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Cheril Tapia, PhD

Principal Investigator

Neurobiology of Aging Lab

Dr. Cheril Cecilia Tapia Rojas is a biochemist who earned her BSc and a PhD in Cellular and Molecular Biology from Pontificia Universidad Católica de Chile. After completing postdoctoral research funded by the ANILLO ACT1411 grant (Chile) at Universidad Autónoma de Chile, she joined Universidad San Sebastián in 2018 as Assistant Professor sponsored by the program that subsidizes installation in academia (PAI77170091), and secured a FONDECYT Initiation grant that same year.

She leads the Neurobiology of Aging Laboratory (NBA‑Lab) at the Centro Basal Ciencia & Vida. Her research focuses on synaptic mitochondrial dysfunction in the aging hippocampus, investigating how factors such as phosphorylated tau and reduced Lonp1 protease activity contribute to memory decline and impaired neuroenergetics. Her team employs mouse primary neuron cultures, organotypic slices, and aged mouse models (strains C57BL6 and SAMP8) to explore these mechanisms.

Dr. Tapia Rojas is actively involved in teaching and mentorship across undergraduate Biochemistry programs and graduate studies, including the PhD in Cell Biology and Biomedicine program and the PhD in Biotechnology and Bioentrepreneurship program at USS. She has more than 55 research publications and multiple funded projects, including FONDECYT grants, and she is recognized nationally and internationally for her contributions to understanding aging and mitochondrial biology.

Grants

FONDECYT R-1221178 [2022-2026]: Degradation Lonp1-mediated of phosphorylated tau inside synaptic mitochondria and its contribution to hippocampal memory loss during aging. (Principal Investigator) FONDECYT R-1221796 [2022-2026]: Cognitive dysfunction mechanisms of anti-ribosomal P protein antibodies in systemic lupus erythematosus (Co-investigator) FONDECYT R-1221374 [2022-2026]: Role of KDELR signaling pathway in cancer cell metabolism: integrating the secretory pathway with lipid droplet and mitochondrial function. (Co-investigator) FONDECYT P-3240174 [2024-2026]: Mitochondrial unfolded protein response (mtUPR) in the aged hippocampus: Elucidating its contribution to mitochondrial, synaptic, and cognitive failure. (Sponsor Investigator) FONDECYT P-3210591 [2021-2024]: Understanding the mechanisms that lead to improved hippocampal function in aging after Red630-Light-Transcranial LED Therapy: mitochondria at the synapses and synaptic plasticity. (Sponsor Investigator)

Collaborations

Marcello Pinti. Department of Life Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy. National Institute for Cardiovascular Research-INRC, Bologna, Italy. Department of Surgery, Medicine, Dentistry and Morphological Sciences, University of Modena and Reggio Emilia, Modena, Italy. Maria José Perez. Department of Chromatin Regulation, Max Planck Institute for Immunobiology and Epigenetics, Stuebeweg, Freiburg, Germany Carolina oliva. Centro para la Transversalización de Género en I + D +i + e, Vicerrectoría de Investigación y Doctorados, Universidad Autónoma de Chile, Santiago, Chile. Daniela Riveras. GEMA Center for Genomics, Ecology and Environment, Facultad de Ciencias, Ingeniería y Tecnología, Universidad Mayor, Santiago, Chile.

Selected Publications

Featured Publications presents a curated selection of the researcher’s most significant scientific contributions, reflecting their expertise, findings, and the broader impact of their work in advancing knowledge within their field.

NPJ Aging
Early mitophagy activation by Urolithin A prevents, but late activation does not reverse, age-related cognitive impairment
Cell Death & Disease
Unraveling sex differences in age-related hippocampal decline: differential mitochondrial dysfunction, Lonp1-dependent mitochondrial proteostasis and mtROS production in aged C57BL/6 mice
Scientific Reports
Identifying a novel Mecp2-mediated epigenetic mechanism controlling Lonp1 in the hippocampus and its disruption by aging
Neural Regeneration Research
Synaptic mitochondria in aging and neurodegenerative diseases: unraveling their functional decline and vulnerability
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