Ulrich J, Anderton B H, Brion J P, Euler M, Probst A
Department of Pathology, University of Basel, Switzerland.
J Neural Transm Suppl. 1987;24:197-204.
The first half of this paper is devoted to a review on the cytoskeletal immunocytochemistry of the various morphological changes in Alzheimer's disease (AD), i.e. neurofibrillary tangles (NFT), senile plaques (SP), granulovacuolar degeneration (GV) and Hirano bodies (HB). In the second half it is demonstrated that sera raised against the paired helical filaments (PHF) in NFT, and monoclonal antibodies to phosphorylated epitopes on neurofilament proteins, also stain structures within neuronal perikarya without PHFs in some diseases. These include Pick bodies and swollen cells in Pick's disease, neurons in old dogs without NFTs, and occasional neurons without NFT in AD. We conclude that PHF constituent proteins can be accumulated in neuronal perikarya of cases with these diseases without being actually assembled to PHFs. In AD and in the old dogs, such accumulations occurring without the formation of PHFs might represent a precursor state of the latter.
本文前半部分致力于综述阿尔茨海默病(AD)中各种形态学变化的细胞骨架免疫细胞化学,即神经原纤维缠结(NFT)、老年斑(SP)、颗粒空泡变性(GV)和平野小体(HB)。后半部分表明,针对NFT中双螺旋丝(PHF)产生的血清以及针对神经丝蛋白上磷酸化表位的单克隆抗体,在某些疾病中也能对神经元胞体中不存在PHF的结构进行染色。这些疾病包括匹克病中的匹克小体和肿胀细胞、无NFT的老龄犬神经元以及AD中偶尔出现的无NFT神经元。我们得出结论,PHF组成蛋白可在这些疾病的病例的神经元胞体中积累,而实际上并未组装成PHF。在AD和老龄犬中,这种未形成PHF的积累可能代表了PHF的前体状态。