Researcher: Prof. Dr. Michael Maes

Prof. Dr. Michael Maes is appointed senior researcher at the Research Institute and Guest Professor in the Department of Psychiatry, Medical University-Plovdiv. He is translational scientist whose research includes epidemiological and clinical investigations, case-control studies, pharmaceutical trials, as well as rodent and molecular experiments.
Dr. Maes is since 2003 a highly cited author (ISI, Thomson Reuters) with a H-index >140 and > 78.000 citations and is listed in the Webometrics Ranking of World Universities as one of the Top Scientists (2016). He is ranked worldwide #1 in CFS, #1 in oxidative stress,
#1 in encephalomyelitis, #1 in nitrosative stress, #1 in nitrosation, #1 in tryptophan, #2 in bacterial translocation, #2 in stress, physiological, #3 in inflammation, #2 in neuroimmune, #5 in depression, #4 in fatigue, #4 in psychiatry, #7 in depressive disorder, #7 in melancholia, #7 in affective disorders, #7 in mood disorders, #9 in cytokines (Bibliometric Website Expertscape, September 2022). He published more than 950 scientific papers in peer-reviewed international journals and gave more than 300 invited lectures at different international symposia. His work has been published in peer-reviewed journals, including Molecular Psychiatry, Molecular Neurobiology, Acta Psychiatrica Scandinavica, Psychiatry Research, Biological Psychiatry, Neuropsychobiology, BMC Medicine, Neuroscience & Biobehavioral Reviews, Journal of Affective Disorders.
The work of Dr. Maes covers the supra-multi-disciplinary field of “pathway and drug discovery processes” in neuro-psychiatric disorders. Dr. Maes's research is focused on biomarkers and pathways of psychiatric disorders, such as major depression, chronic fatigue syndrome, bipolar disorder and schizophrenia, and (neuro-)immune disorders, including Parkinson’s disorder, multiple sclerosis, lupus erythematosus, stroke, rheumatoid arthritis and Alzheimer’s disease.
Dr. Maes discovered that “clinical depression” is a systemic illness characterized by peripheral a) increases in pro-inflammatory cytokine levels, an acute phase response; b) cell-mediated immune (CMI) activation; c) lowered omega-3 PUFA levels; d) lowered plasma tryptophan, which determines brain serotonin contents and is an inflammatory sequel; and e) IFNα-induced depression is associated with increased synthesis of neurotoxic tryptophan catabolites.
Other ground-breaking discoveries were that psychological stressors may cause immune activation, inflammation and Th1 responses in humans; gut-derived inflammation is a new pathway in depression and ME/CFS; chronic apical periodontitis-derived oxidative stress plays a role in depression; increased oxidative and nitrosative stress at the end of pregnancy is associated with the onset of perinatal depression; deficit schizophrenia is an immune disorder with specific deficits in the innate immune system, which is associated with specific neurocognitive impairments; and stress-related disorders are associated with nitrosative stress and autoimmunity secondary to oxidative and nitrosative stress. The work of Dr. Maes not only showed the role of vulnerability or risk factors (e.g. lower dipeptidyl peptidase IV and prolyl endopeptidase and lowered anti-cytokines, e.g. CC16), but also gene pathways that increase the risk to develop depression following stressors.
In 1995, Maes et al. also launched the monocyte-T lymphocyte theory of schizophrenia considering that activated immuno-inflammatory pathways may account for the higher neurodevelopmental pathology linked with gestational infections through the detrimental effects of activated microglia, oxidative and nitrosative stress, cytokine-induced activation of the tryptophan catabolite pathway and consequent modulation of the NMDAR. Recently, he discovered that deficit schizophrenia is an immune disorder.
Dr. Maes also defined biomarkers of staging of depression, bipolar disorder and schizophrenia, e.g. single nucleotide polymorphisms in inflammatory and O&NS genes and lowered antioxidant and increased cytokine levels predicting treatment nonresponse or recurrence. His translational work showed that antidepressants and mood stabilizers have negative immunoregulatory effects.
The clinical and translational work of Dr. Maes contributed to the delineation of new drug targets in depression thereby opening the way to novel treatments of psychiatric disorders, such as ω3-PUFAs, antioxidants, curcumin, anti-inflammatory compounds, minocycline, etc.