Impaired hepatic amyloid-beta degradation in Alzheimer’s disease

• Published in: PloS one Vol. 13; no. 9; p. e0203659
• Main Authors: Maarouf, Chera L., Walker, Jessica E., Sue, Lucia I., Dugger, Brittany N., Beach, Thomas G., Serrano, Geidy E.
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 07.09.2018; Public Library of Science (PLoS)
• Subjects: Aged, 80 and over; Aging; Alzheimer Disease - metabolism; Alzheimer's disease; Amyloid beta-Peptides - chemistry; Amyloid beta-Peptides - metabolism; Amyloid beta-protein; Apolipoprotein E; Biology and Life Sciences; Blood & organ donations; Blood levels; Brain; Brain research; Cathepsin D; Degradation; Dementia; Development and progression; Down syndrome; Enzymes; Female; Fluorescein; Gene expression; Genetic aspects; Genotypes; Humans; Insulin; Insulysin; Liver; Liver - metabolism; Male; Medical research; Medicine and Health Sciences; Neprilysin; Neuropathology; Pathogenesis; Pathology; Peptides; Physiological aspects; Protein Aggregates; Proteins; Proteolysis; Research and Analysis Methods; Studies; Sucrose; Working groups; United States; United States > US; Arizona

Extensive research strongly suggests that amyloid beta (Aβ) aggregates in the brain have a central role in Alzheimer's disease (AD) pathogenesis. Pathological Aβ deposition is likely due to an altered balance between overproduction and elimination. Rodent studies have suggested that the liver h...