Patricio Chrem Mendez, Gabriela Cohen, Julieta Russo Maria, Marcos Fernandez Suarez, Federico Nahas, Griselda Russo, Claudio Wierszylo, Santiago Paz, Leonardo Tabaschi, Jorge Campos, Alejandra Amengual, Janus Kremer, Salvador Guinjoan, Ramon Leiguarda, Gustavo Sevlever, Silvia Vázquez, Ricardo Allegri
Ageing and Memory Center, Instituto de Investigaciones Neurologicas "Raúl Carrea" (FLENI), Buenos Aires, Argentina
Ageing and Memory Center, Instituto de Investigaciones Neurologicas "Raúl Carrea" (FLENI), Buenos Aires, Argentina.
Am J Alzheimers Dis Other Demen. 2015 Sep;30(6):599-606. doi: 10.1177/1533317515576387. Epub 2015 Mar 26.
Today, ligands that bind to fibrillar β-amyloid are detectable by Positron Emission Tomography (PET) allowing for in vivo visualization for Abeta burden. However, amyloid plaques detection per se does not establish Alzheimer's Disease diagnosis. In this sense, the utility of amyloid imaging to improve clinical diagnosis was settled only for specific clinical scenarios and few studies have assessed amyloid molecular neuroimaging in a broader clinical setting. The aim of this study is to determine the frequency of PiB amyloid findings in different diagnostic syndromes grouped into high and low probability pre- test categories, taking into account pre-test clinical assumption of the presence of AD related pathology.
144 patients were assigned into categories of high or low pretest probability according to clinical suspicion of AD pathology. The high probability group included: amnestic Mild Cognitive Impairment (MCI), amnestic and other domains MCI, Dementia of Alzheimer's Type (DAT), Posterior Cortical Atrophy (PCA), logopenic Primary Progressive Aphasia (PPA), Cerebral Amyloid Angiopathy and mixed dementia. The low assumption group included: normal controls, non-amnestic MCI, non-logopenic PPA and Frontotemporal Dementia (FTD).
Only normal controls and DAT patients (typical and atypical presentation) were the most consistent across clinical and molecular diagnostics. MCI, non-logopenic PPA and FTD were the syndromic diagnoses that most discrepancies were found.
This study demonstrates that detecting in vivo amyloid plaques by molecular imaging is considerably frequent in most of the dementia syndromes and shows that there are frequent discordance between molecular diagnosis and clinical assumption.
如今,正电子发射断层扫描(PET)可检测出与纤维状β淀粉样蛋白结合的配体,从而实现对体内β淀粉样蛋白负荷的可视化。然而,淀粉样斑块的检测本身并不能确诊阿尔茨海默病。从这个意义上讲,淀粉样蛋白成像在改善临床诊断方面的效用仅在特定临床场景中得到确立,很少有研究在更广泛的临床环境中评估淀粉样蛋白分子神经成像。本研究的目的是确定在分为高概率和低概率预测试类别的不同诊断综合征中,匹兹堡化合物B(PiB)淀粉样蛋白发现的频率,同时考虑到AD相关病理学存在的预测试临床假设。
根据对AD病理学的临床怀疑,将144名患者分为预测试高概率或低概率类别。高概率组包括:遗忘型轻度认知障碍(MCI)、遗忘型和其他领域MCI、阿尔茨海默病型痴呆(DAT)、后皮质萎缩(PCA)、非流利性原发性进行性失语(PPA)、脑淀粉样血管病和混合性痴呆。低假设组包括:正常对照、非遗忘型MCI、非非流利性PPA和额颞叶痴呆(FTD)。
只有正常对照和DAT患者(典型和非典型表现)在临床和分子诊断中最为一致。MCI、非非流利性PPA和FTD是发现差异最大的综合征诊断。
本研究表明,在大多数痴呆综合征中,通过分子成像检测体内淀粉样斑块相当常见,并且表明分子诊断与临床假设之间经常存在不一致。