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Tremblay, J.C., Phivilay, C.A., Berthiaume, L., Emond, V., Julien, P. and Calon, F. (2010) High-Fat Diet Aggravates Amyloid-Beta and Tau Pathologies in the 3xTg-AD Mouse Model. Neurobiology of Aging, 9, 1516-1531.

has been cited by the following article:

• TITLE: LPS Regulates Apolipoprotein E and Aβ Interactionswith Effects on Acute Phase Proteins and Amyloidosis

  AUTHORS: Ian James Martins

  KEYWORDS: Lipopolysaccharides, Apolipoprotein E, Amyloid Beta, Acute Phase Protein, Diet

  JOURNAL NAME: Advances in Aging Research, Vol.4 No.2, March 27, 2015

  ABSTRACT: Interactions between apolipoprotein E (apo E) and amyloid beta (Aβ) are associated with the peripheral clearance of Aβ and are important to the development of neurodegenerative diseases. Interests in acute phase proteins (APP) as biomarkers for the early progression of Alzheimer’s disease indicate that the peripheral Aβ metabolism is perturbed and the role of nutritional diets are important to reduce APPs to maintain peripheral Aβ clearance with relevance to hepatic cholesterol homeostasis and brain amyloidosis. The role of nutriproteomic diets that reverse the effects of high fat diets are associated with the reduction in APPs, cholesterol homeostasis and improved clearance of Aβ. Nutritional diets that reduce the increase in plasma endotoxins (gut microbiotica) such as lipopolysaccarides (LPS) reduce the effects of LPS on cell membranes and increase the cellular uptake of Aβ by interactions with apo E. LPS alter hepatic lipid metabolism with an increase hepatic cytokines and APPs in plasma. Interactions between apo E and Aβ are altered by LPS with increased binding of LPS to apo E with effects on electrostatic alterations in Aβ oligomers. The role of LPS in neurodegenerative diseases includes the effects of LPS on alpha-synuclein metabolism with relevance to Parkinson’s disease and Alzheimer’s disease