Evidence map›Paper›PMID 39061473›Full record

ReviewBrain sciences2024

Dopamine Dysregulation in Reward and Autism Spectrum Disorder.

Kenneth Blum, Abdalla Bowirrat, Keerthy Sunder, Panayotis K Thanos, Colin Hanna, Mark S Gold, Catherine A Dennen, Igor Elman, Kevin T Murphy, Milan T Makale

Abstract readReview
In one paragraph

Review in Brain sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Circadian rhythm lncRNABiochemistry and biophysics reports · 2026
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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

10 authors.

Kenneth BlumDivision of Addiction Research & Education, Center for Exercise Sports, Mental Health, Western University of Health Sciences, Pomona, CA 91766, USA.ORCID 0000-0001-6727-803X
Abdalla BowirratDepartment of Molecular Biology, Adelson School of Medicine, Ariel University, Ariel 40700, Israel.ORCID 0000-0001-8185-0688
Keerthy SunderSunder Foundation, Palm Springs, CA 92264, USA.
Panayotis K ThanosDepartment of Pharmacology and Toxicology, State University of New York, SUNY, Buffalo, NY 14215, USA.
Colin HannaDepartment of Pharmacology and Toxicology, State University of New York, SUNY, Buffalo, NY 14215, USA.
Mark S GoldDepartment of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USA.
Catherine A DennenDepartment of Family Medicine, Jefferson Health Northeast, Philadelphia, PA 19145, USA.
Igor ElmanDepartment of Psychiatry, Harvard University School of Medicine, Cambridge, MA 02215, USA.
Kevin T MurphyDivision of Personalized Neuromodulations, PeakLogic, LLC, Del Mar, CA 92130, USA.
Milan T MakaleDepartment of Radiation Medicine and Applied Sciences, University of California San Diego, La Jolla, CA 92093, USA.ORCID 0000-0002-0507-5883

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is primarily characterized by core deficits in social skills, communication, and cognition and by repetitive stereotyped behaviors. These manifestations are variable between individuals, and ASD pathogenesis is complex, with over a thousand implicated genes, many epigenetic factors, and multiple environmental influences. The mesolimbic dopamine (DA) mediated brain reward system is held to play a key role, but the rapidly expanding literature reveals intricate, nuanced signaling involving a wide array of mesolimbic loci, neurotransmitters and receptor subtypes, and neuronal variants. How altered DA signaling may constitute a downstream convergence of the manifold causal origins of ASD is not well understood. A clear working framework of ASD pathogenesis may help delineate common stages and potential diagnostic and interventional opportunities. Hence, we summarize the known natural history of ASD in the context of emerging data and perspectives to update ASD reward signaling. Then, against this backdrop, we proffer a provisional framework that organizes ASD pathogenesis into successive levels, including (1) genetic and epigenetic changes, (2) disrupted mesolimbic reward signaling pathways, (3) dysregulated neurotransmitter/DA signaling, and finally, (4) altered neurocognitive and social behavior and possible antagonist/agonist based ASD interventions. This subdivision of ASD into a logical progression of potentially addressable parts may help facilitate the rational formulation of diagnostics and targeted treatments.

Indexed as

anhedoniaautism spectrum disorder (ASD)dopamine (DA)EEGGABAmesolimbicreward system

Identifiers

PMID39061473
PMCPMC11274922

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.