神経性過食症に対する認知行動療法のメカニズムの解明 ―治療効果に関わる脳機能変化と、治療反応を予測する脳機能の探索―

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2026-09-25 千葉大学

千葉大学の研究チームは、がんの転移を調節するタンパク質Mdm2の新たな機能を明らかにした。Mdm2は従来、がん抑制タンパク質p53を制御する因子として知られていたが、本研究では、Mdm2が別のタンパク質との相互作用を通じて、がん細胞の移動・浸潤に関わる細胞内機構を調節することを示した。Mdm2のこの機能を阻害することで、がんの転移を抑制できる可能性が示され、Mdm2を標的とした新しい抗がん剤開発につながることが期待される。研究成果は『Nature Communications』に掲載されている。千葉大学の研究成果一覧でも、2026年9月25日の医学・薬学・看護分野の成果として掲載されている。

神経性過食症に対する認知行動療法のメカニズムの解明 ―治療効果に関わる脳機能変化と、治療反応を予測する脳機能の探索―
治療効果と相関していた治療後のrsFCの変化
青線:結合性低下 赤線:結合性増加

<関連情報>

神経性過食症に対する認知行動療法後の症状改善に関連する安静時機能的結合の変化と治療前の特徴 Resting-state functional connectivity changes and pretreatment features associated with symptom improvement after cognitive behavioral therapy for bulimia nervosa

Yusuke Sudo, Ritu Bhusal Chhatkuli, Tsunehiko Takamura, Rio Kamashita, Koji Matsumoto, Noriko Numata, Sayo Hamatani, Yoshiya Moriguchi, Keiko Ino, Tetsuya Ando, Chisato Ohara, Misako Funaba, Masanori Isobe, Tomomi Noda, Keima Tose, Toshiya Murai, Momo Sunada, Kana Morimoto, Momoka Taniguchi, Yasuhiro Sato, Yumi Hamamoto, Liu Yu, Jeyoon Choi, Kentaro Oba, EDNI Working Group
Journal of Eating Disorders  Published:15 September 2026
DOI:https://doi.org/10.1186/s40337-026-01754-z  Early provide

Abstract

Background
Bulimia nervosa (BN) is a serious eating disorder, and cognitive behavioral therapy (CBT) is the first-line treatment; however, remission rates remain modest, and the neural correlates of CBT response are unclear. Resting-state functional connectivity (rsFC) may clarify CBT-related brain changes and pretreatment correlates of response, yet longitudinal whole-brain rsFC studies in BN are lacking.

Methods
Thirty Japanese women with BN (mean age, 33.6 ± 9.9 years) received multi-site CBT (enhanced CBT: n = 24; videoconference CBT: n = 4; guided internet-based CBT: n = 2). Resting-state fMRI and symptom measures, including the Eating Disorder Examination Questionnaire (EDE-Q), were obtained pre- and post-treatment, with an interval of 5.6 ± 1.5 months between assessments. Whole-brain region of interest (ROI)-to-ROI rsFC was computed and harmonized across sites. Multiple regression analyses adjusting for age and pretreatment psychotropic medication examined associations between improvement in EDE-Q global score and (1) rsFC changes and (2) pretreatment rsFC. Significance was assessed using seed-level FDR correction (q < 0.05), applied across all connections from each seed ROI to all target ROIs, and analysis-level FDR correction (q < 0.05), applied across all tested ROI-to-ROI connections.

Results
No associations survived analysis-level FDR correction across the ROI-to-ROI feature set. Exploratory seed-level findings indicated that greater improvement in EDE-Q global score was associated with decreased rsFC between the right orbitofrontal cortex and right posterior supramarginal gyrus, increased rsFC between the right anterior temporal fusiform cortex and cerebellar regions, and increased rsFC between the right caudate nucleus and right cerebellar hemisphere IX. Greater improvement was associated with stronger pretreatment rsFCs between the right superior parietal lobule and inferior frontal/temporo-occipital temporal regions, and between the left postcentral gyrus and bilateral temporo-occipital inferior temporal gyri.

Conclusions
This exploratory longitudinal analysis suggests that symptom improvement following CBT-based treatment may be associated with ROI-to-ROI rsFC changes in regions implicated in reward processing and higher-order visual or affective processing. Pretreatment connectivity in regions related to somatosensory processing and cognitive control may be relevant to CBT responsiveness. These findings should be interpreted cautiously because they did not survive analysis-level FDR correction and require replication in larger controlled cohorts.

医療・健康
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