Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
VA Connecticut Healthcare System, West Haven, CT, USA.
J Alzheimers Dis. 2022;90(4):1615-1628. doi: 10.3233/JAD-220708.
Earlier studies have described the neural markers of apathy in Alzheimer's disease (AD) and mild cognitive impairment (MCI), but few focused on the motivation circuits. Here, we targeted hypothalamus, a hub of the motivation circuit.
To examine hypothalamic resting state functional connectivity (rsFC) in relation to apathy.
We performed whole-brain regression of hypothalamic rsFC against Apathy Evaluation Scale (AES) total score and behavioral, cognitive, and emotional subscores in 29 patients with AD/MCI and 28 healthy controls (HC), controlling for age, sex, education, cognitive status, and depression. We evaluated the results at a corrected threshold and employed path analyses to assess possible interaction between hypothalamic rsFCs, apathy and depression/memory. Finally, we re-examined the findings in a subsample of amyloid-β-verified AD.
AES total score correlated negatively with hypothalamic precuneus (PCu)/posterior cingulate cortex (PCC) and positively with left middle temporal gyrus (MTG) and supramarginal gyrus rsFCs. Behavioral subscore correlated negatively with hypothalamic PCu/PCC and positively with middle frontal gyrus rsFC. Cognitive subscore correlated positively with hypothalamic MTG rsFC. Emotional subscore correlated negatively with hypothalamic calcarine cortex rsFC. In path analyses, hypothalamic-PCu/PCC rsFC negatively modulated apathy and, in turn, depression. The model where hypothalamic MTG rsFC and memory independently modulated apathy also showed a good fit. The findings of diminished hypothalamic-PCu/PCC rsFC in relation to apathy and, in turn, depression were confirmed in amyloid-verified AD.
The findings together support a role of altered hypothalamic connectivity in relation to apathy and depression, and modulation of apathy by memory dysfunction.
早期的研究已经描述了阿尔茨海默病(AD)和轻度认知障碍(MCI)患者的冷漠的神经标志物,但很少关注动机回路。在这里,我们以下丘脑为目标,这是动机回路的一个枢纽。
研究下丘脑静息状态功能连接(rsFC)与冷漠的关系。
我们对 29 名 AD/MCI 患者和 28 名健康对照者(HC)的下丘脑 rsFC 与冷漠评价量表(AES)总分以及行为、认知和情感子评分进行了全脑回归,同时控制年龄、性别、教育程度、认知状态和抑郁情况。我们在修正阈值下评估结果,并采用路径分析来评估下丘脑 rsFC、冷漠和抑郁/记忆之间可能的相互作用。最后,我们在一个经过验证的淀粉样蛋白-β的 AD 亚样本中重新检查了这些发现。
AES 总分与下丘脑楔前叶(PCu)/后扣带回(PCC)呈负相关,与左侧颞中回(MTG)和缘上回 rsFC 呈正相关。行为子评分与下丘脑 PCu/PCC 呈负相关,与额中回 rsFC 呈正相关。认知子评分与下丘脑 MTG rsFC 呈正相关。情感子评分与下丘脑楔状回 rsFC 呈负相关。在路径分析中,下丘脑 PCu/PCC rsFC 负调节冷漠,进而调节抑郁。下丘脑 MTG rsFC 和记忆独立调节冷漠的模型也表现出较好的拟合。在经淀粉样蛋白验证的 AD 中,与冷漠相关的下丘脑 PCu/PCC rsFC 减少,以及与冷漠相关的抑郁,这些发现得到了证实。
这些发现共同支持了改变的下丘脑连接与冷漠和抑郁有关,以及记忆功能障碍对冷漠的调节作用。