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Cited by 101Attention Deficit Hyperactivity DisorderGenetics and Neurodevelopmental DisordersNeurotransmitter Receptor Influence on Behavior

The role of ADHD associated genes in neurodevelopment

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Dark, Callum, Homman-Ludiye, Jihane, Bryson-Richardson, Robert J.·2018·Developmental Biology
DOI 10.1016/j.ydbio.2018.03.023
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Abstract

Attention deficit hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder of childhood. It is primarily characterised by high levels of activity, inattention, and impulsivity, and has strong negative impacts on academic functioning. Children with ADHD show a reduction in volume, and hypoactivity, in a range of brain regions. The underlying mechanisms behind these phenotypes are unknown, however, variants in several genes with known roles in neurodevelopment are associated with ADHD. In this review we discuss how these ADHD associated genes contribute to neurodevelopment, and how variants in these genes could give rise to the neurological phenotypes seen in ADHD.

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Crossref · 10.1016/j.ydbio.2018.03.023

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  • Oxidative stress results in a notable problem in terms of neuronal damage which can lead to all of the defects mentioned above.

    “Besides, oxidative stress results in a notable problem in terms of neuronal damage which can lead to all of the defects mentioned above [92].”

    From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [92]

    Section 8, “Selective cell death” (page not provided), says excess glutamate can cause oxidative stress and cell death, and links increased neuronal death to reduced neuronal number and brain volume. It does not say oxidative stress can cause all the defects referred to in the citing sentence. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Other proteins related to 5-HT metabolism, such as TPH2 and NOS-1, which reduces SERT cell surface localization increasing the levels of extracellular serotonin, might be involved in the pathophysiology of ADHD.

    “In addition, other proteins related to 5-HT metabolism, such as tryptophan 5-hydroxylase 2 (TPH2) and nitrous oxide synthase 1 (NOS-1), which reduces the serotonin transporter (SERT or SLC6A4) cell surface localization increasing the levels of extracellular serotonin, might be involved in the pathophysiology of ADHD [90, 92].”

    From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [92]

    The Neurogenesis section (page unavailable) says NOS1 is associated with ADHD and that its interaction with SERT reduces SERT cell-surface localisation and serotonin uptake in HEK293 cells. The Migration section (page unavailable) links impaired SERT reuptake to increased extracellular serotonin, but in transporter-knockout mice, not NOS1-expressing cells. The retrieved passages do not address TPH2, so the claim about both proteins is only partly supported. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • Other proteins related to proliferation and neurodevelopment that are altered in ADHD are CREB, cyclin D1, NOS-1, CADH13 and PARK2.

    “Other proteins related to proliferation and neurodevelopment that are altered in ADHD are cyclic AMP response element-binding protein (CREB), cyclin D1 and NOS-1, cadherin-13 (CADH13) and E3 ubiquitin-protein ligase parkin (PARK2) [92].”

    From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [92]

    The Neurogenesis section links CREB and cyclin D1 to proliferation through ADHD-associated glutamate receptors, and identifies NOS1 as associated with ADHD. The passages on CDH13 and PARK2 likewise describe ADHD associations and neurodevelopmental roles. They do not establish that all five proteins are altered in people with ADHD; the CDH13 passage explicitly says whether its function increases or decreases in ADHD is unknown. Page numbers were not available in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Ephrin family members have a role in ADHD-related synaptogenesis alterations.

    “Moreover, it has been suggested that ephrin family members have a role in ADHD-related synaptogenesis alterations [92, 130].”

    From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [92]

    Section 5, “Synaptogenesis” (page unavailable), identifies ephrin type-B receptor 2 (EPHB2) as a surface protein involved in stabilising synaptic contacts. It also discusses possible synaptic-density alterations in ADHD, but does not specifically link ephrin family members to ADHD-related alterations. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • ADHD seems to present a morphogenesis dysregulation, with a high number of neurophysiological difficulties caused by neuronal network dysfunctions in the brain.

    “ADHD seems to present a morphogenesis dysregulation [92, 121], with a high number of neurophysiological difficulties caused by neuronal network dysfunctions in the brain.”

    From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [92]

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Cited by

Sorted by citations

Authors
Dark, C., Homman-Ludiye, J., & Bryson-Richardson, R. J.
Affiliations
Monash University (AU)
Venue
Developmental Biology
Publisher
Elsevier BV
Published
2018-06
Volume
438
Issue
2
Pages
69-83
ISSN
0012-1606 (ISSN-L)
DOI
10.1016/j.ydbio.2018.03.023
OpenAlex
W2794829772
Cited by
101
References
21
Citations by year
2026: 6 · 2025: 14 · 2024: 22 · 2023: 13 · 2022: 20 · 2021: 11 · 2020: 10 · 2019: 3 · 2018: 1 · 2017: 1
FWCI
0.97
Type
journal article
Language
en
Open access
Licence
Locations
  • Developmental Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Australian Government Research Training Program
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
attention deficit hyperactivity disorder, brain development, genetic variants, brain atrophy, hypoactivity, inattention, impulsivity, heritability, academic functioning
MeSH terms
Attention Deficit Disorder with Hyperactivity, Brain, Humans, Impulsive Behavior, Neurons, Synapses, Neurodevelopmental Disorders

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