摘要:The understanding
of cholesterol and its pathogenesis to Alzheimer’s disease (AD) pathogenic
process is important for the possible prevention of AD. High fibre diets that contain phytosterols have been shown to lower
LDL and increase HDL cholesterol and are implicated in membrane cholesterol and
amyloid beta (Aβ) homeostasis. The convergence of diet and AD may be related to
the effects of phytosterols since plasma cholesterol is closely linked and regulated
by phytosterols. Dietary fibre modifications that are low
in fat and glucose reduce the risk for AD by not only effecting cell membranes and nutrient sensing G coupled receptors but also by regulating number of nuclear receptors such as
histone deacetylases (HDAC) and peroxisome
proliferator activated receptors (PPAR) that control glucose, fatty
acids and cholesterol and have significant effects on the brain cholesterol
homeostasis and amyloidosis. The peripheral
sink Aβ hypothesis indicates that the
peripheral clearance of Aβ and its
regulation by dietary phytosterols
is of substantial interest since it may delay hypercholesterolemia and the
early onset of amyloid plaque development. Liver disease
has been of central importance with aging and programmed cell death pathways.
Nutritional therapy has emerged as a novel approach to control appetite and the
role of nutrigenomics as an early nutritional therapy may assist genes to delay liver and brain diseases such as Parkinson’s disease (PD) and Huntington’s
disease (HD) that are associated with aging. The understanding of phytosterols and the
role of these lipids in drug therapy such as cholesterol lowering drugs may
provide molecular mechanisms that are involved in the regulation of cell Aβ clearance and metabolism. High fibre
diets also contain various fatty acids such as the short chain fatty acids
(SCFA) and the understanding of synergistic effects of SCFA and phytosterols in
glucose regulation and cholesterol homeostasisis important to our understanding
of diet, lifestyle and drugs in relation to peripheral amyloidosis and gene
expression that play an early role
in the development of AD.