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• W2057404854 abstract "The mechanism how neurofibrillary tangles (NFTs) and senile plaques (SPs) are formed in Alzheimer's disease (AD) brain is not clear. The human lysosomal protein transmembrane 4 beta is a novel hepatocellular carcinoma-associated gene. LAPTM4B is a type III transmembrane protein with four putative transmembrane regions. The isoform LAPTM4B- 24 misses 91 amino acids in the N-terminal than the isoform LAPTM4B-35, the longer isoform inhibits cell apoptosis, promotes cell proliferation, migration and invasion, while the shorter isoform inhibits cell survival or growth. LAPTM4B is mainly localized on plasma membrane and membranous organelles including endosomes and lysosomes, which has recently been proposed as candidate subcellular sites for AD pathogenesis. Meanwhile, LAPTM4B-35 activates PI3K-AKT signaling pathway through interaction of proline-rich motif in the N- terminus of LAPTM4B-35 with the p85a regulatory subunit of PI3K. PI3K-AKT signaling pathway plays an important role in AD pathologies Methods: The polyclonal antibody (pAb) Nl- 99 LAPTM4B that specifically recognizes LAPTM4B-35, pAb EC2 to LAPTM4B that recognizes both LAPTM4B-35 and LAPTM4B-24 isoforms were used to immunostain paraffin- embedded sections of post-mortem human brains. Results: We observed a dramatically reduced intensity and number of neurons positive for both Nl-99 and EC2 in the CA1 and CA4 of the hippocampus, as well as in the pyramidal neurons of the layers III and V in the temporal cortex in 6 AD as compared to 6 control cases. Using antibodies to phospho-tau (PHF-1 and pAb S422) as markers to NFTs, our double immunostaining data revealed that most normal looking neurons show a stronger immunoreactivity of LAPTM4B than tangle bearing neurons labeled by PHF-1 or pS422. The immunostainings of Nl-99 and EC2 are relatively weaker in most tangle bearing neurons including those with a few intra-neuronal punctuates positive for PHF-1 and pS422, some neurons showed the co-existence of moderate immunoreactivies of Nl-99 /EC2 and that of PHF-1 and pS422. The dystrophic neurites positive for N1-99/EC2 were also observed in SPs. Conclusions: Our data suggested that LAPTM4B might play an important role in the pathogenesis of AD pathologies." @default.
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• W2057404854 date "2011-07-01" @default.
• W2057404854 modified "2023-10-16" @default.
• W2057404854 title "P3-131: Relationship of tumor-promoting factors LAPTM4B and alzheimer's disease pathologies" @default.
• W2057404854 doi "https://doi.org/10.1016/j.jalz.2011.05.2446" @default.
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