Robert K. Naviaux
| Robert K. Naviaux MD, PhD | |
|---|---|
| File:RKN.jpgRKN.jpg | |
| Born | Robert Keith Naviaux June 27, 1956 Woodland, California, U.S. |
| 🏳️ Citizenship | US |
| 🏫 Education | Georg August University, Göttingen, Germany (undergraduate biochemistry) University of California, Davis (BS) |
| 💼 Occupation | |
| Known for | Discovery 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), Co-founder of the Mitochondrial Medicine Society (MMS), Hyperpurinergia hypothesis for the genesis and treatment of autism |
| 👩 Spouse(s) | Jane Crowley Naviaux, MD, PhD (1987-Present; 2 children) |
| 🏅 Awards | Inaugural Kelsey Wright Award, UMDF (2001)
Autism trailblazer award, Autism Speaks (2011) Lifetime achievement award, MMS (2018) Pioneering achievement award, ISEAI (2019) |
| 🌐 Website | https://naviauxlab.ucsd.edu |
Robert K. Naviaux (born in 1956) is an American physician-scientist specializing in mitochondrial medicine and complex chronic disorders. He discovered the cause of Alpers syndrome..[1] and developed the first DNA test to diagnose it. The cause of Alpers was unknown for over 70 years since it was first described in 1931[2]. His team at the University of California, San Diego (UCSD) also discovered the first mitochondrial DNA (mtDNA) mutation to cause genetic forms of autism[3]. Naviaux is the originator of the cell danger response (CDR) hypothesis[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]
Known internationally for his expertise in human genetics, inborn errors of metabolism, metabolomics, and mitochondrial medicine, 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.
The Naviaux Lab has developed new methods in metabolomics[6][7] and environmental toxicology that have shown that many complex chronic disorders like ASD, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)[8], Gulf War Illness[9], and recurrent Major Depressive Disorder (rMDD)[10] have a metabolic signature that can be used in diagnosis and lead to fresh insights to treatment[11][12]
Naviaux characterized the mitochondrial and metabolic features of the healing cycle[11], showed the connection between healing and aging[13], and how mitochondria respond to environmental pollution and ecosystem stress by activating the CDR and creating a link between environmental health and human health[14]. The Naviaux Lab also developed some of the first methods to isolate environmental DNA from beach sand and ocean floor core sediments for use in the molecular reconstruction of modern and ancient marine ecosystems[15]. Naviaux also helped develop new methods of using the biocavity laser spectroscopy to characterize the mitochondrial response to genetic and environmental stress[16][17][18].
Early years[edit]
Naviaux is the oldest of four sons born to Barbara and Dr. James L. Naviaux, DVM. His father, a veterinarian specializing in horses, also had a lifelong interest in wildlife medicine and was the founder of the National Wildlife Health Foundation. After his parents divorced, he was raised by his maternal grandparents in Fairfax in Marin County, California, north of San Francisco.
Training[edit]
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, Naviaux earned a master’s in zoology and microbiology from Indiana University in Bloomington, Indiana. He was trained in the medical scientist training program 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 popular pCL retroviral gene transfer vectors[19]. 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.
Research Career[edit]
Naviaux joined the faculty of UCSD in 1997. In 1999, he reported the cause of the classical neurogenetic disease Alpers-Huttenlocher syndrome[1][2] From 2003 to 2007, Naviaux studied the biophysical response of mitochondria to genetic and environmental stress[16][18]. Studies on the role of mitochondria in regeneration and healing in the MRL mouse followed[20]. In 2008, he developed the concept of the cell danger response (CDR) and the hyperpurinergia hypothesis[21] 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[22][23][24], the antipurinergic drug suramin was tested as a new treatment of autism in a small clinical trial of 10 children in the SAT1 trial[5]. The effects from a single dose of suramin resulted in improvements in the ASD core symptoms of language, social behavior, and reductions in repetitive behaviors six weeks after a single dose in all children who received suramin and in none of the children who received placebo[5]. That work was independently reproduced in 2021 in a study of nearly 50 children with ASD[25]. In other research, Naviaux showed the connection between mitochondria, incomplete healing, and the process of aging[26].
References[edit]
- ↑ 1.0 1.1 Naviaux, Robert K.; Nyhan, William L.; Barshop, Bruce A.; Poulton, Joanna; Markusic, David; Karpinski, Nancy C.; Haas, Richard H. (1999-01-XX). <54::aid-art10>3.0.co;2-b "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. Check date values in:
|date=(help) - ↑ 2.0 2.1 ALPERS, BERNARD J. (1931-03-01). "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.
- ↑ Graf, William D.; Marin-Garcia, Jose; Gao, H.G.; Pizzo, Senia; Naviaux, Robert K.; Markusic, David; Barshop, Bruce A.; Courchesne, Eric; Haas, Richard H. (2000-06-01). "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.
- ↑ "Metabolic features of the cell danger response". Mitochondrion. 16: 7–17. 2014-05-01. doi:10.1016/j.mito.2013.08.006. ISSN 1567-7249.
- ↑ 5.0 5.1 5.2 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.
- ↑ Li, Kefeng; Naviaux, Jane C.; Bright, A. Taylor; Wang, Lin; Naviaux, Robert K. (2017-09-04). "A robust, single-injection method for targeted, broad-spectrum plasma metabolomics". Metabolomics. 13 (10): 122. doi:10.1007/s11306-017-1264-1. ISSN 1573-3890. PMC 5583274. PMID 28943831.
- ↑ Li, Kefeng; Naviaux, Jane C.; Monk, Jonathan M.; Wang, Lin; Naviaux, Robert K. (March 2020). "Improved Dried Blood Spot-Based Metabolomics: A Targeted, Broad-Spectrum, Single-Injection Method". Metabolites. 10 (3): 82. doi:10.3390/metabo10030082. PMC 7143494 Check
|pmc=value (help). PMID 32120852 Check|pmid=value (help). - ↑ Naviaux, Robert K.; Naviaux, Jane C.; Li, Kefeng; Bright, A. Taylor; Alaynick, William A.; Wang, Lin; Baxter, Asha; Nathan, Neil; Anderson, Wayne; Gordon, Eric (2016-09-13). "Metabolic features of chronic fatigue syndrome". Proceedings of the National Academy of Sciences. 113 (37): E5472–E5480. doi:10.1073/pnas.1607571113. ISSN 0027-8424. PMC 5027464. PMID 27573827.
- ↑ Naviaux, Robert K.; Naviaux, Jane C.; Li, Kefeng; Wang, Lin; Monk, Jonathan M.; Bright, A. Taylor; Koslik, Hayley J.; Ritchie, Janis B.; Golomb, Beatrice A. (2019-07-26). "Metabolic features of Gulf War illness". PLOS ONE. 14 (7): e0219531. doi:10.1371/journal.pone.0219531. ISSN 1932-6203. PMC 6660083 Check
|pmc=value (help). PMID 31348786. - ↑ Mocking, Roel J. T.; Naviaux, Jane C.; Li, Kefeng; Wang, Lin; Monk, Jonathan M.; Bright, A. Taylor; Figueroa, Caroline A.; Schene, Aart H.; Ruhé, Henricus G.; Assies, Johanna; Naviaux, Robert K. (2021-01-11). "Metabolic features of recurrent major depressive disorder in remission, and the risk of future recurrence". Translational Psychiatry. 11 (1): 1–13. doi:10.1038/s41398-020-01182-w. ISSN 2158-3188. PMC 7801396 Check
|pmc=value (help). PMID 33431800 Check|pmid=value (help). - ↑ 11.0 11.1 "Metabolic features and regulation of the healing cycle—A new model for chronic disease pathogenesis and treatment". Mitochondrion. 46: 278–297. 2019-05-01. doi:10.1016/j.mito.2018.08.001. ISSN 1567-7249.
- ↑ "Antipurinergic therapy for autism—An in-depth review". Mitochondrion. 43: 1–15. 2018-11-01. doi:10.1016/j.mito.2017.12.007. ISSN 1567-7249.
- ↑ 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 Check
|pmc=value (help). PMID 31083530. - ↑ "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. 2020-03-01. doi:10.1016/j.mito.2019.12.005. ISSN 1567-7249.
- ↑ Naviaux, Robert K.; Good, Benjamin; Mcpherson, John Douglas; Steffen, David L.; Markusic, David; Ransom, Barbara; Corbeil, Jacques (2005-10-11). "Sand DNA - A genetic library of life at the water's edge". Marine Ecology Progress Series. 301: 9–22. ISSN 0171-8630.
- ↑ 16.0 16.1 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. doi:10.1117/1.2799198. ISSN 1083-3668.
- ↑ Gourley, P.L.; Naviaux, R.K. (2005-07-XX). "Optical phenotyping of human mitochondria in a biocavity laser". IEEE Journal of Selected Topics in Quantum Electronics. 11 (4): 818–826. doi:10.1109/JSTQE.2005.857680. ISSN 1558-4542. Check date values in:
|date=(help) - ↑ 18.0 18.1 Gourley, Paul L.; Hendricks, Judy K.; McDonald, Anthony E.; Copeland, R. Guild; Barrett, Keith E.; Gourley, Cheryl R.; Singh, Keshav K; Naviaux, Robert K. (2005-12-XX). "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. Check date values in:
|date=(help) - ↑ Naviaux, R. K.; Costanzi, E.; Haas, M.; Verma, I. M. (1996-08-01). "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. PMID 8764092.
- ↑ "Retained features of embryonic metabolism in the adult MRL mouse". Molecular Genetics and Metabolism. 96 (3): 133–144. 2009-03-01. doi:10.1016/j.ymgme.2008.11.164. ISSN 1096-7192. PMC 3646557. PMID 19131261.
- ↑ "The Neuroscience of Autism Spectrum Disorders - 1st Edition". www.elsevier.com. Retrieved 2021-04-28.
- ↑ Naviaux, Jane C.; Wang, Lin; Li, Kefeng; Bright, A. Taylor; Alaynick, William A.; Williams, Kenneth R.; Powell, Susan B.; Naviaux, Robert K. (2015-01-13). "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.
- ↑ 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–e400. doi:10.1038/tp.2014.33. ISSN 2158-3188. PMC 4080315. PMID 24937094.
- ↑ 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. (2013-03-13). "Antipurinergic Therapy Corrects the Autism-Like Features in the Poly(IC) Mouse Model". PLOS ONE. 8 (3): e57380. doi:10.1371/journal.pone.0057380. ISSN 1932-6203. PMC 3596371. PMID 23516405.
- ↑ "News". PaxMedica. Retrieved 2021-04-28.
- ↑ 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 Check
|pmc=value (help). PMID 31083530.
[COI] This article was contributed by Jonathan Monk, a computational biologist and systems scientist who has worked with Dr. Naviaux since 2017 and is a coauthor on several publications.
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