Evidence map›Paper›PMID 37629164›Full record

ReviewInternational journal of molecular sciences2023

Molecular Mechanisms Underlying NMDARs Dysfunction and Their Role in ADHD Pathogenesis.

Justyna Kuś, Kamil Saramowicz, Maria Czerniawska, Wojciech Wiese, Natalia Siwecka, Wioletta Rozpędek-Kamińska, Aleksandra Kucharska-Lusina, Dominik Strzelecki, Ireneusz Majsterek

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
4.5field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Justyna KuśDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.
Kamil SaramowiczDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.ORCID 0009-0000-0395-5986
Maria CzerniawskaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.
Wojciech WieseDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.ORCID 0000-0002-0796-9717
Natalia SiweckaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.ORCID 0000-0002-0308-580X
Wioletta Rozpędek-KamińskaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.ORCID 0000-0001-9206-1203
Aleksandra Kucharska-LusinaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.
Dominik StrzeleckiDepartment of Affective and Psychotic Disorders, Medical University of Lodz, Czechoslowacka 8/10, 92-216 Lodz, Poland.ORCID 0000-0002-8559-1078
Ireneusz MajsterekDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.
Medical University of Lodz · PL

Funding

Medical University of Lodz 503/5-156-07/503-11-001National Science Center 2021/43/O/NZ5/02068
6 · The paper itself

Abstract

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.

Indexed as

Attention Deficit Disorder with HyperactivityCentral Nervous System StimulantsMethylphenidateAnimalsBrainReceptors, N-Methyl-D-AspartateCentral Nervous System StimulantsMethylphenidateReceptors, N-Methyl-D-Aspartateattention deficit hyperactivity disorder (ADHD)genetic variantsglutamatelong-term depressionlong-term potentiationneurodevelopmentN-methyl-D-aspartate receptor (NMDAR)synaptic plasticity

Identifiers

PMID37629164
PMCPMC10454781
OpenAlexW4386030222

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.