Lower levels of tubulin alpha 1b in the frontal pole in schizophrenia supports a role for changed cytoskeletal dynamics in the aetiology of the disorder. (September 2021)

• Record Type: Journal Article
• Authors: Snelleksz, Megan; Dean, Brian
• Is Part Of: Psychiatry research. Volume 303(2021)
• Publication Date: 2021-09
• Subjects: Schizophrenia -- Bipolar disorders -- Major depressive disorders -- Tubulin -- Cortex -- Cytoskeleton; Psychiatry -- Periodicals; Psychiatry -- periodicals; Psychiatrie -- Périodiques; 616.89
• DOI: 10.1016/j.psychres.2021.114096
• Languages: English
• ISSNs: 0165-1781

Abstract

Highlights: Lower of tubulin alpha 1b (TUBA1B) in Brodmann's area (BA) 10 in schizophrenia. TUBA1B is part of the neuronal cytoskeleton. There may be disruptions in the neuronal cytoskeleton in schizophrenia. No change in TUBA1B in mood disorders showing some diagnostic selectivity. Data from humans and rats argue changes in TUBA1B are not simple drug effects. Abstract: Our transcriptomic study suggested there were markedly lower levels of tubulin alpha 1b (TUBA1B) expression in BA 10, but not BA 9, from patients with schizophrenia. We now use Western blotting to compare levels of TUBA1B protein in BA 9 and 10 from patients with schizophrenia and BA 10 from patients with mood disorders to controls as well as in the frontal cortex from rats after treatment with haloperidol, chlorpromazine or vehicle for 28 days. Levels of TUBA1B were significantly lower (- 18.6%) in BA 10, but not BA 9, from patients with schizophrenia. Levels of TUBA1B did not differ significantly from controls in BA 10 from patients with mood disorders or in the cortex of rats after antipsychotic drug treatments. Levels of TUBA1B were significantly lower (- 30%) in BA 10 from patients with schizophrenia who were not being treated with antipsychotic drugs close to death compared to those who were treated close to death. These data suggest that lower levels of TUBA1B, a cytoskeletal protein, in BA 10 from patients with schizophrenia are not a simple drug effect and therefore add to the hypothesis that a breakdown in cytoskeletal homoeostasis may be contributing to the genesis of the symptoms of the disorder.