Identifying the Role of PTL-1 in C. elegans Learning and Memory

Abstract

Alzheimer’s disease (AD) and other neurodegenerative diseases impact a great portion of the United States’ population, and deaths due to AD have only grown in recent years. Despite this dire need, there is currently no cure or efficacious treatment for these disorders. Animal models of neurodegenerative diseases are invaluable to researchers, providing a way to study how these diseases occur and what drugs and therapies may help cure them. Caenorhabditis elegans is frequently used to study learning and memory with age, as its neurobiology is extremely well-studied. Despite this, little is known about protein with tau-like repeats (PTL-1), a C. elegans protein which is similar in structure and in vivo function to mammalian tau protein. Tau is implicated in AD and related neurodegenerative diseases known as tauopathies; many have argued that pathology involving tau protein is the cause of AD. Since PTL-1 has many similarities to tau, it would be useful to understand its role in learning and memory for C. elegans. Such understanding would allow researchers to create better C. elegans models for Alzheimer’s disease and provide more information on what might cause neurodegenerative disease. In this study, we use a PTL-1 knockout strain to perform short- and long-term associative memory assays as C. elegans age, and find no significant difference between this knockout strain and wild-type worms, except at day 6 of adulthood, where the knockout memory declines more slowly than wild-type worms. Ultimately, we conclude that further study is needed, but that our work is a tentative argument for aggregated tau causing cognitive decline.