Chang Jeryn, Shaw Thomas B, McCombe Pamela A, Henderson Robert D, Lucia Diana, Guo Christine C, Lv Jinglei, Garner Kelly, Bollmann Saskia, Ngo Shyuan T, Steyn Frederik J
School of Biomedical Sciences, Faculty of Medicine, The University of Queensland, Brisbane, QLD 4072, Australia.
School of Electrical Engineering and Computer Science, The University of Queensland, Brisbane, QLD 4072, Australia.
Brain Commun. 2025 Mar 14;7(2):fcaf111. doi: 10.1093/braincomms/fcaf111. eCollection 2025.
Motor Neuron Disease (MND) is associated with significant non-motor symptoms, including the loss of appetite. Loss of appetite has emerged as a dominant feature of the disease that may contribute to negative energy balance, faster disease progression and earlier death. We examined the prevalence and impact of appetite loss and analysed neural correlates of visual food stimuli with prandial status and appetite in people living with MND (plwMND). 157 plwMND and 120 non-neurodegenerative controls (NND Controls) were assessed for anthropometric, metabolic, appetite and clinical measures. Of these, 35 plwMND and 23 NND Controls underwent further functional MRI assessment of fasting and post-prandial responses to visual food cues. plwMND presented with reduced appetite ( < 0.001), with loss of appetite being more prevalent in plwMND than NND controls [OR = 2.59 (95% CI: = 1.46-4.61)]. Loss of appetite was not associated with hypermetabolism; however, was associated with fat mass loss ( < 0.05). Imaging assessment revealed no overall difference in response between plwMND and NND controls when viewing non-food and food images. In contrast, we found no prandial response in the temporal pole of plwMND compared with NND controls, and decreased activity in the cerebellum relative to appetite in plwMND. Loss of appetite, not hypermetabolism, contributes to negative energy balance in MND. Alterations in the temporal pole and cerebellum could contribute to altered appetite responses in some plwMND-brain regions not widely considered in appetite control-providing additional evidence to support widespread involvement of non-motor areas in the disease.
运动神经元病（MND）与显著的非运动症状相关，包括食欲减退。食欲减退已成为该疾病的一个主要特征，可能导致负能量平衡、疾病进展加快和过早死亡。我们研究了食欲减退的患病率和影响，并分析了MND患者（plwMND）视觉食物刺激与用餐状态和食欲的神经关联。对157名plwMND患者和120名非神经退行性对照者（NND对照）进行了人体测量、代谢、食欲和临床指标评估。其中，35名plwMND患者和23名NND对照者接受了进一步的功能磁共振成像评估，以观察禁食和餐后对视觉食物线索的反应。plwMND患者出现食欲减退（<0.001），食欲减退在plwMND患者中比NND对照者更普遍[比值比=2.59（95%置信区间：1.46 - 4.61）]。食欲减退与高代谢无关；然而，与脂肪量减少有关（<0.05）。成像评估显示，plwMND患者和NND对照者在观看非食物和食物图像时的反应没有总体差异。相比之下，我们发现与NND对照者相比，plwMND患者颞叶极区没有餐后反应，且相对于食欲，plwMND患者小脑活动减少。食欲减退而非高代谢导致了MND患者的负能量平衡。颞叶极区和小脑的改变可能导致一些plwMND患者食欲反应改变，而这些脑区在食欲控制中未被广泛考虑——这为支持该疾病中非运动区域广泛受累提供了额外证据。
