Abstract
| Original language | English |
|---|---|
| Publication status | Published - 20 May 2016 |
| Event | 7th Annual World Congress of Neurotalk-2016 - Beijing, United States Duration: 20 May 2016 → 22 May 2016 |
Conference
| Conference | 7th Annual World Congress of Neurotalk-2016 |
|---|---|
| Country | United States |
| City | Beijing |
| Period | 20/05/16 → 22/05/16 |
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Unhealthy diets determine Benign or Toxic Amyloid Beta States and Promote Brain Amyloid Beta Aggregation. / Martins, Ian.
2016. Abstract from 7th Annual World Congress of Neurotalk-2016, Beijing, United States.Research output: Contribution to conference › Abstract
TY - CONF
T1 - Unhealthy diets determine Benign or Toxic Amyloid Beta States and Promote Brain Amyloid Beta Aggregation
AU - Martins, Ian
PY - 2016/5/20
Y1 - 2016/5/20
N2 - Interests in amyloid beta oligomers and their relevance to 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 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 amyloid beta states may be altered by bacterial lipopolysaccharides that involve membrane amphiphilic and charge polarization. Lipopolysaccharides partition in cell membranes and its interaction with apolipoprotein E corrupts 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 lipolysaccharides in brain cells that determine neuroinflammation with relevance to toxic amyloid beta behaviour and memory disorders.
AB - Interests in amyloid beta oligomers and their relevance to 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 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 amyloid beta states may be altered by bacterial lipopolysaccharides that involve membrane amphiphilic and charge polarization. Lipopolysaccharides partition in cell membranes and its interaction with apolipoprotein E corrupts 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 lipolysaccharides in brain cells that determine neuroinflammation with relevance to toxic amyloid beta behaviour and memory disorders.
M3 - Abstract
ER -