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Updated: May 2, 2026

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Hyperdynamic microtubule-based structural changes in Monocyte-Derived-Neuronal-like cells from patients with

Alfredo Bellon^1,2, Alonso Cortez-Resendiz³, Lauren N Forrest⁴

¹Penn State Hershey Medical Center, Department of Psychiatry and Behavioral Health, Hershey, PA, USA. abellon@pennstatehealth.psu.edu.

Schizophrenia (Heidelberg, Germany)

|April 30, 2026

Summary

Schizophrenia (SCZ) patients

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Author Spotlight: Induced Microglia-Like Cell Technology to Shed Light on the Role of Microglial Dysfunction in Neuropsychiatric Disorders

Author Spotlight: Induced Microglia-Like Cell Technology to Shed Light on the Role of Microglial Dysfunction in Neuropsychiatric Disorders

Published on: September 6, 2024

Area of Science:

Neuroscience
Cell Biology
Psychiatry

Background:

Postmortem studies reveal altered dendritic structures in schizophrenia.
In vitro studies show variable neuronal morphology in schizophrenia patient cells.
Microtubule dynamics are crucial for neuronal structure and have been implicated in schizophrenia.

Purpose of the Study:

To investigate dynamic neurostructural changes in living cells from schizophrenia patients.
To explore the role of microtubule dynamics in schizophrenia-related neuronal abnormalities.
To assess the impact of colchicine and antipsychotics on these cellular changes.

Main Methods:

Utilized Monocyte-Derived-Neuronal-like cells (MDNCs) from schizophrenia patients and controls.
Assessed neurostructural plasticity and dynamic changes in MDNCs.
Applied colchicine, a microtubule-targeting agent, to evaluate cellular responses.

Main Results:

MDNCs from schizophrenia patients exhibited hyperdynamic microtubule-based neurostructural changes.
Colchicine disrupted neurostructural dynamics in control cells but not in schizophrenia cells at low concentrations.
Antipsychotic effects on cellular dynamics were inconclusive.

Conclusions:

Living neuronal-like cells from schizophrenia patients show altered microtubule dynamics.
These findings link microtubule deficits to neuronal shape anomalies in schizophrenia.
Further research is needed to clarify the role of medications and confirm these cellular observations.