In this study, the effects of dopamine, D-DOPA, and L-DOPA were analyzed in the extent of inhibition of amyloid β-42 (Aβ42) aggregation, a peptide prone to aggregation that is thought to be the major contributing factor in Alzheimer’s disease (AD). The goal of this research was to determine if these catecholamine compounds reduce the extent aggregation of Aβ42 through interaction with aggregated fibrils, providing a possible curative mechanism for AD. Fluorescence correlation spectroscopy was used to measure the degree of aggregation by determining diffusion coefficients and size of aggregates of Aβ42 with and without dopamine, D-DOPA, and L-DOPA. This was performed using a nitrogen laser setup designed to measure random fluctuations of fluorescence, with reactions containing Aβ42 peptide, thioflavin T (a fluorescent dye used to measure the extent of aggregation), and catecholamine compounds at varying concentrations. Using autocorrelation analysis, the size and relative diffusions of Aβ42 aggregates were determined, giving an indication of how effective each small molecule was at inhibiting aggregation of Aβ42. Autocorrelation analysis relates random fluctuations in fluorescence to autocorrelation functions, which determine correlation between lag times of fluctuations and give information relating to size and diffusion of an aggregate. By determining these parameters, dopamine, D-DOPA, and L-DOPA may be classified as effective molecules of reducing aggregation of Aβ42, providing evidence to support a possible curative or preventative mechanism for Alzheimer’s disease.

Catecholamine compounds as inhibitors of amyloid β-42 aggregation in Alzheimer's disease

255th National Meeting (2018)

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