Amyloid protein fibril (null)

Amyloid protein fibril Overview

Amyloid protein fibrils are insoluble, β-sheet–rich aggregates formed by the misfolding and self-assembly of specific proteins, most notably amyloid β (Aβ), tau, and alpha-synuclein, within neural tissue[1][5]. These fibrils compose the characteristic plaques and tangles observed in neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease[5]. Fibrils form through a hierarchical aggregation pathway involving soluble oligomers and protofibrils that mature into highly stable, often neurotoxic fibrillar structures[3][5]. Amyloid fibril formation is central to disease progression, and therapeutic strategies target the inhibition, clearance, or disruption of these aggregates through monoclonal antibodies or small molecules[1][4]. The presence of amyloid fibrils can be detected using imaging or cerebrospinal fluid biomarkers, and several drugs (e.g., Aducanumab, Lecanemab) directly target amyloid deposits to alter disease progression[4].

Mechanism of Action

Monoclonal antibody-mediated amyloid removal, Inhibition of amyloid aggregation, Fibril capping, Disruption of β-sheet structure

Biological Functions

Safety Considerations

Interacting Drugs

Associated Biomarkers