Authors:

Cheryl Yee

Date Created:

Not specified

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About Paper:

In the cell, microtubules provide structural support and serve as tracks for cargo transport. Within neurons, the mutated form of a microtubule-associated protein called tau tends to self-aggregate, leading to neurodegenerative diseases known as tauopathies. In humans, traumatic brain injury (TBI) can cause neuronal death and the development of the tauopathy Alzheimer's disease. There is evidence that TBI may lead to acute neuronal hyperexcitability, which drives tau pathology. However, it is unknown how neuronal excitability leads to eventual neuronal death. My project will serve to determine how TBI coupled with tau expression leads to increased neuronal activity on a cellular level and delineate the timeline from hyperactivity to degeneration. To do this, I will employ the calcium-based neuronal activity sensor, CaLexA-LUC (luciferase), in Drosophila melanogaster. After administering TBI on the tau-expressing flies, if increased neuronal activity is maintained 2 or 3 weeks post-injury, this suggests that tau could promote its own disease progression. Overall, I expect to see an increase in neuronal activity in the tau-expressing TBI flies followed by neuronal death. Therefore, if I can outline the time course from head trauma to disease, preventative and therapeutic strategies can be developed in the future to interfere with tau pathogenesis. The Health Highlight Student-Run Podcast: Identifying Inequities in Modern Healthcare Systems Jennifer Yee

Source:

UC Davis / Molecular & Cellular Bio / 2024

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Co-authors:

Cheryl Yee