Preprint / Version 1

Abnormalities in Cytoskeleton and Molecular Motors in Psychiatric Disorders: Focus on Schizophrenia and Autism Spectrum Disorder

##article.authors##

  • Koki Higuchi Laboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba
  • Kenyu Nakamura Laboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba
  • Asumi Kubo Laboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba
  • Sae Sanaka Laboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba
  • Sara Kamiya Laboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba
  • Tetsuya Sasaki Laboratory of Anatomy and Neuroscience, Department of Biomedical Sciences, Institute of Medicine, University of Tsukuba https://orcid.org/0000-0002-7723-4417 https://researchmap.jp/tsasak

DOI:

https://doi.org/10.51094/jxiv.885

Keywords:

Cytoskeleton, Molecular motors, Schizophrenia, Autism Spectrum Disorder, Microglia

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). 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 synaptic plasticity disturbances. In ASD, Myosin Id has been identified as a risk gene, with its localization in dendritic spines recently elucidated. 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.

Conflicts of Interest Disclosure

The authors declare that they have no competing interests.

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Posted


Submitted: 2024-09-05 23:50:52 UTC

Published: 2024-09-06 08:14:31 UTC
Section
Biology, Life Sciences & Basic Medicine