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  1. 原著論文

Prefronto-thalamic hypoconnectivity in schizophrenia: Monkey to human translation of critical pathways for symptom-related functions

https://repo.qst.go.jp/records/2002827
https://repo.qst.go.jp/records/2002827
d69ab2d6-e228-4e88-8df9-6970b3d352f5
アイテムタイプ 学術雑誌論文 / Journal Article(1)
公開日 2026-02-25
タイトル
タイトル Prefronto-thalamic hypoconnectivity in schizophrenia: Monkey to human translation of critical pathways for symptom-related functions
言語 en
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
著者 Yahata Noriaki

× Yahata Noriaki

Yahata Noriaki

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Hirabayashi Toshiyuki

× Hirabayashi Toshiyuki

Hirabayashi Toshiyuki

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Minamimoto Takafumi

× Minamimoto Takafumi

Minamimoto Takafumi

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抄録
内容記述タイプ Abstract
内容記述 Aim: Recent advances in genetic neuromodulation technology have enabled circuit-specific interventions in nonhuman primates (NHPs), thereby revealing the causal functions of specific neural circuits. Using this technology, we recently identified in NHPs the causal roles of the dorsolateral prefrontal cortex (DLPFC) to the lateral part of the mediodorsal thalamic nucleus (MDl) pathway in working memory, a core deficit in schizophrenia (SCZ) patients. Here, we aimed to examine if this alteration was translational to the human patients with SCZ.Methods: Using the publicly available, multisite, multi-disorder magnetic resonance imaging (MRI) dataset, we evaluated the resting-state functional connectivity in this DLPFC-MDl pathway and examined whether the alteration was, if any, specific to SCZ (N = 91) and not to healthy controls (HCs, N = 511), patients with major depressive disorder (MDD, N = 133), and autism spectrum disorders (ASDs, N = 120).Results: We found that the DLPFC-MDl connectivity was significantly reduced in the SCZ group compared to HCs, whereas no such hypoconnectivity was observed in the ASD or MDD groups, suggesting a disease-dependent profile of altered connectivity at rest. This hypoconnectivity was not observed between the DLPFC and other neighboring thalamic nuclei, suggesting a focal thalamic anomaly underlying the altered connectivity in SCZ.Conclusion: These results support the potential of translating pathway-specific causal insights from NHP studies to identify disease-specific connectivity alterations in neuropsychiatric disorders with related symptoms in humans.Keywords: functional connectivity; pathway‐specific silencing; resting‐state functional MRI; schizophrenia; thalamus.
書誌情報 PCN Reports

巻 4, 号 4, p. e70206, 発行日 2025-10
出版者
出版者 John Wiley & Sons, Inc.
ISSN
収録物識別子タイプ ISSN
収録物識別子 2769-2558
PubMed番号
識別子タイプ PMID
関連識別子 41041143
DOI
識別子タイプ DOI
関連識別子 10.1002/pcn5.70206
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