PT - JOURNAL ARTICLE AU - Masataka Wada AU - Shinichiro Nakajima AU - Shiori Honda AU - Mayuko Takano AU - Keita Taniguchi AU - Sakiko Tsugawa AU - Yu Mimura AU - Nanao Hattori AU - Shinsuke Koike AU - Reza Zomorrodi AU - Daniel M. Blumberger AU - Zafiris J. Daskalakis AU - Masaru Mimura AU - Yoshihiro Noda TI - Reduced signal propagation elicited by frontal transcranial magnetic stimulation is associated with oligodendrocyte abnormalities in treatment-resistant depression AID - 10.1503/jpn.220102 DP - 2022 Sep 14 TA - Journal of Psychiatry and Neuroscience PG - E325--E335 VI - 47 IP - 5 4099 - http://jpn.ca/content/47/5/E325.short 4100 - http://jpn.ca/content/47/5/E325.full SO - JPN2022 Sep 14; 47 AB - Background: The efficacy of repetitive transcranial magnetic stimulation (rTMS) to the left dorsolateral prefrontal cortex (dlPFC) has been established in patients with treatment-resistant depression (TRD), suggesting that alterations in signal propagation from the left dlPFC to other brain regions may be linked to the pathophysiology of TRD. Alterations at the cellular level, including dysfunction of oligodendrocytes, may contribute to these network abnormalities. The objectives of the present study were to compare signal propagation from the left dlPFC to other neural networks in patients with TRD and healthy controls. We used TMS combined with electroencephalography to explore links between cell-specific gene expression and signal propagation in TRD using a virtual-histology approach.Methods: We examined source-level estimated signal propagation from the left dlPFC to the 7 neural networks in 60 patients with TRD and 30 healthy controls. We also calculated correlations between the interregional profiles of altered signal propagation and gene expression for 9 neural cell types derived from the Allen Human Brain Atlas data set.Results: Signal propagation from the left dlPFC to the salience network was reduced in the θ and α bands in patients with TRD (p = 0.0055). Furthermore, this decreased signal propagation was correlated with cellspecific gene expression of oligodendrocytes (p < 0.000001).Limitations: These results show only part of the pathophysiology of TRD, because stimulation was limited to the left dlPFC.Conclusion: Reduced signal propagation from the left dlPFC to the salience network may represent a pathophysiological endophenotype of TRD; this finding may be associated with reduced expression of oligodendrocytes.