Juan Pablo Palavicini, PhD
I have a broad background in biochemistry and neuroscience, with more than 16 years of research experience. During my graduate studies at the Institute of Neurobiology of the University of Puerto Rico, I studied protein-RNA interactions within the central nervous system, where I became proficient at multiple biochemical, molecular biology, genetic, and neuroscience techniques using bacteria, yeast, and squid systems. I joined the field of neurodegenerative diseases in 2011, first through a postdoctoral appointment at the laboratory of Dr. Madepalli Lakshmana at the Torrey Pines Institute for Molecular Studies, Florida, where I studied the molecular mechanisms underlying the role of RanBP9 on Alzheimer’s disease (AD) using cell culture systems and transgenic mouse models.
In 2013, I joined the laboratory of Dr. Xianlin Han as a postdoctoral fellow, formerly at the Sanford Burnham Prebys Medical Discovery Institute and since 2017 at UT Health SA, where I studied the role of myelin lipids on the pathogenesis of AD, aging, and diabetes using shotgun lipidomics, biochemical, genetic, and histological approaches and multiple murine models. To this end, I received a Postdoctoral Fellowship from the American Diabetes Association (2015-2017) entitled “Mechanistic study of sulfatide deficiency in diabetes and its relationship with dementia”.
In 2019, I was appointed as an Assistant Professor, at UT Health SA’s Barshop Institute for Longevity and Aging studies and the Department of Medicine, Diabetes Division. My current research efforts are focused on studying the role of ceramides, important signaling molecules that in excess become lipotoxic, in the context of AD, diabetes, and aging. In addition, I am starting to develop a new line of research in collaboration with Dr. Sarah Hopp focused on studying phospholipase C gamma 2 (PLCγ2), whose gene has been recently strongly associated with Alzheimer’s disease. Finally, I continue collaborating with Dr. Han in multiple lipid metabolism-oriented AD, aging, and diabetes projects.
|1.||Qiu, S., Palavicini, J. P., Wang, J., Gonzalez, N. S., He, S., Dustin, E., Zou, C., Ding, L., Bhattacharjee, A., Van Skike, C. E., Galvan, V., Dupree, J. L., & Han, X. (2021). Adult-onset CNS myelin sulfatide deficiency is sufficient to cause Alzheimer’s disease-like neuroinflammation and cognitive impairment. Molecular Neurodegeneration, 16(1), . https://doi.org/10.1186/s13024-021-00488-7|
|2.||Wang, C., Palavicini, J. P., & Han, X. (2021). A lipidomics atlas of selected sphingolipids in multiple mouse nervous system regions. International journal of molecular sciences, 22(21), . https://doi.org/10.3390/ijms222111358|
|3.||Shannon, C. E., Ragavan, M., Palavicini, J. P., Fourcaudot, M., Bakewell, T. M., Valdez, I. A., Ayala, I., Jin, E. S., Madesh, M., Han, X., Merritt, M. E., & Norton, L. (2021). Insulin resistance is mechanistically linked to hepatic mitochondrial remodeling in non-alcoholic fatty liver disease. Molecular Metabolism, 45, . https://doi.org/10.1016/j.molmet.2020.101154|
|4.||Palavicini, J. P., Chavez-Velazquez, A., Fourcaudot, M., Tripathy, D., Pan, M., Norton, L., DeFronzo, R. A., & Shannon, C. E. (2021). The Insulin-Sensitizer Pioglitazone Remodels Adipose Tissue Phospholipids in Humans. Frontiers in Physiology, 12, . https://doi.org/10.3389/fphys.2021.784391|
|5.||Palavicini, J. P., Chen, J., Wang, C., Wang, J., Qin, C., Baeuerle, E., Wang, X., Woo, J. A., Kang, D. E., Musi, N., Dupree, J. L., & Han, X. (2020). Early disruption of nerve mitochondrial and myelin lipid homeostasis in obesity-induced diabetes. JCI Insight, 5(21), [e137286]. https://doi.org/10.1172/jci.insight.137286|
|6.||Singha, A., Palavicini, J. P., Pan, M., Farmer, S., Sandoval, D., Han, X., & Fujikawa, T. (2020). Leptin Receptors in RIP-Cre25Mgn Neurons Mediate Anti-dyslipidemia Effects of Leptin in Insulin-Deficient Mice. Frontiers in Endocrinology, 11, . https://doi.org/10.3389/fendo.2020.588447|
|7.||Palavicini, J. P., Wang, C., Chen, L., Hosang, K., Wang, J., Tomiyama, T., Mori, H., & Han, X. (2017). Oligomeric amyloid-beta induces MAPK-mediated activation of brain cytosolic and calcium-independent phospholipase A2 in a spatial-specific manner. Acta Neuropathologica Communications, 5(1), 56. https://doi.org/10.1186/s40478-017-0460-6|
|8.||Wang, M., Palavicini, J. P., Cseresznye, A., & Han, X. (2017). Strategy for Quantitative Analysis of Isomeric Bis(monoacylglycero)phosphate and Phosphatidylglycerol Species by Shotgun Lipidomics after One-Step Methylation. Analytical Chemistry, 89(16), 8490-8495. https://doi.org/10.1021/acs.analchem.7b02058|
|9.||Wang, C., Palavicini, J. P., Wang, M., Chen, L., Yang, K., Crawford, P. A., & Han, X. (2016). Comprehensive and quantitative analysis of polyphosphoinositide species by shotgun lipidomics revealed their alterations in db/db mouse brain. Analytical Chemistry, 88(24), 12137-12144. https://doi.org/10.1021/acs.analchem.6b02947|
|10.||Palavicini, J. P., Wang, C., Chen, L., Ahmar, S., Higuera, J. D., Dupree, J. L., & Han, X. (2016). Novel molecular insights into the critical role of sulfatide in myelin maintenance/function. Journal of neurochemistry, 139(1), 40-54. https://doi.org/10.1111/jnc.13738|
|11.||Wang, R., Palavicini, J. P., Wang, H., Maiti, P., Bianchi, E., Xu, S., Lloyd, B. N., Dawson-Scully, K., Kang, D. E., & Lakshmana, M. K. (2014). RanBP9 overexpression accelerates loss of dendritic spines in a mouse model of Alzheimer's disease. Neurobiology of Disease, 69, 169-179. https://doi.org/10.1016/j.nbd.2014.05.029|
|12.||Palavicini, J. P., Wang, H., Minond, D., Bianchi, E., Xu, S., & Lakshmana, M. K. (2014). RanBP9 overexpression down-regulates phospho-cofilin, causes early synaptic deficits and impaired learning, and accelerates accumulation of amyloid plaques in the mouse brain. Journal of Alzheimer's Disease, 39(4), 727-740. https://doi.org/10.3233/JAD-131550|