![]() ![]() The researchers noticed amyloid beta was found in lipoprotein complexes (fat+protein), then experimentally modified the liver to produce it. We knew amyloid beta was highly associated with Alzheimer's. This study provides causal evidence of a lipoprotein-Aß /capillary axis for onset and progression of a neurodegenerative process. Transmission electron microscopy shows marked neurovascular disruption in HSHA mice. Moreover, the HSHA mice showed impaired performance in the passive avoidance test, suggesting impairment in hippocampal-dependent learning. In this study, we report that genetic modification of C57BL/6J mice engineered to synthesise human Aß only in liver (hepatocyte-specific human amyloid (HSHA) strain) has marked neurodegeneration concomitant with capillary dysfunction, parenchymal extravasation of lipoprotein-Aß, and neurovascular inflammation. ![]() ![]() In blood, greater than 90% of Aß is complexed as an apolipoprotein, raising the possibility of a lipoprotein-mediated axis for AD risk. > Several lines of study suggest that peripheral metabolism of amyloid beta (Aß) is associated with risk for Alzheimer disease (AD). The paper: Synthesis of human amyloid restricted to liver results in an Alzheimer disease–like neurodegenerative phenotype It's a very plausible mechanism that worked end-to-end and seems to fit all of the observational evidence we've gathered. This setup was shown to trigger the disease. Now they've found a way to trigger the disease by generating amyloid in the liver and shown that it can reach the brain (by crossing the blood brain barrier). (Reposting again since it wasn't noticed ~1.5 months ago.)Īmyloid beta has long been implicated in Alzheimer's. ![]()
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