Platelet monoamine oxidase activity in children with attention-deficit/hyperactivity disorder

Nedić, Gordana; Pivac, Nela; Hercigonja, Dubravka Kocijan; Jovančević, Milivoj; Ćurković, Katarina Dodig; Mück‐Šeler, Dorotea

doi:10.1016/j.psychres.2009.08.013

Cited by 23 publications

(11 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The enzyme preferentially degrades benzylamine and phenylethylamine and targets a wide variety of specific neurotransmitters involved in the primary substrates of MAO in the brain, including epinephrine (EP), norepinephrine (NE), dopamine (DA), serotonin (5-HT), and β-phenylethylamine (PEA) (1,2). The unique position of MAO in modulating the function of a diverse series of specific neurotransmitters in association with various conditions, including mood disorders (3), anxiety and depression (4,5), schizophrenia (6), attention deficit hyperactivity disorder (7)(8)(9), migraine (10), sexual maturation (11) and neurodegenerative diseases (12), has attracted significant attention to the protein as a therapeutic target.…”

Section: Introductionmentioning

confidence: 99%

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

180

View full text Add to dashboard Cite

Abstract. Activated monoamine oxidase (MAO) has a critical role in the pathogenesis of Alzheimer's disease (AD), including the formation of amyloid plaques from amyloid β peptide (Aβ) production and accumulation, formation of neurofibrillary tangles, and cognitive impairment via the destruction of cholinergic neurons and disorder of the cholinergic system. Several studies have indicated that MAO inhibitors improve cognitive deficits and reverse Aβ pathology by modulating proteolytic cleavage of amyloid precursor protein and decreasing Aβ protein fragments. Thus, MAO inhibitors may be considered as promising therapeutic agents for AD.

show abstract

Section: Introductionmentioning

confidence: 99%

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

180

View full text Add to dashboard Cite

show abstract

“…Children with ADHD and ASD frequently share symptoms of impaired communication skills, impaired social interactions (4), and develop difficulties in familial, educational, and academic functioning (5,6). The abnormal functioning of the dopaminergic and serotonergic systems (5,(7)(8)(9), among other neurotransmitters, were repeatedly found in ADHD and ASD, and therefore the candidate genes common for both disorders are the dopaminergic transporter gene, dopaminergic receptor type 3 and type 4 genes, serotonin transporter gene, and genes for catechol-o-methyl-transferase and monoamine oxidase type A (4), although genome-wide association studies did not confirm with certainty all these candidates (10). A shared genetic basis is further suggested by the higher frequency of ADHD and ASD traits in children with a defined genetic diagnosis such as 22q11 deletion syndrome, XXYY syndrome, and microdeletions or duplications in the chromosome 15q13.2-q13.3 region (11,12).…”

mentioning

confidence: 99%

Human Plasma Glycome in Attention-Deficit Hyperactivity Disorder and Autism Spectrum Disorders

Pivac

Knežević

Gornik

et al. 2011

Molecular & Cellular Proteomics

Self Cite

View full text Add to dashboard Cite

Over a half of all proteins are glycosylated, and their proper glycosylation is essential for normal function. Unfortunately, because of structural complexity of nonlinear branched glycans and the absence of genetic template for their synthesis, the knowledge about glycans is lagging significantly behind the knowledge about proteins or DNA. Using a recently developed quantitative high throughput glycan analysis method we quantified components of the plasma N-glycome in 99 children with attention-deficit hyperactivity disorder (ADHD), 81 child and 5 adults with autism spectrum disorder, and a total of 340 matching healthy controls. No changes in plasma glycome were found to associate with autism spectrum disorder, but several highly significant associations were observed with ADHD. Further structural analysis of plasma glycans revealed that ADHD is associated with increased antennary fucosylation of biantennary glycans and decreased levels of some complex glycans with three or four antennas. The design of this study prevented any functional conclusions about the observed associations, but specific differences in glycosylation appears to be strongly associated with ADHD and warrants further studies in this direction. Molecular & Cellular Proteomics 10: 10.1074/mcp.M110.004200, 1-7, 2011. Attention-deficit hyperactivity disorder (ADHD)1 and autism spectrum disorders (ASDs) are both highly heritable multifactorial and clinically heterogeneous childhood-onset neurodevelopmental disorders (1, 2). The hallmarks of ADHD are severe inattention, hyperactivity, and impulsivity whereas the characteristic symptoms of ASD include impaired communication and social interaction skills as well as repetitive and restricted behavior and interests (3). Several pieces of evidence point toward some shared heritability and thus genetic factors contributing to the occurrence of both ADHD an ASD (4). Children with ADHD and ASD frequently share symptoms of impaired communication skills, impaired social interactions (4), and develop difficulties in familial, educational, and academic functioning (5, 6). The abnormal functioning of the dopaminergic and serotonergic systems (5, 7-9), among other neurotransmitters, were repeatedly found in ADHD and ASD, and therefore the candidate genes common for both disorders are the dopaminergic transporter gene, dopaminergic receptor type 3 and type 4 genes, serotonin transporter gene, and genes for catechol-o-methyl-transferase and monoamine oxidase type A (4), although genome-wide association studies did not confirm with certainty all these candidates (10). A shared genetic basis is further suggested by the higher frequency of ADHD and ASD traits in children with a defined genetic diagnosis such as 22q11 deletion syndrome, XXYY syndrome, and microdeletions or duplications in the chromosome 15q13.2-q13.3 region (11,12). However, the molecular agents related to various biological processes and interactions between different risk factors responsible for development of ADHD and ASD remain elusive (6).Prote...

show abstract

“…For these reasons, p-MAO-B activity was proposed as a predictive peripheral marker of various psychopathologies [23], neurodegenerative diseases [24], and CNS neurotoxic alterations [21]; further, alterations in MAO levels have been implicated in the pathogenesis of psychiatric disorders. As such, decreased platelet MAO-B activity was found in children with ADHD [22, 25]. Altered p-MAO-B has been also suggested as a biomarker of alcohol dependence or alcohol consumption [14, 26].…”

Section: Discussionmentioning

confidence: 99%

Mercury Vapour Long-Lasting Exposure: Lymphocyte Muscarinic Receptors as Neurochemical Markers of Accidental Intoxication

Roda¹,

Giampreti²,

Vecchio³

et al. 2016

Case Reports in Medicine

View full text Add to dashboard Cite

Introduction. Chronic poisoning may result in home setting after mercury (Hg) vapours inhalation from damaged devices. We report a chronic, nonoccupational Hg poisoning due to 10-year indoor exposure to mercury spillage. Case Report. A 72-year-old man with polyneuropathy of suspected toxic origin. At hospitalization, toxicological clinical evaluations confirmed the altered neurological picture documented across the last decade. Periodic blood and urine Hg levels (BHg, UHg) monitoring were performed from admission (t 0), until 1 year later (t 2), paralleled by blood neurochemical markers assessment, that is, lymphocytes muscarinic receptors (l-MRs). At t 0: BHg and UHg were 27 and 1.4 microg/L, respectively (normal values: BHg 1–4.5; UHg 0.1–4.5), associated with l-MRs increase, 185.82 femtomoL/million lymphocytes (normal range: 8.0–16.0). At t 1 (two days after DMSA-mobilization test), BHg weak reduction, paralleled by UHg 3.7-fold increase, was measured together with further l-MRs enhancement (205.43 femtomoL/million lymphocytes). At t 2 (eight months after two cycles of DMSA chelating therapy ending), gradual improving of clinical manifestations was accompanied by progressive decrease of BHg and UHg (4.0 and 2.8 microg/L, resp.) and peripheral l-MRs neurochemical marker (24.89 femtomoL/million lymphocytes). Conclusion. l-MRs modulatory effect supports their use as peripheral neurochemical marker in Hg poisoning diagnosis and chelation therapy monitoring.

show abstract

Platelet monoamine oxidase activity in children with attention-deficit/hyperactivity disorder

Cited by 23 publications

References 36 publications

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Human Plasma Glycome in Attention-Deficit Hyperactivity Disorder and Autism Spectrum Disorders

Mercury Vapour Long-Lasting Exposure: Lymphocyte Muscarinic Receptors as Neurochemical Markers of Accidental Intoxication

Contact Info

Product

Resources

About