研究背景：雙相情緒障礙症（bipolar disorder, BD）是一種慢性精神疾病，其特徵為反覆發作的異常情緒與逐漸惡化的神經認知功能。雖然BD患者的神經認知缺損已有充分的研究，但其社會認知缺損在整個生命歷程中的變化仍不明確。本研究主要探討 BD 患者社會認知缺損的年齡模式，將神經認知作為此之次要探討以注意它與社會認知之間的對照與差異。並先分析精神病性特徵之病史的調節作用，再進一步探討周邊胰島素阻抗（insulin resistance, IR）及多巴胺轉運體（dopamine transporter, DAT）的三方互動效果對年齡相關認知缺損的影響。
研究方法：本研究採用橫斷面設計，分析108名BD患者與90名健康對照組（HC）。依據患者病史中是否曾有精神病性特徵，將BD患者分為精神病性BD（psychotic BD, PBD）與非精神病性BD（non-psychotic BD, NPBD）。社會認知功能以Diagnostic Analysis of Nonverbal Accuracy 2-Taiwan Version（DANVA-2-TW）、Mayer-Salovey-Caruso Emotional Intelligence Test（MSCEIT）、Chinese Theory of Mind Tasks（CToM）與Reading the Mind in the Eyes Test（RMET）進行評估。神經認知功能則採用Wisconsin Card Sorting Test（WCST）與Continuous Performance Test（CPT）評估。胰島素阻抗透過HOMA-IR公式計算，並使用[99mTc]TRODAT-1單光子發射電腦斷層掃描（SPECT）量測多巴胺轉運體可用性。
研究結果：BD患者在神經認知與社會認知表現上皆顯著低於健康對照組。BD患者在隨年齡增長下，情緒辨識（DANVA-2-TW）與執行功能（WCST）方面的退化更為明顯，次族群分析則顯示此趨勢主要由PBD組貢獻。高胰島素阻抗對於與BD患者的執行功能表現隨年齡增加而下降有關，但多巴胺轉運體可用性對此不具有顯著的調節作用。
結論：本研究突顯BD患者的認知與社會認知功能具有隨年齡增長而惡化的趨勢，其中精神病性特徵與胰島素阻抗為主要影響因素。研究結果顯示，代謝功能異常可能加劇BD患者的認知退化，可作為為早期介入的潛在目標。未來應進一步進行縱貫性研究，以釐清因果關係並評估相關干預措施的有效性。

Background: Bipolar disorder (BD) is a chronic psychiatric condition marked by episodic mood disturbances and progressive neurocognitive decline. While neurocognitive impairments in BD are well-documented, less is known about the trajectory of social cognition deficits across the lifespan. This study primarily investigates age-related patterns of social cognitive deficits in BD, with neurocognition examined as a secondary reference to highlight potential overlaps and distinctions between general and social cognitive functions. Additionally, the moderating effect of psychotic features is first examined, followed by the three-way interaction effects of peripheral insulin resistance (IR) and dopamine transporter (DAT) availability on age-related cognitive deficits.
Methods: A cross-sectional design was utilized, combining data from 108 BD patients and 90 healthy controls (HC). Participants were categorized into psychotic BD (PBD) and non-psychotic BD (NPBD) based on lifetime history of psychotic symptoms. Social cognition was assessed using the Diagnostic Analysis of Nonverbal Accuracy 2-Taiwan Version (DANVA-2-TW), Mayer-Salovey-Caruso Emotional Intelligence Test (MSCEIT), Chinese Theory of Mind Tasks (CToM), and Reading the Mind in the Eyes Test (RMET). Neurocognition was evaluated using the Wisconsin Card Sorting Test (WCST) and Continuous Performance Test (CPT). Peripheral IR was assessed via HOMA-IR, and dopamine transporter (DAT) availability was measured using [99mTc]TRODAT-1 SPECT imaging.
Results: BD patients exhibited significant impairments in both neurocognitive and social cognitive domains compared to HC. Notably, BD individuals demonstrated more deficits than HC in emotion recognition (DANVA-2-TW) and executive function (WCST) with increasing age, which is mainly contributed by the PBD group. Higher IR levels were associated with greater age-related executive function deficits in BD individuals. However, DAT availability did not significantly moderate age-related cognitive deficits.
Conclusion: This study highlights the progressive nature of cognitive and social cognitive impairments in BD, with history of psychotic features and insulin resistance as key contributing factors. The findings suggest that metabolic dysfunction may exacerbate cognitive decline in BD, indicating potential targets for early intervention. Future longitudinal studies are warranted to establish causal relationships and assess intervention efficacy.

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