Evidence map›Paper›PMID 41972553›Full record

ReviewBiology2026

Cytoskeletal Dynamics and Molecular Motor Dysfunction in Psychiatric Disorders: Insights from Schizophrenia and Autism Spectrum Disorder.

Kenyu Nakamura, Asumi Kubo, Sae Sanaka, Sara Kamiya, Kentaro Itagaki, Tetsuya Sasaki

Abstract readReview
In one paragraph

Review in Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Kenyu NakamuraLaboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Ibaraki, Japan.
Asumi KuboLaboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Ibaraki, Japan.
Sae SanakaLaboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Ibaraki, Japan.
Sara KamiyaLaboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Ibaraki, Japan.
Kentaro ItagakiLaboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Ibaraki, Japan.
Tetsuya SasakiLaboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Ibaraki, Japan.ORCID 0000-0002-7723-4417

Funding

Japan Society for the Promotion of Science 16H06276Japan Society for the Promotion of Science 19H05201Japan Society for the Promotion of Science 19K08065Japan Society for the Promotion of Science 22K07611
6 · The paper itself

Abstract

Elucidating the pathophysiological mechanisms of mental disorders remains a critical challenge in psychiatric research. Recent studies have highlighted the potential involvement of cytoskeletal and molecular motor abnormalities in the development of mental disorders such as schizophrenia and autism spectrum disorder (ASD). Although schizophrenia and ASD differ clinically, both disorders are increasingly regarded as neurodevelopmental conditions and share vulnerabilities in synapse formation and neural circuit maturation. This review synthesizes the latest findings on the relationship between cytoskeletal and molecular motor abnormalities and mental disorders. The cytoskeleton, composed of microtubules, actin filaments, and intermediate filaments, along with molecular motors such as kinesins, dyneins, and myosins, plays crucial roles in neurodevelopment, synapse formation, and neurotransmission. In schizophrenia, decreased expression of the microtubule-associated protein MAP2 and abnormalities in the DISC1 gene have been reported, potentially leading to dendritic morphological abnormalities and neurodevelopmental disorders. Additionally, abnormalities in molecular motors such as KIF17 and KIF1A have been implicated in schizophrenia pathophysiology. Myosin Id has been identified as a risk gene for ASD. Furthermore, abnormalities in actin-related proteins such as SHANK3 and CYFIP1 have been shown to cause synaptic dysfunction. These findings suggest that mental disorders arise from complex pathologies involving multiple cytoskeletal and molecular motor-related protein abnormalities. Future research should focus on elucidating the functions of individual proteins and adopting a comprehensive approach that includes glial cells. Advances in this field may deepen our understanding of the pathophysiological mechanisms of mental disorders and potentially lead to the development of novel therapeutic strategies.

Indexed as

autism spectrum disordercytoskeletonmicrogliamolecular motorsschizophrenia

Identifiers

PMID41972553
PMCPMC13072259

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.