Charlotte Mankovich | 2026 I.S. Symposium
Name: Charlotte Mankovich
Title: Exercise May Prevent the Development of Alzheimer’s by Modulating Biomarkers in Rat Hippocampal Tissue​
Major: Neuroscience
²Ñ¾±²Ô´Ç°ù:ÌýPhilosophy
Advisor: Destiny Brakey
Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder that impairs memory, placing emotional and physical strain on patients and their caregivers. Despite the projected rise in cases, there is still no cure; current treatments are limited in their ability to reverse memory-impairing brain damage. This calls for research on accessible preventative strategies, such as exercise. Exercise is thought to reduce the risk of AD by modulating associated-biomarkers such as: (1) IL-1β and (2) Brain-derived growth factor (BDNF). Exercise-induced reductions in pro-inflammatory cytokine IL-1β prevent the activation of neurodegenerative pathways. Exercise can also upregulate BDNF levels, promoting neuron growth to combat AD. However, most of this literature focuses solely on mature BDNF (mBDNF), without accounting for the presence of its apoptosis-promoting precursor, proBDNF. Research suggests that IL-1B may also mediate this mBDNF/proBDNF ratio. Therefore, failure to collectively assess all three biomarkers limits the mechanistic understanding of exercise’s preventative effect. The current study addresses this gap by examining the impact of voluntary wheel-running on both IL-1β and the mBDNF/proBDNF ratio. Twelve Sprague Dawley rats were randomly assigned to either a 12-week exercise group or a sedentary control group. Following the intervention, rat hippocampal brain tissue was extracted, and Western Blots were performed to assess relative biomarker levels. It is hypothesized that exercise will decrease levels of IL-1β, while increasing the mBDNF/proBDNF ratio. This hypothesis suggests that exercise may play a preventative role against AD by reducing neuroinflammation and supporting the maintenance of optimal neuronal health.
Posted in Symposium 2026 on May 1, 2026.
