Abstract
Alzheimer's disease is characterized by inflammatory proteinaceous deposits comprised principally of the protein amyloid-beta (Aβ). Presently, the origins of cerebral amyloid deposits are controversial, though pivotal for the prevention of Alzheimer's disease. Recent evidence suggests that in blood, Aβ may serve as a regulating apoprotein of the triglyceride-rich-lipoproteins and we have found that the synthesis of Aβ in enterocytes and thereafter secretion as part of the chylomicron cascade is regulated by dietary fats. It is our contention that chronically elevated plasma levels of Aβ in response to diets rich in saturated fats may lead to disturbances within the cerebrovasculature and exaggerated blood-to-brain delivery of circulating Aβ, thereby exacerbating amyloidosis. Consistent with this hypothesis we show that enterocytic Aβ is increased concomitant with apolipoprotein B48. Furthermore, cerebral extravasation of immunoglobulin G, a surrogate marker of plasma proteins is observed in a murine model of Alzheimer's disease maintained on a saturated-fat diet and there is diminished expression of occludin within the cerebrovasculature, an endothelial tight junction protein.
Published Version
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