The Physiology of BDNF and Its Relationship with ADHD

Liu, Deyi; Shen, Xuemei; Yuan, Fang-fen; Guo, Ouyang; Zhong, Yan; Chen, Jianguo; Zhu, Ling‐Qiang; Wu, Jing

doi:10.1007/s12035-014-8956-6

Cited by 84 publications

(57 citation statements)

References 98 publications

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“…Lower concentrations of neurotrophins such as brain-derived neurotrophin factor (BDNF) have also been identified in people with ADHD (Liu et al 2014). BDNF has a critical role in hippocampal functioning, long-term potentiation for learning and memory, synaptic plasticity, neurogenesis, and neuroprotection (Leal et al 2014).…”

Section: How Oandns and Inflammation Might Influence Biological Pathwaymentioning

confidence: 99%

Oxidative and nitrosative stress in ADHD: possible causes and the potential of antioxidant-targeted therapies

Lopresti

2015

ADHD Atten Def Hyp Disord

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Attention deficit hyperactivity disorder (ADHD) has a complex etiology although theories associated with disturbances in dopaminergic and noradrenergic activity are most commonly cited.The importance of these catecholamines in ADHD is supported by its effective treatment utilising stimulant and non-stimulant medications that modify their activity. Recently there has been interest in oxidative and nitrosative stress (O&NS) in ADHD and its potential to contribute to this condition. In this article, research investigating O&NS in ADHD is reviewed and its impact on catecholaminergic activity and neurological structure is discussed. Lifestyle, environmental, ADHD is most commonly treated with stimulant medications such as methylphenidate and amphetamines, non-stimulants such as atomoxetine, and alpha2-adrenergic agonists such as clonidine and guanfacine. Through their effects on dopamine and noradrenaline transporters, stimulants inhibit the reuptake of dopamine and noradrenaline, thereby increasing the extracellular levels of these neurotransmitters. These stimulants also inhibit monoamine oxidase, the enzyme that metabolises these catecholamines (Wilens et al. 2011). Atomoxetine works as a selective reuptake inhibitor of noradrenaline leading to its increased extracellular concentration (Garnock- Jones and Keating 2009).While effective, these medications are associated with several adverse effects. These include loss of appetite, growth delay and sleep disturbances (Cortese et al. 2013). It is important to note that despite their widely accepted short-term efficacy, the long-term effectiveness of pharmacological treatments on social, educational and occupational functioning in people with ADHD continues to be debated (Huang and Tsai 2011;Langberg and Becker 2012;Nijmeijer et al. 2008). On a positive note, recent analyses using the Swedish national registrar suggests that long-term stimulant use in people with ADHD is associated with reduced rates of substance use, criminality, and serious traffic accidents (Chang et al. 2014a;Chang et al. 2014b;Lichtenstein et al. 2012).Despite wide appreciation of catecholaminergic theories associated with ADHD, there has been increased research into other biological mechanisms associated with ADHD. For example, in psychiatry there has been interest in immune-inflammatory pathways and oxidative and nitrosative stress (O&NS). In particular, it has been confirmed through recent meta-analyses that depression is Increased O&NS has also been found in bipolar disorder (Andreazza et al. 2008;Brown et al. 2014),

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Section: How Oandns and Inflammation Might Influence Biological Pathwaymentioning

confidence: 99%

Oxidative and nitrosative stress in ADHD: possible causes and the potential of antioxidant-targeted therapies

Lopresti

2015

ADHD Atten Def Hyp Disord

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“…BDNF has been linked to a number of neurologic disorders including neurodevelopmental disorders [155–157] and is now a gene of interest to investigate the neurological effects of environmental toxicants. Prenatal exposure to maternal cigarette smoking has been reported to induce a long-term effect on adolescent behavior possibly by inducing hypermethylation at BDNF promoter VI and 5′ untranslated region (UTR) [158].…”

Section: Epigenetic Alterations By Environmental Toxicantsmentioning

confidence: 99%

Neurodevelopmental Disorders and Environmental Toxicants: Epigenetics as an Underlying Mechanism

Tran

Miyake

2017

International Journal of Genomics

123

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The increasing prevalence of neurodevelopmental disorders, especially autism spectrum disorders (ASD) and attention deficit hyperactivity disorder (ADHD), calls for more research into the identification of etiologic and risk factors. The Developmental Origin of Health and Disease (DOHaD) hypothesizes that the environment during fetal and childhood development affects the risk for many chronic diseases in later stages of life, including neurodevelopmental disorders. Epigenetics, a term describing mechanisms that cause changes in the chromosome state without affecting DNA sequences, is suggested to be the underlying mechanism, according to the DOHaD hypothesis. Moreover, many neurodevelopmental disorders are also related to epigenetic abnormalities. Experimental and epidemiological studies suggest that exposure to prenatal environmental toxicants is associated with neurodevelopmental disorders. In addition, there is also evidence that environmental toxicants can result in epigenetic alterations, notably DNA methylation. In this review, we first focus on the relationship between neurodevelopmental disorders and environmental toxicants, in particular maternal smoking, plastic-derived chemicals (bisphenol A and phthalates), persistent organic pollutants, and heavy metals. We then review studies showing the epigenetic effects of those environmental factors in humans that may affect normal neurodevelopment.

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“…During development, BDNF and its receptors TrkB not only promote survival and differentiation of neurons but also are involved in neural plasticity in adulthood (13). Alteration in BDNF/TrkB activity is implicated in midbrain dopaminergic dysfunction reported in ADHD, which may explain the development of the main symptoms (45). Low serum levels of BDNF in ADHD can persist until adulthood (12).…”

Section: Attention-deficit/hyperactivity Disordermentioning

confidence: 99%

“…In dopamine transporter knockout mice (DAT −/− ), another animal model for ADHD, low expression level of BDNF mRNA and TrkB receptors were found in frontal cortex (20). BDNF regulates two crucial circuits, the fronto-striatal-cerebellar and the ventral striatal-limbic circuits in normal brain (45). Neural circuits in prefrontal cortex and cerebellum, which modulate the attentional process, thoughts, emotions, social behavior, and motor control, are implicated in ADHD symptomatology (37).…”

Section: Attention-deficit/hyperactivity Disordermentioning

confidence: 99%

Alterations of Growth Factors in Autism and Attention-Deficit/Hyperactivity Disorder

et al. 2017

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Growth factors (GFs) are cytokines that regulate the neural development. Recent evidence indicates that alterations in the expression level of GFs during embryogenesis are linked to the pathophysiology and clinical manifestations of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorders (ASD). In this concise review, we summarize the current evidence that supports the role of brain-derived neurotrophic factor, insulin-like growth factor 2, hepatocyte growth factor (HGF), glial-derived neurotrophic factor, nerve growth factor, neurotrophins 3 and 4, and epidermal growth factor in the pathogenesis of ADHD and ASD. We also highlight the potential use of these GFs as clinical markers for diagnosis and prognosis of these neurodevelopmental disorders.

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The Physiology of BDNF and Its Relationship with ADHD

Cited by 84 publications

References 98 publications

Oxidative and nitrosative stress in ADHD: possible causes and the potential of antioxidant-targeted therapies

Oxidative and nitrosative stress in ADHD: possible causes and the potential of antioxidant-targeted therapies

Neurodevelopmental Disorders and Environmental Toxicants: Epigenetics as an Underlying Mechanism

Alterations of Growth Factors in Autism and Attention-Deficit/Hyperactivity Disorder

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