Neuropathologic Correlates of Psychiatric Symptoms in Alzheimer's Disease.
Neuropathologic Correlates of Psychiatric Symptoms in Alzheimer's Disease.
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DOI：
10.3233/jad-180688
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发表时间：
2018
期刊：
影响因子：
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通讯作者：
Grinberg LT
中科院分区：
文献类型：
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作者：
Ehrenberg AJ;Suemoto CK;França Resende EP;Petersen C;Leite REP;Rodriguez RD;Ferretti-Rebustini REL;You M;Oh J;Nitrini R;Pasqualucci CA;Jacob-Filho W;Kramer JH;Gatchel JR;Grinberg LT
阐明神经精神症状和阿尔茨海默病（AD）相关病理之间的关系可能为有效治疗开辟道路。在这里，我们调查了神经系统缠结和淀粉样蛋白-β病理学负担增加时发生神经精神症状的几率。2004年至2014年期间去世的参与者在圣保罗大学医学院衰老研究生物库进行了全面的神经病理学评估。与可靠的线人进行死后访谈，以收集有关神经精神和认知状态的信息。在收集的1，092例病例中，排除了任何非阿尔茨海默病病理学，使队列达到455例。Braak分期用于评估神经系统缠结负荷，CERAD神经病理学评分用于评估淀粉样蛋白-β负荷。采用12项神经精神症状量表评估神经精神症状，采用CDR-Risk评分评估痴呆状态。在Braak I/II中，与对照组相比，检测到激越、焦虑、食欲变化、抑郁和睡眠障碍的几率显著增加。在Braak III/IV期，躁动的可能性继续增加。Braak V/VI与较高的妄想几率相关。没有发现神经精神症状的几率增加与淀粉样蛋白-β病理学相关。神经精神症状的几率增加与早期神经系统缠结病理学相关，表明皮质下神经系统缠结积聚伴最小皮质病理学足以影响生活质量，神经精神症状是AD生物学过程的表现。
Clarifying the relationships between neuropsychiatric symptoms and Alzheimer’s disease (AD)-related pathology may open avenues for effective treatments. Here, we investigate the odds of developing neuropsychiatric symptoms across increasing burdens of neurofibrillary tangle and amyloid-β pathology. Participants who passed away between 2004 and 2014 underwent comprehensive neuropathologic evaluation at the Biobank for Aging Studies from the Faculty of Medicine at the University of São Paulo. Postmortem interviews with reliable informants were used to collect information regarding neuropsychiatric and cognitive status. Of 1,092 cases collected, those with any non-Alzheimer pathology were excluded, bringing the cohort to 455 cases. Braak staging was used to evaluate neurofibrillary tangle burden, and the CERAD neuropathology score was used to evaluate amyloid-β burden. The 12-item neuropsychiatric inventory was used to evaluate neuropsychiatric symptoms and CDR-SOB score was used to evaluate dementia status. In Braak I/II, significantly increased odds were detected for agitation, anxiety, appetite changes, depression, and sleep disturbances, compared to controls. Increased odds of agitation continue into Braak III/IV. Braak V/VI is associated with higher odds for delusions. No increased odds for neuropsychiatric symptoms were found to correlate with amyloid-β pathology. Increased odds of neuropsychiatric symptoms are associated with early neurofibrillary tangle pathology, suggesting that subcortical neurofibrillary tangle accumulation with minimal cortical pathology is sufficient to impact quality of life and that neuropsychiatric symptoms are a manifestation of AD biological processes.