BDNF and TRiC-inspired reagent rescue cortical synaptic deficits in a mouse model of Huntington's disease

Authors: Yingli Gu, Alexander Pope, Charlene Smith, Christopher Carmona, Aaron Johnstone, Linda Shi, Xuqiao Chen, Sarai Santos, Claire Cecile Bacon-Brenes, Thomas Shoff, Korbin M. Kleczko, Judith Frydman, Leslie M. Thompson, William C. Mobley, and Chengbiao Wu

Neurobiology of Disease, 10 April 2024

Scientists used Maestro MEA to evaluate neural activity in vitro with no labs, dyes, or complicated steps.

Huntington’s disease (HD) is a fatal inherited disorder that causes neurons to break down over time, resulting in cognitive, motor, and psychiatric symptoms. In this study, researchers assessed mechanisms underlying synaptic dysfunction in a Huntington's disease (HD) mouse model. To compare neural activity between WT and HD neurons in vitro, the team used Axion’s noninvasive Maestro MEA system, finding that at day 28, HD neurons exhibited disrupted synaptic activity, indicated by decreased synchrony and burst metrics. These changes corroborated similar decreases in synaptogenesis markers and were rescued by treatment with brain derived neurotrophic factor (BDNF). Taken together with other assessments, the team concluded that “the culture paradigm we employed can be used to further explore HD synaptic pathogenesis and treatments to intercept synaptic pathology in HD.”