Aída Guzmán
This is a likely match — the affiliation was inferred from OpenAlex, ORCID, and web sources but has not been fully confirmed. Treat with appropriate caution.
Researcher
Also affiliated: United States Food and Drug Administration (2022); École Nationale Supérieure de Chimie de Lille (2003); Instituto Nacional de Enfermedades Respiratorias (2003); Instituto Nacional de Neurología y Neurocirugía (2001–2003); Universidad Nacional Autónoma de México (1999–2020)
Faculty Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Aída Guzmán's research investigates mechanisms of neurodegeneration, specifically focusing on autophagy and protein aggregation in dopaminergic neurons. Her work utilizes a primary human dopaminergic neuronal model to study these processes. She has published 10 papers with 148 citations and an h-index of 6. Guzmán collaborates with researchers at the National Center for Toxicological Research, including Susan M. Burks, Manuel Alejandro Ramirez-Lee, Syed F. Ali, and Syed Z. Imam, with whom she has co-authored publications. Her recent publication in 2022 addressed the role of autophagy and protein aggregation in dopaminergic degeneration.
Metrics
- h-index: 6
- Publications: 10
- Citations: 151
Selected Publications
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Autophagy and protein aggregation as a mechanism of dopaminergic degeneration in a primary human dopaminergic neuronal model (2022)
Collaboration Network
Top Collaborators
- Autophagy and protein aggregation as a mechanism of dopaminergic degeneration in a primary human dopaminergic neuronal model
- Autophagy and protein aggregation as a mechanism of dopaminergic degeneration in a primary human dopaminergic neuronal model
- Autophagy and protein aggregation as a mechanism of dopaminergic degeneration in a primary human dopaminergic neuronal model
- Autophagy and protein aggregation as a mechanism of dopaminergic degeneration in a primary human dopaminergic neuronal model
- Autophagy and protein aggregation as a mechanism of dopaminergic degeneration in a primary human dopaminergic neuronal model
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