Evaluating amyloid-beta aggregation and toxicity in transgenic Caenorhabditis elegans models of Alzheimer's disease

Alzheimer's disease (AD) is the leading cause of dementia in the elderly, clinically characterized by memory loss, cognitive decline, and behavioral disturbances. Its pathogenesis is not fully comprehended but involves intracellular depositions of amyloid beta peptide (Aβ) and neurofibrillary tangles of hyperphosphorylated tau. Currently, pharmacological interventions solely slow the progression of symptoms. Caenorhabditis elegans (C. elegans) is a simple and valuable organism to study the dynamics of Aβ. It may contribute to advancing our comprehension of AD development and progression, as well as to discovering new treatments. Herein, we describe usual protocols for evaluating Aβ aggregation and toxicity in transgenic C. elegans models of AD (CL2006, CL4176, GMC101, and CL2355 strains) through the visualization and quantification of the peptide with specific fluorescent dyes, in addition to the analysis of particular behaviors (paralysis and chemotaxis associated with learning).