Pomara Nunzio, Bruno Davide, Osorio Ricardo S, Reichert Chelsea, Nierenberg Jay, Sarreal Antero S, Hernando Raymundo T, Marmar Charles R, Wisniewski Thomas, Zetterberg Henrik, Blennow Kaj
aGeriatric Psychiatry Division, Nathan S. Kline Institute, Orangeburg Departments of bPsychiatry cSteve and Alexandra Cohen Veterans Center dNeurology, Pathology and Psychiatry eCenter for Brain Health, NYU Langone Medical Center fProgram in Behavioral and Cognitive Neuroscience, The Graduate Center of the City University of New York, New York City, New York, USA gSchool of Natural Sciences and Psychology, Liverpool John Moores University, Liverpool hDepartment of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK iClinical Neurochemistry Laboratory, Sahlgrenska University Hospital jDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Neuroreport. 2016 Sep 28;27(14):1068-71. doi: 10.1097/WNR.0000000000000658.
Depression has been linked to Alzheimer's disease as either an increased risk factor for its development or as a prodromal symptom. The neurobiological basis for such an association, however, remains poorly understood. Numerous studies have examined whether changes in amyloid beta (Aβ) metabolism, which are implicated in the pathogenesis of Alzheimer's disease, are also found in depression. In this paper, we investigated the relationship between depressive symptoms and cerebrospinal fluid (CSF) Aβ indices in otherwise healthy, cognitively normal elderly with late-life major depression (LLMD) and controls using a longitudinal approach, which is a novel contribution toward the literature. Significantly lower levels of CSF Aβ42 were observed in the LLMD group at baseline and were associated with more severe depressive symptoms. During longitudinal follow-up, the depressed group remained cognitively unchanged, but was significantly less depressed than at baseline. A greater improvement in depressive symptoms was associated with increases in CSF Aβ42 levels in both groups. Increases in CSF Aβ42 and Aβ40 were also associated with increased CSF total-tau levels. Our results suggest that LLMD may be associated with state-dependent effects of CSF Aβ42 levels. Future studies should determine whether the association reflects state-dependent changes in neuronal activity and/or brain amyloid burden in depression.
抑郁症已被认为与阿尔茨海默病有关，要么是其发病的风险增加因素，要么是前驱症状。然而，这种关联的神经生物学基础仍知之甚少。许多研究探讨了在抑郁症中是否也存在与阿尔茨海默病发病机制相关的β淀粉样蛋白（Aβ）代谢变化。在本文中，我们采用纵向研究方法，对患有老年期重度抑郁症（LLMD）的健康、认知正常的老年人及对照组的抑郁症状与脑脊液（CSF）Aβ指标之间的关系进行了研究，这是对该领域文献的一项新贡献。在基线时，LLMD组的脑脊液Aβ42水平显著降低，且与更严重的抑郁症状相关。在纵向随访期间，抑郁组认知状态未发生变化，但抑郁程度明显低于基线水平。两组中抑郁症状的更大改善与脑脊液Aβ42水平的升高有关。脑脊液Aβ42和Aβ40的升高也与脑脊液总tau蛋白水平的升高有关。我们的结果表明，LLMD可能与脑脊液Aβ42水平的状态依赖性效应有关。未来的研究应确定这种关联是否反映了抑郁症中神经元活动和/或脑淀粉样蛋白负荷的状态依赖性变化。
