> This study provides, for the first time, direct evidence that hepatic expression of genes leading to the synthesis of human-Aβ is causally associated with cor

> This study provides, for the first time, direct evidence that hepatic expression of genes leading to the synthesis of human-Aβ is causally associated with corruption of the NVU, with cell death and brain atrophy realised. [...] Consistent with the hypothesis of increased neurovascular insult as a consequence of hepatic synthesis of TRL-Aβ, PET findings clearly demonstrated an age-associated increase in [Pittsburgh compound] uptake. We suggest that this was indicative of the marked abundance of amyloid-rich lipofuscin aggregates distributed within brain parenchyma and within vessel lumen. They definitely seem to lean into the neurovascular damage angle. I.e. liver produces amyloid-beta complexes, high levels of which result in neurovascular damage, resulting in lipids making it through and accreting in the brain. Which makes sense, as if your capillaries are less functional, how would you body clear plaques from a difficult to reach organ (the brain)?