The protein leaks out of the liver and causes neurodegeneration. 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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