Effect of aggregation states of Aβ42-Monomer and Fibril on the Dynamics of a Neuronal Model Membrane

Amyloid Aβ (1-42), Aβ42 is predominantly found in the form of plaques in the brain tissues in Alzheimer's disease. Studies have shown that Aβ42 plaques are mainly responsible for cognitive dysfunctionality in Alzheimer’s. Aβ42 exist in different aggregation states namely monomer (M), β-sheets, oligomer (O), or fibril (F). Studies have shown that the incorporation of amyloid, depending upon the amino acid length and aggregation states, can affect the phospholipid membrane distinctively. This can lead to structural and dynamic changes in the membrane and hence can affect membrane functions. Therefore, it is essential to investigate the effect of the aggregation states of Aβ42 on the dynamics and physiological relevant neuronal phospholipid membrane extracted from mammalian brain tissues on the picosecond time scale. This study can be useful to understand amyloid membrane interaction and add to our understanding of Alzheimer's disease. Here, we wish to investigate the effect of aggregation states of human Aβ42, a neurotoxic peptide, monomer (M) and fibril (F) on the dynamics of neuronal phospholipid membrane extracted from mammalian brain tissues