Molecular Mechanisms Underlying NMDARs Dysfunction and Their Role in ADHD Pathogenesis

Attention deficit hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders, although the aetiology of ADHD is not yet understood. One proposed theory for developing ADHD is N-methyl-D-aspartate receptors (NMDARs) dysfunction. NMDARs are involved in regulating synaptic pla...

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Published in:International journal of molecular sciences 2023-08, Vol.24 (16), p.12983
Main Authors: Kuś, Justyna, Saramowicz, Kamil, Czerniawska, Maria, Wiese, Wojciech, Siwecka, Natalia, Rozpędek-Kamińska, Wioletta, Kucharska-Lusina, Aleksandra, Strzelecki, Dominik, Majsterek, Ireneusz
Format: Article
Language:English
Subjects:
Aspartate
Attention deficit hyperactivity disorder
Brain research
Child & adolescent psychiatry
Dopamine
Genes
Genetic aspects
Genetic polymorphisms
Hyperactivity
Impulsivity
Kinases
Ligands
Memory
Methyl aspartate
Neurodevelopmental disorders
Pathogenesis
Pediatrics
Review
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Summary:Attention deficit hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders, although the aetiology of ADHD is not yet understood. One proposed theory for developing ADHD is N-methyl-D-aspartate receptors (NMDARs) dysfunction. NMDARs are involved in regulating synaptic plasticity and memory function in the brain. Abnormal expression or polymorphism of some genes associated with ADHD results in NMDAR dysfunction. Correspondingly, NMDAR malfunction in animal models results in ADHD-like symptoms, such as impulsivity and hyperactivity. Currently, there are no drugs for ADHD that specifically target NMDARs. However, NMDAR-stabilizing drugs have shown promise in improving ADHD symptoms with fewer side effects than the currently most widely used psychostimulant in ADHD treatment, methylphenidate. In this review, we outline the molecular and genetic basis of NMDAR malfunction and how it affects the course of ADHD. We also present new therapeutic options related to treating ADHD by targeting NMDAR.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms241612983