Decreased serum levels of adiponectin in adult attention deficit hyperactivity disorder

Mavroconstanti, Thegna; Halmøy, Anne; Haavik, Jan

doi:10.1016/j.psychres.2014.01.025

Cited by 19 publications

(15 citation statements)

References 69 publications

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“…70, 73, 74, 104, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129 Some studies regarded the circadian rhythms analyzing the melatonin levels, 70, 118 others the oxidative stress pathway. In particular in a pioneering study, 120 plasma homocysteine levels were lower and serum folic acid levels higher in adult ADHD patients when compared with controls, whereas no difference was found in serum vitamin B12, total antioxidant status, total oxidant status and the oxidative stress index.…”

Section: Resultsmentioning

confidence: 99%

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Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies

2016

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The adult form of attention-deficit/hyperactivity disorder has a prevalence of up to 5% and is the most severe long-term outcome of this common disorder. Family studies in clinical samples as well as twin studies suggest a familial liability and consequently different genes were investigated in association studies. Pharmacotherapy with methylphenidate (MPH) seems to be the first-line treatment of choice in adults with attention-deficit hyperactive disorder (ADHD) and some studies were conducted on the genes influencing the response to this drug. Finally some peripheral biomarkers were identified in ADHD adult patients. We believe this work is the first systematic review and meta-analysis of candidate gene association studies, pharmacogenetic and biochemical (metabolomics) studies performed in adults with ADHD to identify potential genetic, predictive and peripheral markers linked specifically to ADHD in adults. After screening 5129 records, we selected 87 studies of which 61 were available for candidate gene association studies, 5 for pharmacogenetics and 21 for biochemical studies. Of these, 15 genetic, 2 pharmacogenetic and 6 biochemical studies were included in the meta-analyses. We obtained an association between adult ADHD and the gene BAIAP2 (brain-specific angiogenesis inhibitor 1-associated protein 2), even after Bonferroni correction, with any heterogeneity in effect size and no publication bias. If we did not apply the Bonferroni correction, a trend was found for the carriers allele 9R of dopamine transporter SLC6A3 40 bp variable tandem repeat polymorphism (VNTR) and for 6/6 homozygotes of SLC6A3 30 bp VNTR. Negative results were obtained for the 9-6 haplotype, the dopamine receptor DRD4 48 bp VNTR, and the enzyme COMT SNP rs4680. Concerning pharmacogenetic studies, no association was found for the SLC6A3 40 bp and response to MPH with only two studies selected. For the metabolomics studies, no differences between ADHD adults and controls were found for salivary cortisol, whereas lower serum docosahexaenoic acid (DHA) levels were found in ADHD adults. This last association was significant even after Bonferroni correction and in absence of heterogeneity. Other polyunsaturated fatty acids (PUFAs) such as AA (arachidonic acid), EPA (eicosapentaenoic acid) and DyLA (dihomogammalinolenic acid) levels were not different between patients and controls. No publication biases were observed for these markers. Genes linked to dopaminergic, serotoninergic and noradrenergic signaling, metabolism (DBH, TPH1, TPH2, DDC, MAOA, MAOB, BCHE and TH), neurodevelopment (BDNF and others), the SNARE system and other forty genes/proteins related to different pathways were not meta-analyzed due to insufficient data. In conclusion, we found that there were not enough genetic, pharmacogenetic and biochemical studies of ADHD in adults and that more investigations are needed. Moreover we confirmed a significant role of BAIAP2 and DHA in the etiology of ADHD exclusively in adults. Future research should be focused on the replication ...

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Section: Resultsmentioning

confidence: 99%

“…Other relevant peripheral biomarkers are represented by the serum BDNF, 126 adiponectin, 124 albumin 125 as we as the cerebrospinal fluid metabolites homovanillic acid and 5-hydroxyindoleacetic acid. 128 …”

Section: Resultsmentioning

confidence: 99%

Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies

2016

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“…34,35 Our best hit, the rs11649622 genotype, has been observed to be linked to CDH13 expression especially in amygdala, 36 and other CDH13 variants have been observed to be associated with working memory 24 and cortical thickness in dorsolateral prefrontal cortex of patients with ADHD. 37 CDH13 codes for T-cadherin, a GPI-anchored protein, which has an important role in the proliferation, migration and connectivity of neurons, 30,32 and disturbed neural connectivity has been proposed as the main pathophysiological mechanism underlying behavioral problems in ADHD. 30 A recent meta-analysis concluded that about 25–30% of prisoners fulfill criteria for ADHD.…”

Section: Discussionmentioning

confidence: 99%

Genetic background of extreme violent behavior

et al. 2014

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In developed countries, the majority of all violent crime is committed by a small group of antisocial recidivistic offenders, but no genes have been shown to contribute to recidivistic violent offending or severe violent behavior, such as homicide. Our results, from two independent cohorts of Finnish prisoners, revealed that a monoamine oxidase A (MAOA) low-activity genotype (contributing to low dopamine turnover rate) as well as the CDH13 gene (coding for neuronal membrane adhesion protein) are associated with extremely violent behavior (at least 10 committed homicides, attempted homicides or batteries). No substantial signal was observed for either MAOA or CDH13 among non-violent offenders, indicating that findings were specific for violent offending, and not largely attributable to substance abuse or antisocial personality disorder. These results indicate both low monoamine metabolism and neuronal membrane dysfunction as plausible factors in the etiology of extreme criminal violent behavior, and imply that at least about 5–10% of all severe violent crime in Finland is attributable to the aforementioned MAOA and CDH13 genotypes.

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“…In addition to its regulation of neural cell growth, cadherin-13 also acts as a receptor for the peptide hormone adiponectin (Hug et al , 2004). Serum adiponectin levels in ADHD patients are inversely correlated with psychiatric symptoms (Mavroconstanti et al , 2014), and can reduce depression-related behaviors in rodents when administered intracerebroventricularly (Liu et al , 2012). Thus, CDH13 actions on psychiatric symptoms may operate in part through its interaction with adiponectin.…”

Section: Introductionmentioning

confidence: 99%

Cdh13 and AdipoQ gene knockout alter instrumental and Pavlovian drug conditioning

King

Militello

Hart

et al. 2017

Genes Brain and Behavior

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Genome-wide association studies in humans have suggested that variants of the cadherin-13 (CDH13) gene are associated with substance use disorder, subjective response to amphetamine, and attention deficit hyperactivity disorder. To examine the role of the Cdh13 and its peptide ligand adiponectin (AdipoQ) in addiction-related behaviors, we assessed Cdh13 knock-out rats and AdipoQ knock-out mice using intravenous cocaine self-administration and conditioned place preference paradigms. During intravenous cocaine self-administration, male Cdh13 heterozygous (+/−) and knock-out (−/−) rats showed increased cue-induced reinstatement compared to wild-type rats when presented with a cocaine-paired stimulus, whereas female Cdh13 rats showed no differences across genotype. Cdh13 −/− rats showed higher responding for a saccharin reinforcer and learned the choice reaction time task more slowly than wild-types. However, we found no differences between Cdh13 −/− and +/+ rats in responding for sensory reinforcement, number of premature responses in the reaction time task, tendency to approach a Pavlovian food cue, conditioned place preference and locomotor activation to cocaine (10 or 20 mg/kg). In AdipoQ −/− mice there was a significant increase in conditioned place preference to methamphetamine (1 mg/kg) but not to a range of d-amphetamine doses (0.5, 1, 2 and 4 mg/kg). Taken together, these data suggest that Cdh13 and AdipoQ regulate sensitivity to psychomotor stimulants and palatable rewards without producing major changes in other behaviors. In humans, these two genes may regulate sensitivity to natural and drug rewards, thus influencing susceptibility to the conditioned drug effects and relapse.

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Decreased serum levels of adiponectin in adult attention deficit hyperactivity disorder

Cited by 19 publications

References 69 publications

Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies

Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies

Genetic background of extreme violent behavior

Cdh13 and AdipoQ gene knockout alter instrumental and Pavlovian drug conditioning

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