Brier Matthew R, Gordon Brian, Friedrichsen Karl, McCarthy John, Stern Ari, Christensen Jon, Owen Christopher, Aldea Patricia, Su Yi, Hassenstab Jason, Cairns Nigel J, Holtzman David M, Fagan Anne M, Morris John C, Benzinger Tammie L S, Ances Beau M
Department of Neurology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Department of Radiology, Washington University in St. Louis, St. Louis, MO 63110, USA. Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO 63110, USA.
Sci Transl Med. 2016 May 11;8(338):338ra66. doi: 10.1126/scitranslmed.aaf2362.
Alzheimer's disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form of neurofibrillary tangles, neuritic plaques, and neuropil threads. Until recently, only Aβ could be studied in humans using positron emission tomography (PET) imaging owing to a lack of tau PET imaging agents. Clinical pathological studies have linked tau pathology closely to the onset and progression of cognitive symptoms in patients with AD. We report PET imaging of tau and Aβ in a cohort of cognitively normal older adults and those with mild AD. Multivariate analyses identified unique disease-related stereotypical spatial patterns (topographies) for deposition of tau and Aβ. These PET imaging tau and Aβ topographies were spatially distinct but correlated with disease progression. Cerebrospinal fluid measures of tau, often used to stage preclinical AD, correlated with tau deposition in the temporal lobe. Tau deposition in the temporal lobe more closely tracked dementia status and was a better predictor of cognitive performance than Aβ deposition in any region of the brain. These data support models of AD where tau pathology closely tracks changes in brain function that are responsible for the onset of early symptoms in AD.
阿尔茨海默病(AD)具有两种分子病理学特征:以β淀粉样蛋白(Aβ)斑块形式存在的脑β淀粉样变性,以及以神经原纤维缠结、神经炎斑块和神经毡丝形式存在的tau蛋白病。直到最近,由于缺乏tau正电子发射断层扫描(PET)成像剂,只有Aβ能够在人体中通过PET成像进行研究。临床病理研究已将tau病理学与AD患者认知症状的发作和进展紧密联系起来。我们报告了一组认知正常的老年人和轻度AD患者的tau和Aβ的PET成像情况。多变量分析确定了tau和Aβ沉积的独特的与疾病相关的典型空间模式(地形图)。这些PET成像的tau和Aβ地形图在空间上是不同的,但与疾病进展相关。常用于临床前AD分期的脑脊液tau测量值与颞叶中的tau沉积相关。颞叶中的tau沉积更紧密地跟踪痴呆状态,并且比大脑任何区域的Aβ沉积更能预测认知表现。这些数据支持AD模型,其中tau病理学紧密跟踪导致AD早期症状发作的脑功能变化。