Prof. Avik Roy
Biography
Dr. Avik Roy, Ph.D serves as the Chief Scientific Officer (CSO) and Principal Investigator at Simmaron Research
He is also an Adjunct Professor of Biochemistry at the University of Wisconsin-Milwaukee and an elected member of the Milwaukee Institute for Drug Discovery (MIDD). Dr. Roy specializes in the molecular mechanisms of neurodegenerative and chronic neuroinflammatory diseases. At Simmaron Research, he applies his extensive background in Parkinson's and Alzheimer's disease to decode the underlying mechanisms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), Long COVID, and Postural Orthostatic Tachycardia Syndrome (POTS). [1, 2, 3, 4, 5, 6]
Core Research Focus & Breakthroughs
- Cellular Energy Failure in ME/CFS: Dr. Roy’s research has revealed that ME/CFS immune cells suffer from a severe dual impairment. Unlike other chronic conditions, both major energy production steps—mitochondrial oxidative phosphorylation and glycolysis—fail simultaneously. This cellular energy collapse is heavily driven by defects in autophagy (the body's cellular quality control process). [1, 2, 3]
- Low-Dose Rapamycin Clinical Trial: Building on findings that the drug rapamycin can restore autophagy, Dr. Roy leads breakthrough clinical trials at Simmaron Research. Initial phase findings show that low-dose rapamycin significantly reduces fatigue, post-exertional malaise (PEM), sleep issues, and orthostatic intolerance for a specific subset of patients—particularly those whose ME/CFS was triggered by viral infections. [1, 2, 3]
- Animal Model Development: His team has successfully developed specialized animal models to study the precise mechanisms driving muscle fatigue and PEM. This enables the testing of potential drugs before they transition to human trials. [1, 2, 3]
- Parkinson's Disease Discoveries: He demonstrated that a loss of function in the bpoz2 gene contributes to Lewy body pathology in Parkinson's. His work targeting alpha-synuclein pathology utilizing the BPOZ2 protein earned him the Rapid Response Innovation Award from the Michael J. Fox Foundation. [1, 2, 3]
Notable Awards & Funding
- NIH Exploratory Award (R21NS129021): Awarded to study specific molecular pathways (like the ATG-13 study) to target neuroinflammation.
- Solve ME/CFS Catalyst Award: Granted by the Solve ME/CFS Initiative to fund and expand decentralized clinical trials for rapamycin.
- Ramsay Research Grant (2022): Awarded by the Solve ME/CFS Initiative to support early-stage innovative studies into ME/CFS pathology.
- Patents: Dr. Roy holds multiple patents, including those for Keptide™ (an intranasal therapeutic candidate) and memory-inducing small molecules designed to improve hippocampal function. [1, 2, 3, 4, 5, 6]
Publications (10 selected):
1. M. A. Toriola et al., Genetic depletion of the early autophagy protein ATG13 impairs mitochondrial energy metabolism, augments oxidative stress, induces the polarization of macrophages to the M1 inflammatory mode, and compromises myelin integrity in skeletal muscle. Inflamm Res 75, 26 (2026).
2. G. Gottschalk et al., Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE). Mol Cell Neurosci 120, 103731 (2022).
3. B. T. Ruan et al., Low-dose rapamycin alleviates clinical symptoms of fatigue and PEM in ME/CFS patients via improvement of autophagy: a pilot study. Journal of Translational Medicine 23, 1148 (2025).
4. A. Roy et al., Identification and characterization of PPARα ligands in the hippocampus. Nat Chem Biol 12, 1075-1083 (2016).
5. A. Roy et al., HMG-CoA Reductase Inhibitors Bind to PPARα to Upregulate Neurotrophin Expression in the Brain and Improve Memory in Mice. Cell Metab 22, 253-265 (2015).
6. A. Roy et al., Regulation of cyclic AMP response element binding and hippocampal plasticity-related genes by peroxisome proliferator-activated receptor α. Cell Rep 4, 724-737 (2013).
7. R. K. Paidi, S. Raha, A. Roy, K. Pahan, Muscle-building supplement β-hydroxy β-methylbutyrate binds to PPARα to improve hippocampal functions in mice. Cell Rep 42, 112717 (2023).
8. D. Patel et al., Aspirin binds to PPARα to stimulate hippocampal plasticity and protect memory. Proc Natl Acad Sci U S A 115, E7408-e7417 (2018).
9. S. B. Rangasamy et al., Selective disruption of TLR2-MyD88 interaction inhibits inflammation and attenuates Alzheimer's pathology. J Clin Invest128, 4297-4312 (2018).
10. T. Ali et al., Exploiting vitamin C as a prooxidant to activate ROS-responsive prodrugs for potent and selective tumor killing. Redox Biol 95, 104229 (2026).
Total Publications: 80
PubMed: https://pubmed.ncbi.nlm.nih.gov/?term=avik+roy
Google Scholar:
https://scholar.google.com.tr/citations?user=cLPRR20AAAAJ&hl=it
( h-index: 38 and i10 index: 58)
https://www.michaeljfox.org/grant/regulation-alpha-synucleinopathy-bpoz-2
Research Grants (As PI):