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• W2101622526 abstract "BRI2 mutations are responsible of familial British and Danish dementias (FBD and FDD) causing amyloid deposits and neurofibrillary tangles similar to those observed in Alzheimer's disease (AD). BRI2 binds APP downregulating the production of amyloid- β. We previously observed increased levels of BRI2 and deposition of a 50kDa wild-type BRI2 form in sporadic AD human hippocampus compared to controls suggesting involvement of BRI2 in AD pathology. Here, we further analyzed in which stage of the disease BRI2 is increased as well as the possible causes of BRI2 accumulation by analyzing the levels of furin, ADAM10 and SPPL2b, the enzymes involved in BRI2 processing. Additionally, we investigated whether BRI2-APP binding is preserved in human AD hippocampus. Post-mortem human hippocampus homogenates from AD patients (n = 14) and controls (n=14) were analyzed by western blot. Polyclonal and monoclonal antibodies against a BRI2 140–153 were produced by Biogenes (Germany) and their specificity has been fully characterized. Anti-FurinB6 (Santa Cruz), anti-ADAM10 ab1997 (Abcam), anti-SPPL2b (Aviva System Biology), anti-APP-22C11 (Millipore) were used. Immunopurification was performed using anti- BRI2 140–153 and anti-BRI2 113–231 (Dr. J. Presto). BRI2 was increased in early pathological stages (Braak-III; Thal-2/3)of AD. While the levels of furin and ADAM10 were decreased in AD human hippocampus, the levels of SPPL2b were increased up to 10-times in AD patients compare to controls. The data revealed a correlation between the levels of ADAM10 with the levels both furin (r=0.67,p<0.0001) and BRI2 (r=0.42,p =0.02). BRI2-APP complexes were observed in the hippocampus homogenates from control cases (n=4) but not in AD patients (n=4). Our data show that BRI2 is increased in early stages of AD, supporting the potential involvement of BRI2 in AD pathology development. The observed inverse correlation between ADAM10 and BRI2 suggest that reduced ADAM10 levels and activity determines BRI2 increased. Processing by ADAM10 leads to the release of the BRI2 ectodomain and may thus promote the observed BRI2 deposition in plaques. Deposition of BRI2 may be the cause of the lack of BRI2-APP complexes in AD. These results strongly suggest that human BRI2 is a relevant player in the early steps of the amyloid cascade and thus, on AD etiology." @default.
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• W2101622526 date "2013-07-01" @default.
• W2101622526 modified "2023-09-27" @default.
• W2101622526 title "P3-066: The increase of BRI2 in early stages of Alzheimer's disease correlates with reduced levels of ADAM10 and may prevent its binding to APP" @default.
• W2101622526 doi "https://doi.org/10.1016/j.jalz.2013.05.1136" @default.
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