Aggregation and accumulation of amyloid β and tau proteins to plaques and neurofibrillary tangles are the key pathogenic events in Alzheimer's disease. Here, we studied the capability of the cyclic d,l-α-peptide CP-2 as a conformational inhibitor of different amyloids to cross-interact with tau-derived AcPHF6 peptide and inhibit its aggregation, membrane perturbation and toxicity.
|Number of pages||4|
|State||Published - 8 Jun 2018|
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© 2018 The Royal Society of Chemistry.