Professor MARIUSZ SACHARCZUK , PhD, DSc

Head of the Department of Experimental Genomics

Field of interest

genetics, neurobiology, hypertension and angiology, oncology

Scientific achievements

ca. 60 publications, 53 papers from the JCR list, including Pain, Addiction Biology, Neuropharmacology, Neuroscience. Author of the book ’Neurogeneza wieku dorosłego‘ (‘Adult neurogenesis’). Total citations ca. 330, including citations in Nature Reviews Cancer. Hirsch Index – 10.

ORCID: 0000-0002-6309-5292

Selected scientific achievements:

1. Demonstration that both the genetically determined, increased stress susceptibility and chronic environmental stress conditions constitute factors predisposing to increased chromosomal aberration frequency and DNA damage (identified with the micronucleus technique) especially in conditions that involve exposure to physical (γ rays) and chemical (mitomycin C) mutagens (Mutation Research, Animal Science Papers and Reports, Behavior Genetics). Moreover, it has been explained that HA mice apart from their enhanced stress and mutagen susceptibility, also show accelerated tumor growth after B16F0 implantation (Journal of Environmental Pathology, Toxicology and Oncology) especially in chronic stress conditions (CMS) (Stress).

2. Indication of the critical role of the δ-opioid receptor polymorphism affecting both endogenous and exogenous opioid. Moreover, we were the first to show that the magnitude of stress-induced analgesia is regulated by δ-opioid receptors (Pain). 

3. Identification of the differences in functional opioid receptor activity associated with G-protein activation as the leading cause for the divergent opioid sensitivity caused by selective breeding, was an important finding (Neuropharmacology). Additionally, divergent G-protein activity also determines cannabinoid system activity where its hyperactivity or dysfunction is related to pain sensitivity and progression of inflammatory processes (Neuroscience).

4. Determining the role of the opioid system and stress susceptibility in the pathogenesis of disorders associated with alcohol abuse, epilepsy or central nervous system (CNS) injuries and explaining the relationships between these disorders (Alcohol, Physiology & Behaviour, Acta Neurobiologiae Experimentalis, Addiction Biology). Moreover, a very important aspect of his research concerning the role of the opioid system in the pathomechanism of addiction, was evidencing the important role of δ-opioid receptors in this disorder. Moreover, the observation that opioid receptor antagonists show unfavourable effects in individuals with opioid system hyperactivity by triggering an uncontrollable increase in alcohol intake and preference accompanied by exacerbated neurodegeneration following CNS injury, was another breakthrough discovery (Neuropharmacology).

5. Demonstration that blood-brain barrier leakage is the main mechanism leading to a temporary decrease in alcohol consumption by suppression of β-endorphin release (Addiction Biology).

6. Demonstration that an increase in endogenous opioid system activity contributes to limiting side effects related to neurodegeneration, like memory and cognitive dysfunction after CNS injury. I have also confirmed the effectiveness of opioid receptor agonists against outcomes brought about by such injuries, whereas the use of opioid receptor antagonists in conditions where the opioid system is upregulated, leads not only to the aforementioned uncontrollable increase in alcohol intake and preference, but also to exacerbation of cognitive dysfunctions that accompany CNS injuries (Neuropharmacology, Behavioural & Brain Research).

7. Indication of a profound increase in epileptic thresholds in mice with upregulated opioid system activity compared to their counterparts showing opioid system dysfunction. Based on the results obtained, a new, innovative therapy featuring combined treatment with opioid receptor agonists and classical antieplieptic drugs was proposed (Annual Reports).

8. Demonstration that divergent endogenous opioid (EOS) and endocannabinoid (ECS) system (ECS) activity play important roles in the pathophysiology and progression of inflammatory and functional diseases. Thus, EOS and ECS modulation could become the novel target for the treatment of such disorders (Neurogastroenterology & Motility, British Journal of Pharmacology, Pharmacological Reports, Journal of Physiology and Pharmacology).

9. Development of a central nervous system protein hydrolysate and the assessment of its effectiveness in the therapy of neurodegenerative diseases, particularly Alzheimer's disease. Studies were conducted on a Tg(Thy1-APPLon)2Vln transgenic mouse model obtained by introduction of the human cDNA coding a 695 APP protein isoform carrying the London mutation (V642I - relative to APP695) into the mouse Thy1 gene that by altering cleavage of the APP protein, increases the amount of the 42-amino acid toxic β-amyloid isoform. The results obtained, proved the high therapeutic effectiveness of the designed preparation in preventing learning and memory impairments (Journal of Molecular Neuroscience, patent application: Nr.: WO2013098415-A1, Nr.: PL409386-A1).

Completed research projects

Coordinator of the OPUS project „The studies on the genetic background of depression in mice with using genetic markers and analysis of genes expression”

IGHZ Coordinator in the IGHZ-IMDIK-UM Lodz consortium joint project:  „Activity of the opioid system in the pathogenesis and therapy inflammatory bowel diseases in mice with high and low sensitivity to stress”

Participation in the project „ Red blood cell distribution width (RDW) as a risk factor of myocardial infarction and stroke” – Warsaw Medical University.

BASTION “From Basic to Translational Research in Oncology”

Organizational activity, dissemination and other

Author of the general public articles in ‘Neurologia i Neurochirurgia Polska’, ‘Prace i Materiały Zootechniczne’, ‘Kosmos’, ‘Wszechświat’, presenting scientific results at the Academic Internet Television Network (ATVN).  ATVN broadcasts were an important contribution to popularizing his scientific work by presenting the latest information on human adult neurogenesis. Participant on behalf of the scientific community in the government subcommittee regarding the medical use of cannabinoids. A member of the organizing committee of the 'Opioid Expert Group' at the Mossakowski Medical Research Centre Polish Academy of Sciences in Warsaw.

Selected publications and patents:1. Sacharczuk M (autor koresp.), Lesniak A, Korostynski M, Przewlocki R, Lipkowski A, Jaszczak K, Sadowski B. A polymorphism in exon 2 of the delta-opioid receptor affects nociception in response to specific agonists and antagonists in mice selectively bred for high and low analgesia. Pain 2010;149:506-513. Q1, IF 5.559, pkt. MNiSW 45.

2. Sacharczuk M (autor koresp.), Lesniak A, Lipkowski AW, Korostynski M, Przewlocki R, Sadowski B. Association between the A107V substitution in the δ-opioid receptors and ethanol drinking in mice selected for high and low analgesia. Addiction Biology. 2014;19(4):643-651. Q1, IF 5.578, pkt. MNiSW 40.

3. Lesniak A, Pick CG, Misicka A, Lipkowski AW, Sacharczuk M (autor koresp.). Biphalin protects against cognitive deficits in a mouse model of mild traumatic brain injury (mTBI). Neuropharmacology. 2016;101:506-518. Q1, IF 5.11, pkt. MNiSW 40.

4. Poznanski P, Lesniak A, Korostynski M, Szklarczyk K, Lazarczyk M, Religa P, Bujalska-Zadrozny M, Sadowski B, Sacharczuk M (autor koresp.). Delta-opioid receptor antagonism leads to excessive ethanol consumption in mice with enhanced activity of the endogenous opioid system. Neuropharmacology. 2017;118:90-101. Q1; IF 5.012; pkt. MNiSW 40.

5. Poznanski P, Lesniak A, Korostynski M, Sacharczuk M (autor koresp.). Ethanol consumption following mild traumatic brain injury is related to the blood-brain barrier permeability. Addiction Biology. 2018; 25(1):e12683. Q1, IF 5.578,  pkt. MNiSW 40.

6. Salaga M, Polepally PR, Zielinska M, Marynowski M, Fabisiak A, Murawska N, Sobczak K, Sacharczuk M, Do Rego JC, Roth BL, Zjawiony JK, Fichna J. 2015. Salvinorin A analogues PR-37 and PR-38 attenuate compound 48/80-induced itch responses in mice. Br J Pharmacol. 172: 4331-4341. IF 5.491

 7. Patent: Lang B, Lipkowski AW, Sacharczuk M, Salinska E. 2013 Enzymatic hydrolysate of proteins of animal tissue of nervous system for use in treatment of memory disorders. NAPCO SARL. Patent no. WO2013098415-A1.

8. Patent: “Oleacein for treating or preventing diseases resulting from atherosclerotic plaques” nr patentu US 9.682.056 B2, EU “Use of oleacein, particularly from Ligustrum vulgare L.” –EP 13742600.3, PCT/IB2014/001940, P.413385, EP 15460037

Links to professional profiles (e.g. Research Gate, Scopus, Linkedin), do not include links to private profiles (e.g. Facebook) 

https://www.researchgate.net/profile/Mariusz_Sacharczuk

https://www-1scopus-1com-1000028yk05d0.han3.wum.edu.pl/authid/detail.uri?authorId=6506134744

https://www.linkedin.com/in/mariusz-sacharczuk-63a21661/