Robert K. Naviaux
Born
Robert Keith Naviaux

(1956-06-27)June 27, 1956
Woodland, California, U.S.
EducationGeorg August University, Göttingen, Germany (undergraduate biochemistry)

University of California, Davis (BS)

Indiana University (MA, MD, PhD; human genetics and virology)
Known forDiscovery of the cause of Alpers syndrome, Metabolic features of the cell danger response (CDR), Mitochondrial and metabolic features and stages of the healing cycle (salugenesis), Hyperpurinergia hypothesis for the genesis and treatment of autism
Spouse(s)
Jane Crowley Naviaux, MD, PhD
​
​
(m. 1987)​
Children2
AwardsInaugural Kelsey Wright Award, UMDF (2001)

Autism trailblazer award, Autism Speaks (2011) Lifetime achievement award, MMS (2018) Pioneering achievement award, ISEAI (2019)

The Vanguard Award, UMDF (2023)
Scientific career
FieldsMitochondrial medicine, molecular and medical genetics, biochemical genetics, inborn errors of metabolism, metabolomics, virology, immunology, ecosystem biology, environmental medicine
InstitutionsUC San Diego
ThesisConstruction and characterization of three infectious molecular clones of encephalomyocarditis virus (1989)
Doctoral advisorW. Dean Fraser, Milton W. Taylor, M. Ed Hodes, Joe C. Christian, George W. Jordan, Stuart H. Cohen
Websitehttps://naviauxlab.ucsd.edu

Robert K. Naviaux (born in 1956) is an American physician-scientist who specializes in mitochondrial medicine and complex chronic disorders. He discovered the cause of Alpers syndrome,[1][2] and was part of the team that reported the first mitochondrial DNA (mtDNA) mutation to cause genetic forms of autism.[3] Naviaux proposed the cell danger response (CDR) and hyperpurinergia hypothesis for complex disorders in 2014[4] and directed the first FDA-approved clinical trial to study the safety and efficacy of the antipurinergic drug suramin as a new treatment for autism spectrum disorder (ASD).[5]

Naviaux is the founder and co-director of the Mitochondrial and Metabolic Disease Center (MMDC) at UCSD and is a Professor of Genetics in the departments of Medicine, Pediatrics, and Pathology at the UCSD School of Medicine, where he directs a core laboratory for metabolomics. He is the co-founder and a former president of the Mitochondrial Medicine Society (MMS) and a founding associate editor of the journal Mitochondrion. Naviaux received the 2023 United Mitochondrial Disease Foundation Vanguard Award.[6][7]

Training

Naviaux received his B.S. in biological sciences from the University of California Davis. He studied natural killer cell biology and cancer immunology as an undergraduate research intern at the National Institutes of Health (NIH) and studied biochemistry and medical sociology at Georg August University in Göttingen, Germany as an education abroad student. In 1981, he earned a master's in zoology and microbiology from Indiana University in Bloomington, Indiana. He was trained in the medical scientist training program (MSTP) at Indiana University and received his MD and PhD in medical genetics and virology in 1989. He was a resident and medical scholar in the clinical investigator pathway of the American Board of Internal Medicine (ABIM) at UC Davis Medical Center from 1986 to 1990. In 1990, Naviaux was named a National Medical Resident of the Year by the National Institute of Diabetes, Digestive, and Kidney Disease (NIDDK, NIH). He did his postdoctoral training in gene therapy and retrovirus biology at the Salk Institute from 1990 to 1994, where he invented the pCL retroviral gene transfer vectors.[8] Naviaux was a Fogarty International scholar in India in 1994. He did his medical subspecialty training in pediatrics as a fellow in biochemical genetics and inborn errors of metabolism from 1994 to 1997 at the University of California, San Diego (UCSD) School of Medicine. In 1996, Naviaux founded the Mitochondrial and Metabolic Disease Center (MMDC) at UCSD.[9]

Research career

Naviaux joined the faculty of the University of California, San Diego in 1997. In 1999, he reported the cause of the classical neurogenetic disease Alpers-Huttenlocher syndrome.[1][2] From 2003 to 2007, he studied the biophysical response of mitochondria to genetic and environmental stress.[10][11] Studies on the role of mitochondria in regeneration and healing in the MRL mouse followed.[12] In 2008, he developed the concept of the cell danger response (CDR) and the hyperpurinergia hypothesis[13] that focused on abnormalities in ATP signaling as a root cause for the genesis and treatment of autism spectrum disorder (ASD). This led to a Trailblazer Award from Autism Speaks in 2011. After successful testing in several mouse models of ASD,[14][15][16] the antipurinergic drug suramin was found to be safe and effective as a new treatment for the core symptoms of autism in a small clinical trial of 10 children in the SAT1 trial.[5] Recent work in the Naviaux lab has showcased the connection between mitochondria, incomplete healing and aging,[17] and the connections between environmental health, mitochondria, the cell danger response, and the rising prevalence of chronic illness.[18]

References

  1. 1 2 Naviaux, Robert K.; Nyhan, William L.; Barshop, Bruce A.; Poulton, Joanna; Markusic, David; Karpinski, Nancy C.; Haas, Richard H. (January 1999). "Mitochondrial DNA polymerase ? deficiency and mtDNA depletion in a child with Alpers' syndrome". Annals of Neurology. 45 (1): 54–58. doi:10.1002/1531-8249(199901)45:1<54::aid-art10>3.0.co;2-b. ISSN 0364-5134. PMID 9894877. S2CID 72829923.
  2. 1 2 ALPERS, BERNARD J. (March 1, 1931). "Diffuse Progressive Degeneration of the Gray Matter of the Cerebrum". Archives of Neurology and Psychiatry. 25 (3): 469. doi:10.1001/archneurpsyc.1931.02230030027002. ISSN 0096-6754.
  3. ↑ Graf, William D.; Marin-Garcia, Jose; Gao, H.G.; Pizzo, Senia; Naviaux, Robert K.; Markusic, David; Barshop, Bruce A.; Courchesne, Eric; Haas, Richard H. (June 1, 2000). "Autism Associated With the Mitochondrial DNA G8363A Transfer RNALys Mutation". Journal of Child Neurology. 15 (6): 357–361. doi:10.1177/088307380001500601. ISSN 0883-0738. PMID 10868777. S2CID 37548666.
  4. ↑ Naviaux, Robert K. (May 1, 2014). "Metabolic features of the cell danger response". Mitochondrion. 16: 7–17. doi:10.1016/j.mito.2013.08.006. ISSN 1567-7249. PMID 23981537.
  5. 1 2 Naviaux, Robert K.; Curtis, Brooke; Li, Kefeng; Naviaux, Jane C.; Bright, A. Taylor; Reiner, Gail E.; Westerfield, Marissa; Goh, Suzanne; Alaynick, William A.; Wang, Lin; Capparelli, Edmund V. (2017). "Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial". Annals of Clinical and Translational Neurology. 4 (7): 491–505. doi:10.1002/acn3.424. ISSN 2328-9503. PMC 5497533. PMID 28695149.
  6. ↑ "UMDF Celebrates 2023 Vanguard Award Winner".
  7. ↑ "Robert K Naviaux Receives United Mitochondrial Disease Foundations Vanguard Award".
  8. ↑ Naviaux, R K; Costanzi, E; Haas, M; Verma, I M (August 1996). "The pCL vector system: rapid production of helper-free, high-titer, recombinant retroviruses". Journal of Virology. 70 (8): 5701–5705. doi:10.1128/jvi.70.8.5701-5705.1996. ISSN 0022-538X. PMC 190538. PMID 8764092.
  9. ↑ Haas, RH; Naviaux, RK (2019). "A brief history of the Mitochondrial Medicine Society—The first 20 years, 1998-2018". Mitochondrial and Metabolic Medicine. 1: 1–7.
  10. ↑ Gourley, Paul Lee; Hendricks, Judy Kay; McDonald, Anthony E.; Copeland, R. G.; Yaffe, Michael P.; Naviaux, Robert K. (September 2007). "Reactive biomolecular divergence in genetically altered yeast cells and isolated mitochondria as measured by biocavity laser spectroscopy: rapid diagnostic method for studying cellular responses to stress and disease". Journal of Biomedical Optics. 12 (5): 054003. Bibcode:2007JBO....12e4003G. doi:10.1117/1.2799198. ISSN 1083-3668. PMID 17994891. S2CID 21850240.
  11. ↑ Gourley, Paul L.; Hendricks, Judy K.; McDonald, Anthony E.; Copeland, R. Guild; Barrett, Keith E.; Gourley, Cheryl R.; Singh, Keshav K; Naviaux, Robert K. (December 2005). "Mitochondrial Correlation Microscopy and Nanolaser Spectroscopy — New Tools for Biophotonic Detection of Cancer in Single Cells". Technology in Cancer Research & Treatment. 4 (6): 585–592. doi:10.1177/153303460500400602. ISSN 1533-0346. PMID 16292878. S2CID 28063390.
  12. ↑ Naviaux, Robert K.; Le, Thuy P.; Bedelbaeva, Khamilia; Leferovich, John; Gourevitch, Dmitri; Sachadyn, Pawel; Zhang, Xiang-Ming; Clark, Lise; Heber-Katz, Ellen (March 1, 2009). "Retained features of embryonic metabolism in the adult MRL mouse". Molecular Genetics and Metabolism. 96 (3): 133–144. doi:10.1016/j.ymgme.2008.11.164. ISSN 1096-7192. PMC 3646557. PMID 19131261.
  13. ↑ "The Neuroscience of Autism Spectrum Disorders - 1st Edition". www.elsevier.com. Retrieved April 28, 2021.
  14. ↑ Naviaux, Jane C.; Wang, Lin; Li, Kefeng; Bright, A. Taylor; Alaynick, William A.; Williams, Kenneth R.; Powell, Susan B.; Naviaux, Robert K. (January 13, 2015). "Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model". Molecular Autism. 6 (1): 1. doi:10.1186/2040-2392-6-1. ISSN 2040-2392. PMC 4334917. PMID 25705365.
  15. ↑ Naviaux, J. C.; Schuchbauer, M. A.; Li, K.; Wang, L.; Risbrough, V. B.; Powell, S. B.; Naviaux, R. K. (June 2014). "Reversal of autism-like behaviors and metabolism in adult mice with single-dose antipurinergic therapy". Translational Psychiatry. 4 (6): e400. doi:10.1038/tp.2014.33. ISSN 2158-3188. PMC 4080315. PMID 24937094.
  16. ↑ Naviaux, Robert K.; Zolkipli, Zarazuela; Wang, Lin; Nakayama, Tomohiro; Naviaux, Jane C.; Le, Thuy P.; Schuchbauer, Michael A.; Rogac, Mihael; Tang, Qingbo; Dugan, Laura L.; Powell, Susan B. (March 13, 2013). "Antipurinergic Therapy Corrects the Autism-Like Features in the Poly(IC) Mouse Model". PLOS ONE. 8 (3): e57380. Bibcode:2013PLoSO...857380N. doi:10.1371/journal.pone.0057380. ISSN 1932-6203. PMC 3596371. PMID 23516405.
  17. ↑ Naviaux, Robert K. (June 2019). "Incomplete Healing as a Cause of Aging: The Role of Mitochondria and the Cell Danger Response". Biology. 8 (2): 27. doi:10.3390/biology8020027. PMC 6627909. PMID 31083530.
  18. ↑ Naviaux, Robert K. (March 2020). "Perspective: Cell danger response Biology—The new science that connects environmental health with mitochondria and the rising tide of chronic illness". Mitochondrion. 51: 40–45. doi:10.1016/j.mito.2019.12.005. ISSN 1567-7249. PMID 31877376. S2CID 209488913.
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