Joseline M. Velazquez-Cintron and Zaira Mateo- Mayol, PhD

Pontifical Catholic University of Puerto Rico – Ponce Campus

Introduction: Melatonin is a hormone produced in the pineal gland, which acts as an antioxidant, promotes neuroprotection and preserves synaptic processes in cells. Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the prevalence of amyloid plaques that subsequently cause some of the symptoms. Most of the initial symptoms appear late in life coinciding with a decrease in melatonin concentration as human ages. It has been observed that melatonin has a reduced effect on β-amyloid and improves associative memory in patients suffering from AD. Thus, to test the hypothesis that melatonin decreases the accumulation of amyloid beta 1-42, Caenorhabditis elegans (C. elegans) CL2122 and CL2120 was used.

Methods: A fluorescence assay was used to measure if melatonin decreases β-amyloid expression in this model.  C. elegans was placed in a 25-degree incubator to activate the expression of the gene (CL2120).  Later 0.10 mM melatonin was added, and incubated for 48 hours in the plate. Subsequently, 10X photographs were taken under a fluorescence microscope and images were analyzed using NIH ImageJ software. To test whether melatonin at 0.10 mM improves associative memory, a chemotaxis assay was performed to understand the effect on short-term memory. The nematodes were acutely pre-exposed (2 hours) to 0.10 mM melatonin. We followed previous protocols combining Diacetyl (odorant) with E. coli OP50 (food) to create the association.

Results: Preliminary results showed a decrease in the percentage (%) of amyloid beta fluorescence when previously exposed to melatonin, demonstrating a p-value < 0.05. However,  results demonstrate the associative memory task to be non-significance with a p-value>0.05.

Conclusion: Finally, the results showed a decrease in beta-amyloid expression to 0.10mM of Melatonin but not in associative memory tasks.