Posterior Accumulation of Tau and Concordant Hypometabolism in an Early-Onset Alzheimer's Disease Patient with Presenilin-1 Mutation
Posterior Accumulation of Tau and Concordant Hypometabolism in an Early-Onset Alzheimer's Disease Patient with Presenilin-1 Mutation
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DOI：
10.3233/jad-151004
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发表时间：
2016-01-01
影响因子：
4
通讯作者：
Hansson, Oskar
中科院分区：
文献类型：
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作者：
Smith, Ruben;Wibom, Moa;Hansson, Oskar
目前尚不清楚tau病理学的分布是否在早发性家族性阿尔茨海默病（AD）和散发性AD病例之间存在差异。我们目前的正电子发射断层扫描（PET）数据从一个年轻的患者早老素-1突变（Thr 116 Asn）。F-18-flutemetalanine PET显示淀粉样蛋白-β原纤维的分布类似于散发性AD。然而，使用F-18-AV 1451 PET揭示的tau病理学模式显示，与晚发型散发性AD相比，后扣带回、楔前叶、顶叶和枕叶皮质中的摄取更高。此外，tau病理学而非淀粉样蛋白病理学表现出与F-18-氟脱氧葡萄糖代谢非常明显的反比关系，表明受tau聚集体影响的区域中的神经元代谢减退。
It is unclear whether the distribution of tau pathology differs between cases with early-onset familial Alzheimer's disease (AD) and sporadic AD. We present positron emission tomography (PET) data from a young patient with a presenilin-1 mutation (Thr116Asn). F-18-flutemetamol PET showed a distribution of amyloid-beta fibrils similar to sporadic AD. However, the pattern of tau pathology, revealed using F-18-AV1451 PET, showed higher uptake in posterior cingulate, precuneus, parietal and occipital cortices compared to late-onset sporadic AD. Further, the tau pathology, but not amyloid pathology, exhibited a very clear inverse relationship with F-18-fluorodeoxyglucose-metabolism, indicating neuronal hypometabolism in regions affected by tau aggregates.