 retrieved articles were analyzed, which investigated a combined 41 single nucleotide polymorphisms (SNPs) of nine candidate genes. Overall, 12 significant SNPs of CNTNAP2, MTHFR, OXTR, SLC25A12, and VDR were identified, of which associations with suggestive evidence included the C677T polymorphism of MTHFR (under allelic, dominant, and heterozygote models) and the rs731236 polymorphism of VDR (under allelic and homozygote models). Associations with weak evidence included the rs2710102 polymorphism of CNTNAP2 (under allelic, homozygote, and recessive models), the rs7794745 polymorphism of CNTNAP2 (under dominant and heterozygote models), the C677T polymorphism of MTHFR (under homozygote model), and the rs731236 polymorphism of VDR (under dominant and recessive models). Our UR summarizes research evidence on the genetics of ASD and provides a broad and detailed overview of risk genes for ASD. The rs2710102 and rs7794745 polymorphisms of CNTNAP2, C677T polymorphism of MTHFR, and rs731236 polymorphism of VDR may confer ASD risks. This study will provide clinicians and healthcare decision-makers with evidence-based information about the most salient candidate genes relevant to ASD and recommendations for future treatment, prevention, and research.
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Project description:EPIC array data were generated from 2 MDD case control cohorts. EWAS was performed in each cohort, followed by meta-analysis between the 2 cohort. Cohort 1: A total of 191 blood samples from 112 patients with MDD was collected up till the interim analysis (wave 1 samples) from an observational clinical study OBSERVEMDD0001 (ClinicalTrials.gov Identifier: NCT02489305) compared to 32 healthy controls; Cohort 2: The MDD cases (N = 359) were drawn from the Molecular Biomarkers of Antidepressant Response study compared to 68 healthy controls.
2022-11-03 | GSE198904 | GEO
Project description:BackgroundGrowing evidence suggests that headache disorders and atopic dermatitis share similar pathological mechanisms and risk factors. The aim of this study was to assess the risk for headache disorders in patients with atopic dermatitis.MethodsWe systematically searched the PubMed and Embase databases from inception to December 1, 2023, for observational studies that examined risk of migraine in subjects with atopic dermatitis. Risk estimates from individual studies were pooled using random-effects models.ResultsTen studies with 12,717,747 subjects were included in the meta-analysis. Our results showed that patients with atopic dermatitis were associated with a higher risk of headache disorder (OR, 1.46, 95% CI = 1.36-1.56; P < 0.001; I2 = 98%) or migraine (OR, 1.32, 95% CI = 1.18-1.47; P < 0.001; I2 = 98.9%). Most of the results of the subgroup analyses were consistent with the overall results.ConclusionThe findings of this meta-analysis suggest that atopic dermatitis is a potential risk indicator for headache disorder or migraine. Further studies are still needed to verify our findings due to the substantial heterogeneity in our analyses.
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Project description:Methamphetamine and Other Substance Use Disorder Genetics in Thailand
| PRJNA955367 | ENA
Project description:Background: Several studies had examined the association between brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and methamphetamine (METH) use disorder, whereas the results were conflicting. The aim of this study was to conduct a meta-analysis to achieve a pooled effect size of the association between BDNF Val66Met polymorphism and METH use disorder. Methods: Literature searches were conducted in PubMed, EMBASE, and Cochrane Library up to July, 2020. All relevant studies on the relationship of BDNF Val66Met polymorphism and METH addiction were retrieved. Pooled odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated in the dominant, recessive, co-dominant, and allele model to appraise the association. Results: Seven case-control studies with a total of 2,204 subjects (956 METH-dependent cases and 1,248 healthy controls) were included in this meta-analysis. The results showed a significant correlation between BDNF Val66Met polymorphism and METH dependence in overall population under different genetic models. However, subgroup analysis indicated that the association only existed in Han Chinese but not in other Asian populations. Conclusion: Although the current data indicate that BDNF Val66Met polymorphism might be a potential genetic factor for METH use disorder, more researches are needed to prove its role in different populations.
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Project description:ImportanceStimulant use disorder is common, affecting between 0.3% and 1.1% of the population, and costs more than $85 billion per year globally. There are no licensed treatments to date. Several lines of evidence implicate the dopamine system in the pathogenesis of substance use disorder. Therefore, understanding the nature of dopamine dysfunction seen in stimulant users has the potential to aid the development of new therapeutics.ObjectiveTo comprehensively review the in vivo imaging evidence for dopaminergic alterations in stimulant (cocaine, amphetamine, or methamphetamine) abuse or dependence.Data sourcesThe entire PubMed, EMBASE, and PsycINFO databases were searched for studies from inception date to May 14, 2016.Study selectionCase-control studies were identified that compared dopaminergic measures between stimulant users and healthy controls using positron emission tomography or single-photon emission computed tomography to measure striatal dopamine synthesis or release or to assess dopamine transporter availability or dopamine receptor availability.Data extraction and synthesisDemographic, clinical, and imaging measures were extracted from each study, and meta-analyses and sensitivity analyses were conducted for stimulants combined, as well as for cocaine and for amphetamine and methamphetamine separately if there were sufficient studies.Main outcomes and measuresDifferences were measured in dopamine release (assessed using change in the D2/D3 receptor availability after administration of amphetamine or methylphenidate), dopamine transporter availability, and dopamine receptor availability in cocaine users, amphetamine and methamphetamine users, and healthy controls.ResultsA total of 31 studies that compared dopaminergic measures between 519 stimulant users and 512 healthy controls were included in the final analysis. In most of the studies, the duration of abstinence varied from 5 days to 3 weeks. There was a significant decrease in striatal dopamine release in stimulant users compared with healthy controls: the effect size was -0.84 (95% CI, -1.08 to -0.60; P < .001) for stimulants combined and -0.87 (95% CI, -1.15 to -0.60; P < .001) for cocaine. In addition, there was a significant decrease in dopamine transporter availability: the effect size was -0.91 (95% CI, -1.50 to -0.32; P < .01) for stimulants combined and -1.47 (95% CI, -1.83 to -1.10; P < .001) for amphetamine and methamphetamine. There was also a significant decrease in D2/D3 receptor availability: the effect size was -0.76 (95% CI, -0.92 to -0.60; P < .001) for stimulants combined, -0.73 (95% CI, -0.94 to -0.53; P < .001) for cocaine, and -0.81 (95% CI, -1.12 to -0.49; P < .001) for amphetamine and methamphetamine. Consistent alterations were not found in vesicular monoamine transporter, dopamine synthesis, or D1 receptor studies.Conclusions and relevanceData suggest that both presynaptic and postsynaptic aspects of the dopamine system in the striatum are down-regulated in stimulant users. The commonality and differences between these findings and the discrepancies with the preclinical literature and models of drug addiction are discussed, as well as their implications for future drug development.
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Project description:Alcohol use disorder (AUD) represents a significant and ongoing public health concern with 12-month prevalence estimates of ?5.6%. Quantitative genetic studies suggest a heritability of approximately 50% for AUD, and as a result, significant efforts have been made to identify specific variation within the genome related to the etiology of AUD. Given the limited number of replicable findings that have emerged from genome-wide linkage and candidate gene association studies, more recent efforts have focused on the use of genome-wide association studies (GWAS). These studies have suggested that hundreds of variants across the genome, most of small effect (R2?<?0.002), contribute to the genetic etiology of AUD. The present review describes the initial, though limited, successes of GWAS to identify loci related to risk for AUD as well as other etiologically relevant traits (e.g. alcohol consumption). In addition, 'Post-GWAS' approaches that rely on GWAS data to estimate the heritability and co-heritability of traits, test causal relations between traits, and aid in gene discovery are described. Together, the described research findings illustrate the importance of molecular genetic research on AUD as we seek to better understand the mechanisms through which genetic variation leads to increased risk for AUD.
| S-EPMC6368900 | biostudies-literature
Project description:The experience of craving via exposure to drug-related cues often leads to relapse in drug users. This study consolidated existing empirical evidences of cue reactivity to methamphetamine to provide an overview of current literature and to inform the directions for future research. The best practice methodological framework for conducting scoping review by Arkey and O'Malley was adopted. Studies that have used a cue paradigm or reported on cue reactivity in persons with a history of methamphetamine use were included. Databases such as Medline, EMBASE, PsycINFO and CINAHL were searched using key terms, in addition to citation check and hand search. The search resulted in a total of 32 original research articles published between 2006 to 2020. Three main themes with regard to cue reactivity were identified and synthesized: (1) effects of cue exposure, (2) individual factors associated with cue reactivity, and (3) strategies that modulate craving or reactivity to cues. Exposure to methamphetamine-associated cues elicits significant craving and other autonomic reactivity. Evidence suggests that drug cue reactivity is strongly associated with indices of drug use and other individual-specific factors. Future studies should focus on high quality studies to support evidence-based interventions for reducing cue reactivity and to examine cue reactivity as an outcome measure.
| S-EPMC7558044 | biostudies-literature
Project description:BackgroundAssociations between endogenous estrogen exposure indicators and risk of subtypes of dementia have been unclear.MethodsDatabases (PubMed, EMBASE and Web of Science) were searched electronically on 1st July and updated regularly until 12nd November 2021. Observational studies of English language were selected if reported an effect estimate [e.g., odds ratio (OR), rate ratio (RR) or hazard ratio (HR)] and 95% CI for the association between any exposure (age of menarche, age at menopause, reproductive period, estradiol level) and any endpoint variable [all-cause dementia, Alzheimer's disease (AD), vascular dementia (VD), cognitive impairment (CI)]. Random-effects models and dose-response meta-analyses were used to calculate estimates and to show the linear/nonlinear relationship. PROSPERO CRD42021274827.FindingsWe included 22 studies (475 9764 women) in this analysis. We found no clear relationship between late menarche (≥14 vs <14 years) and dementia, CI in categorical meta-analysis compared to a J-shape relationship in dose-response meta-analyses. Later menopause (≥45 vs <45 years) was consistently associated with a lower risk of all-cause dementia (pooled RR: 0.87, 95%CI: 0.78-0.97, I2=56.0%), AD (0.67, 0.44-0.99, I2=78.3%), VD (0.87, 0.80-0.94) and CI (0.82, 0.71-0.94, I2=19.3%) in categorical meta-analysis, showing similar results in dose-response meta-analyses. An inverse relationship between longer reproductive duration (≥35 vs <35 years) and dementia was observed in dose-response meta-analysis. In addition, estradiol levels after menopause were inversely correlated with the risk of AD and CI.InterpretationIn this study, later menopause and longer reproductive period were associated with a lower risk of dementia, while the relationship for menarchal age was J-shaped. There was an inverse relationship between higher postmenopausal estrogen levels and risk of AD and CI. Longitudinal study are needed to further explore the association between life-time estrogen exposure and risk of subtypes of dementia.FundingStart-up Foundation for Scientific Research in Shandong University.
| S-EPMC8683685 | biostudies-literature
Project description:Post-traumatic stress disorder (PTSD) is a prevalent, disabling anxiety disorder that constitutes a major health care burden. Despite evidence supporting a genetic predisposition to PTSD, the precise genetic loci remain unclear. Herein we review the current state and limitations of genetic research on PTSD. Although recent years have seen an exponential increase in the number of studies examining the influence of candidate genes on PTSD diagnosis and symptomatology, most studies have been characterized by relatively low rates of PTSD, with apparent inconsistencies in gene associations linked to marked differences in methodology. We further discuss how current advances in the genetics field can be applied to studies of PTSD, emphasizing the need to adapt a genome-wide approach that facilitates discovery rather than hypothesis testing. Genome-wide association studies offer the best opportunity to identify novel "true" risk variants for the disorder that in turn has the potential to inform our understanding of PTSD etiology.
| S-EPMC3108177 | biostudies-literature