Constanza J Cortes

Constanza J Cortes

Adjunct Assistant Professor in the Department of Neurology


I am interested in understanding how our brain ages, and in particular, how it ages as an integrated part of a physiological system. My research represents a cutting edge approach to our understanding of brain plasticity and aging, as it suggests that distant tissues such as skeletal muscle may be fundamentally influencing the rate at which our brain ages. Importantly, as these conversations may be disrupted in age-associated neurodegenerative diseases (such as Alzheimer's disease), I am to uncover and develop novel therapeutics for these disorders.

Education & Training

  • Postdoctoral Fellowship, Dept. Of Pediatrics, University of California - San Diego 2010 - 2016

  • Ph.D., The University of Chicago 2010

Selected Grants

Enhanced skeletal muscle proteostasis as a determinant of CNS protein quality control and neural function in the aging brain awarded by National Institutes of Health (Co-Principal Investigator). 2018 to 2022

Enhanced Skeletal Muscle Proteostasis as a Modulator of Alzheimer's Disease awarded by National Institutes of Health (Principal Investigator). 2019 to 2020

SBMA motor neuron degeneration: From cellular and molecular basis to therapy awarded by Muscular Dystrophy Association (Investigator). 2017 to 2020

Wang, Shiyi, and Constanza J. Cortes. “Interactions with PDZ proteins diversify voltage-gated calcium channel signaling.J Neurosci Res, vol. 99, no. 1, Jan. 2021, pp. 332–48. Pubmed, doi:10.1002/jnr.24650. Full Text

Cortes, Constanza J. “Women in neuroscience special issue: Pandemic edition.J Neurosci Res, vol. 99, no. 1, Jan. 2021, pp. 5–6. Pubmed, doi:10.1002/jnr.24726. Full Text

Wertman, Virginia, et al. “Low-Cost Gait Analysis for Behavioral Phenotyping of Mouse Models of Neuromuscular Disease.J Vis Exp, no. 149, July 2019. Pubmed, doi:10.3791/59878. Full Text

Pizarro, Theresa T., et al. “Challenges in IBD Research: Preclinical Human IBD Mechanisms.Inflamm Bowel Dis, vol. 25, no. Suppl 2, May 2019, pp. S5–12. Pubmed, doi:10.1093/ibd/izz075. Full Text

Cortes, Constanza J., and Albert R. La Spada. “TFEB dysregulation as a driver of autophagy dysfunction in neurodegenerative disease: Molecular mechanisms, cellular processes, and emerging therapeutic opportunities.Neurobiol Dis, vol. 122, Feb. 2019, pp. 83–93. Pubmed, doi:10.1016/j.nbd.2018.05.012. Full Text

Cortes, Constanza J., and Albert R. La Spada. “X-Linked Spinal and Bulbar Muscular Atrophy: From Clinical Genetic Features and Molecular Pathology to Mechanisms Underlying Disease Toxicity.Adv Exp Med Biol, vol. 1049, 2018, pp. 103–33. Pubmed, doi:10.1007/978-3-319-71779-1_5. Full Text

Blessing, Alicia M., et al. “Transcriptional regulation of core autophagy and lysosomal genes by the androgen receptor promotes prostate cancer progression.Autophagy, vol. 13, no. 3, Mar. 2017, pp. 506–21. Pubmed, doi:10.1080/15548627.2016.1268300. Full Text

Todd, Tiffany W., et al. “Nemo-like kinase is a novel regulator of spinal and bulbar muscular atrophy.Elife, vol. 4, Aug. 2015, p. e08493. Pubmed, doi:10.7554/eLife.08493. Full Text

Cortes, Constanza J., and Albert R. La Spada. “Autophagy in polyglutamine disease: Imposing order on disorder or contributing to the chaos?Mol Cell Neurosci, vol. 66, no. Pt A, May 2015, pp. 53–61. Pubmed, doi:10.1016/j.mcn.2015.03.010. Full Text

Cortes, Constanza J., et al. “Polyglutamine-expanded androgen receptor interferes with TFEB to elicit autophagy defects in SBMA.Nat Neurosci, vol. 17, no. 9, Sept. 2014, pp. 1180–89. Pubmed, doi:10.1038/nn.3787. Full Text


Cortes, C., and A. R. La Spada. “Transcription Factor E-B enhances protein - organelle quality control and modulates insulin signaling in skeletal muscle.” Molecular Biology of the Cell, vol. 26, AMER SOC CELL BIOLOGY, 2015.

Moreno, R. D., et al. “Cross-reactivity of monoclonal antibodies against human acrosin to dog spermatozoa.” Reproduction in Domestic Animals, vol. 41, no. 4, BLACKWELL PUBLISHING, 2006, pp. 317–317.

Retamal, M. A., et al. “Hemichannels formed by connexin43 are sensitive to changes in cellular redox potential.” Placenta, vol. 27, no. 1, W B SAUNDERS CO LTD, 2006, pp. A65–A65.