The interactions of amyloid β aggregates with phospholipid membranes and the implications for neurodegeneration

Misfolding, aggregation and accumulation of Amyloid-0 peptides (A0) in neuronal tissue and extracellular matrix are hallmark features of Alzheimer's disease (AD) pathology. Soluble A0 oligomers are involved in neuronal toxicity by interacting with the lipid membrane, compromising its integrity, and affecting the function of receptors. These facts indicate that the interaction between A0 oligomers and cell membranes may be one of the central molecular level factors responsible for the onset of neurodegeneration. The present review provides a structural understanding of A0 neurotoxicity via membrane interactions and contributes to understanding early events in Alzheimer's disease.

Automated summary

Misfolding, aggregation, and accumulation of Amyloid-0 peptides (A0) in neuronal tissue and extracellular matrix are key pathological features of Alzheimer's disease (AD). The interaction between soluble A0 oligomers and cell membranes leads to neuronal toxicity by compromising the integrity of the lipid membrane and affecting receptor function. Understanding A0 neurotoxicity through membrane interactions contributes to unraveling early events in AD.