Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathology

Introduction: Neuroinflammation is a key contributor to the pathogenesis of Alzheimer's disease (AD), and impaired clearance of amyloid-β (Aβ) by microglia is closely associated with disease progression. Oxytocin (OXT), a hypothalamic neuropeptide, has recently been reported to exert anti-infla...

Full description

Saved in:
Bibliographic Details
Main Authors: Tomoki Asaba, Sayuri Hamano, Ayaka Nanmo, Jieun Seo, Tatsuto Kageyama, Junji Fukuda
Format: Article
Language:English
Published: Elsevier 2025-12-01
Series:Regenerative Therapy
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2352320425001464
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849473209284427776
author Tomoki Asaba
Sayuri Hamano
Ayaka Nanmo
Jieun Seo
Tatsuto Kageyama
Junji Fukuda
author_facet Tomoki Asaba
Sayuri Hamano
Ayaka Nanmo
Jieun Seo
Tatsuto Kageyama
Junji Fukuda
author_sort Tomoki Asaba
collection DOAJ
description Introduction: Neuroinflammation is a key contributor to the pathogenesis of Alzheimer's disease (AD), and impaired clearance of amyloid-β (Aβ) by microglia is closely associated with disease progression. Oxytocin (OXT), a hypothalamic neuropeptide, has recently been reported to exert anti-inflammatory effects on microglia; however, its therapeutic potential in the human brain remains unclear. Methods: We generated human cerebral organoids (hCOs) from induced pluripotent stem cells (iPSCs) to model early AD-like pathology. Aβ toxicity was induced by applying 3 μM Aβ1–42 for 48 h. The protective effects of OXT were evaluated through immunohistochemistry, RT-qPCR, calcium imaging, and multielectrode array (MEA) recordings. The involvement of microglia in Aβ clearance was assessed by immunostaining and gene expression analysis of TREM2. Results: Aβ exposure led to significant deposition of Aβ in the outer layers of hCOs, accompanied by suppressed neural activity and increased apoptotic signaling. Pretreatment with OXT attenuated Aβ deposition and caspase-3-mediated apoptosis in a concentration-dependent manner. OXT also restored calcium oscillations and neuronal network activity as measured by MEA. Notably, OXT enhanced the recruitment of microglia to Aβ deposits and upregulated the expression of TREM2, a key regulator of microglial phagocytosis. Co-expression of oxytocin receptors (OXTR) on Iba1-positive microglia suggests that OXT directly modulates microglial activation and Aβ clearance. Conclusions: OXT has neuroprotective effects on human cortical organoids by preserving their neuronal activity and promoting microglial-mediated Aβ clearance. This study provides novel insights into the therapeutic potential of OXT for targeting neuroinflammation and Aβ pathology in patients with AD.
format Article
id doaj-art-d2bd27110b364690bf49dc47591cd82f
institution Kabale University
issn 2352-3204
language English
publishDate 2025-12-01
publisher Elsevier
record_format Article
series Regenerative Therapy
spelling doaj-art-d2bd27110b364690bf49dc47591cd82f2025-08-20T03:24:13ZengElsevierRegenerative Therapy2352-32042025-12-013025926710.1016/j.reth.2025.06.013Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathologyTomoki Asaba0Sayuri Hamano1Ayaka Nanmo2Jieun Seo3Tatsuto Kageyama4Junji Fukuda5Faculty of Engineering, Yokohama National University, 79-5 Tokiwadai, Hodogaya-ku, Yokohama, Kanagawa, 240-8501, JapanFaculty of Engineering, Yokohama National University, 79-5 Tokiwadai, Hodogaya-ku, Yokohama, Kanagawa, 240-8501, JapanFaculty of Engineering, Yokohama National University, 79-5 Tokiwadai, Hodogaya-ku, Yokohama, Kanagawa, 240-8501, JapanFaculty of Engineering, Yokohama National University, 79-5 Tokiwadai, Hodogaya-ku, Yokohama, Kanagawa, 240-8501, JapanFaculty of Engineering, Yokohama National University, 79-5 Tokiwadai, Hodogaya-ku, Yokohama, Kanagawa, 240-8501, JapanCorresponding author.; Faculty of Engineering, Yokohama National University, 79-5 Tokiwadai, Hodogaya-ku, Yokohama, Kanagawa, 240-8501, JapanIntroduction: Neuroinflammation is a key contributor to the pathogenesis of Alzheimer's disease (AD), and impaired clearance of amyloid-β (Aβ) by microglia is closely associated with disease progression. Oxytocin (OXT), a hypothalamic neuropeptide, has recently been reported to exert anti-inflammatory effects on microglia; however, its therapeutic potential in the human brain remains unclear. Methods: We generated human cerebral organoids (hCOs) from induced pluripotent stem cells (iPSCs) to model early AD-like pathology. Aβ toxicity was induced by applying 3 μM Aβ1–42 for 48 h. The protective effects of OXT were evaluated through immunohistochemistry, RT-qPCR, calcium imaging, and multielectrode array (MEA) recordings. The involvement of microglia in Aβ clearance was assessed by immunostaining and gene expression analysis of TREM2. Results: Aβ exposure led to significant deposition of Aβ in the outer layers of hCOs, accompanied by suppressed neural activity and increased apoptotic signaling. Pretreatment with OXT attenuated Aβ deposition and caspase-3-mediated apoptosis in a concentration-dependent manner. OXT also restored calcium oscillations and neuronal network activity as measured by MEA. Notably, OXT enhanced the recruitment of microglia to Aβ deposits and upregulated the expression of TREM2, a key regulator of microglial phagocytosis. Co-expression of oxytocin receptors (OXTR) on Iba1-positive microglia suggests that OXT directly modulates microglial activation and Aβ clearance. Conclusions: OXT has neuroprotective effects on human cortical organoids by preserving their neuronal activity and promoting microglial-mediated Aβ clearance. This study provides novel insights into the therapeutic potential of OXT for targeting neuroinflammation and Aβ pathology in patients with AD.http://www.sciencedirect.com/science/article/pii/S2352320425001464Alzheimer's diseaseAmyloid-betaCerebral organoidsMicrogliaOxytocinAnti-inflammatory signaling
spellingShingle Tomoki Asaba
Sayuri Hamano
Ayaka Nanmo
Jieun Seo
Tatsuto Kageyama
Junji Fukuda
Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathology
Regenerative Therapy
Alzheimer's disease
Amyloid-beta
Cerebral organoids
Microglia
Oxytocin
Anti-inflammatory signaling
title Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathology
title_full Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathology
title_fullStr Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathology
title_full_unstemmed Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathology
title_short Human iPSC-derived cerebral organoids reveal oxytocin-mediated protection against amyloid-β pathology
title_sort human ipsc derived cerebral organoids reveal oxytocin mediated protection against amyloid β pathology
topic Alzheimer's disease
Amyloid-beta
Cerebral organoids
Microglia
Oxytocin
Anti-inflammatory signaling
url http://www.sciencedirect.com/science/article/pii/S2352320425001464
work_keys_str_mv AT tomokiasaba humanipscderivedcerebralorganoidsrevealoxytocinmediatedprotectionagainstamyloidbpathology
AT sayurihamano humanipscderivedcerebralorganoidsrevealoxytocinmediatedprotectionagainstamyloidbpathology
AT ayakananmo humanipscderivedcerebralorganoidsrevealoxytocinmediatedprotectionagainstamyloidbpathology
AT jieunseo humanipscderivedcerebralorganoidsrevealoxytocinmediatedprotectionagainstamyloidbpathology
AT tatsutokageyama humanipscderivedcerebralorganoidsrevealoxytocinmediatedprotectionagainstamyloidbpathology
AT junjifukuda humanipscderivedcerebralorganoidsrevealoxytocinmediatedprotectionagainstamyloidbpathology