Interests in amyloid beta oligomers and their relevance to mechanisms for toxic amyloid beta species has accelerated with effects on neuronal apoptosis in Alzheimer’s disease. Unhealthy diets that accelerate amyloidogenic pathways may involve lipids such as palmitic acid and cholesterol that promote hydrophobic self association reactions with amyloid beta aggregation in the brain. These diets corrupt membrane amyloid beta homeostasis and determine neuron senescence and the aging process. Amyloid beta oligomers generated by cell membrane cholesterol and phospholipids interact with acute phase reactants that determine the benign or toxic amyloid beta conformational states. In yeast amyloid beta oligomers have different toxicities and are relevant to human amyloid beta oligomers in the brain. In mammalian cells the dynamic nature of the amyloid beta oligomer states may be altered by bacterial lipopolysaccharides that involve membrane amphiphilic and charge polarization. Lipopolysaccarides partition in cell membranes and its interaction with apolipoprotein E corrupts the peripheral amyloid beta metabolism with effects on toxic amyloid beta generation in the brain with relevance to neurodegeneration and Alzheimer’s disease. The role of atherogenic diets involve dysregulation of peripheral lipopolysaccharide metabolism with effects on apolipoprotein E/amyloid beta and albumin/amyloid beta interactions associated with increased lipopolysaccharides in brain cells that determine neuroinflammation with relevance to toxic amyloid beta behaviour and memory disorders.
|Number of pages||6|
|Journal||Austin Journal of Clinical Neurology|
|Publication status||Published - 29 Jun 2015|