| Affiliations: | Aggie Research Mentoring Program |
| Project Leader: | Daniela Ayala
danielaaimee@tamu.edu Neuroscience & Experimental Therapeutics |
| Faculty Mentor: | Rahul Srinivasan, Ph.D. |
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Meeting Times:
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TBA |
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Team Size:
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3
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| Open Spots: | 0 |
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Special Opportunities:
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Opportunities for hands-on lab work beyond basic house keeping, encouragement to have your own mini-project, participate in research symposiums, writing a senior thesis, receiving letters of recommendation for internships, medical school and graduate school applications, summer research programs, and more.
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Team Needs:
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Ambitious and reliable students with interest in neurodegenerative research and expanding their basic science and benchwork skills. Must come in to lab in person for at least 3/4 of their available time (>8 hours per week). Interest in working with animal models (mice), behavior experiments, histology and/or computer data analysis. |
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Description:
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Parkinson’s disease (PD) is the most common movement disorder in the world, caused by significant degeneration of dopaminergic (DA) neurons in the midbrain’s substantia nigra pars compacta (SNc). Given the lack of knowledge on the underlying mechanisms for DA neuron cell loss in this context, there is currently no known cure for PD. Recent research shows astrocytes play a paramount role in modulating neuronal function via spontaneous calcium (Ca2+) signals that manage critical aspects of brain function. Our lab has shown that astrocytes in live dorsolateral striatum (DLS) brain slices exhibit robust and spontaneous Ca2+ influx events emanating from their mitochondria, suggesting that these organelles actively participate in neuronal function. Based on these findings, this project aims to assess whether specific disruption of astrocytic mitochondria function in the SNc accelerates DA neuron loss and the progression of neurodegeneration. We plan to observe whether astrocytic mitochondrial dysfunction in PD-related brain regions. To do so, we have created an adeno-associated virus (AAV) tool specifically target astrocytic mitochondrial DNA, coding for the restriction enzyme PstI, called Mito-PstI, which damages mitochondrial function. We intend to use this tool to observe changes in mitochondrial function and morphology, astrocyte and neuronal function, glial and microglial reactivity, and the development of PD-like symptoms in mice. |