Gradual changes in steady-state levels of beta amyloid peptides (Aβ) in the brain are considered as initial step in the amyloid cascade hypothesis of Alzheimers disease (AD). Aβ is a product of the secretase cleavage of the amyloid precursor protein and there is evidence that the membrane lipid environment may modulate secretase activity and alters its function. Aβ disturbs membrane properties of artificial and isolated biological membranes and of plasma membranes in living cells. Aβ induced changes in membrane fluidity could be explained by physico-chemical interactions of the peptide with membrane components such as cholesterol, phospholipids and gangliosides. Thus, cell membranes may be the location where the neurotoxic cascade of Aβ is initiated. Perturbation of membranes, binding to lipids and alteration of cellular calcium signaling by Aβ have been reported by several studies and these topics are examined in this review.
Keywords: Amyloid, membrane, membrane fluidity, cholesterol, ganglioside, Alzheimer, calcium, pyrene, diphenylhexatriene
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