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- W149471864 abstract "In the past few years it has become increasingly clear that the neuronal microtubular system is involved in the pathogenesis of Alzheimer neurofibrillary tangles (NFT). Electron microscopists were among the first to observe the relative paucity of microtubules in NFT-containing neurons. The microtubular system was later implicated immunochemically, based on an antiserum that cross-reacted with NFT and microtubules.1 In 1980 Eng et al.2 demonstrated that the cross-reactive element between microtubules and NFT was not the tubulin, which is the most abundant component of microtubules, because antibodies to tubulin did not cross-react with NFT. Attention turned to the microtubule-associated proteins (MAPs) which are a class of proteins that cycle with microtubules through temperature-dependent phases of polymerization/depolymerization and are morphologically associated with the microtubule system. One of the possible functions of the MAPs is to stabilize the microtubules against depolymerization3 and modulate their dynamic instability.4 Relative to other tissues the brain contains an abundance of microtubules and appears to have evolved its own system of MAPs. Brain MAPs have been divided into a high molecular weight group and a heterogeneous protein of 55–62 kDa designated tau. As seen on SDS-PAGE the high molecular weight group consists of a complex series of bands designated MAP15 and a doublet of approximately 280 kDa designated MAP2. Additional MAPs with unique tissue distributions and developmental chronologies have been described as well as “light chains” and kinases that bear a close association with those MAPs mentioned above.6 Of the various MAPs in brain, MAP2 is the most abundant." @default.
- W149471864 created "2016-06-24" @default.
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- W149471864 date "1987-01-01" @default.
- W149471864 modified "2023-10-14" @default.
- W149471864 title "Cloning of Neurofibrillary Tangle-Related Genes" @default.
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- W149471864 doi "https://doi.org/10.1007/978-1-4613-1657-2_4" @default.
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