Division of Applied Health Sciences, School of Medicine and Dentistry, Institute of Medical Sciences, University of Aberdeen, Liberty Building, Foresterhill Road, Aberdeen AB25 2ZP, Scotland, UK.
Neuroimaging Clin N Am. 2012 Feb;22(1):11-22, vii. doi: 10.1016/j.nic.2011.11.003.
Neurofibrillary pathology in Alzheimer's disease consists of paired helical filaments comprising tau protein. This pathology is correlated with dementia, but can appear in the first two decades of life. Extracellular amyloid β-protein arises through proteolytic processing of a transmembrane precursor, which involves the action of several enzymes. Mutations in the genes for the precursor and presenilin proteins accelerate the deposition of Aβ. Tau mutations cause other tauopathies in the absence of amyloid deposition, indicating that amyloid deposition is not a prerequisite for dementia. An improved understanding of Alzheimer's disease awaits to be obtained by molecular imaging of these pathologies.
阿尔茨海默病的神经纤维缠结病理由包含 tau 蛋白的双螺旋丝组成。这种病理与痴呆有关，但也可能在生命的头二十年出现。细胞外淀粉样 β-蛋白通过跨膜前体的蛋白水解加工产生，其中涉及几种酶的作用。前体和早老素蛋白基因的突变会加速 Aβ的沉积。tau 突变导致在没有淀粉样沉积的情况下出现其他 tau 病，这表明淀粉样沉积不是痴呆的先决条件。通过对这些病理的分子成像，可以进一步了解阿尔茨海默病。
