@article{MTMT:34780914,
	title = {Disease Modifying Strategies in Multiple Sclerosis: New Rays of Hope to Combat Disability?},
	url = {https://m2.mtmt.hu/api/publication/34780914},
	author = {Bellanca, C.M. and Augello, E. and Mariottini, A. and Bonaventura, G. and La, Cognata V. and Di, Benedetto G. and Cantone, A.F. and Attaguile, G. and Di, Mauro R. and Cantarella, G. and Massacesi, L. and Bernardini, R.},
	doi = {10.2174/1570159X22666240124114126},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34780914},
	issn = {1570-159X},
	abstract = {multiple sclerosis (MS) is the most prevalent chronic autoimmune inflammatory- demyelinating disorder of the central nervous system (CNS). It usually begins in young adulthood, mainly between the second and fourth decades of life. Usually, the clinical course is characterized by the involvement of multiple CNS functional systems and by different, often overlapping phenotypes. In the last decades, remarkable results have been achieved in the treatment of MS, particularly in the relapsing-remitting (RRMS) form, thus improving the long-term outcome for many patients. As deeper knowledge of MS pathogenesis and respective molecular targets keeps growing, nowadays, several lines of disease-modifying treatments (DMT) are available, an impressive change compared to the relative poverty of options available in the past. Current MS management by DMTs is aimed at reducing relapse frequency, ameliorating symptoms, and preventing clinical disability and progression. Notwithstanding the relevant increase in pharmacological options for the management of RRMS, research is now increasingly pointing to identify new molecules with high efficacy, particularly in progressive forms. Hence, future efforts should be concentrated on achieving a more extensive, if not exhaustive, understanding of the pathogenetic mechanisms underlying this phase of the disease in order to characterize novel molecules for therapeutic intervention. The purpose of this review is to provide a compact overview of the numerous currently approved treatments and future innovative approaches, including neuroprotective treatments as anti-LINGO-1 monoclonal antibody and cell therapies, for effective and safe management of MS, potentially leading to a cure for this disease. © 2024, Bentham Science Publishers. All rights reserved.},
	keywords = {THROMBOCYTOPENIA; VIRUS INFECTION; Pathogenesis; Stem Cells; review; human; heart disease; azathioprine; HYPERTENSION; nuclear magnetic resonance imaging; disease course; central nervous system disease; fatigue; ANEMIA; vascular disease; urticaria; dizziness; drug safety; drug efficacy; interleukin 6; Clinical Trials; vomiting; headache; coughing; bradycardia; flushing; autoimmune disease; MULTIPLE SCLEROSIS; MULTIPLE SCLEROSIS; neuroprotection; disability; URINARY TRACT INFECTION; rituximab; bacterial infection; backache; drug administration; diarrhea; lymphoproliferative disease; neutropenia; rheumatoid arthritis; demyelination; mental disease; nausea and vomiting; blood brain barrier; Melanoma; patient safety; eye disease; off label drug use; B7 antigen; dyspepsia; abdominal pain; INFLUENZA; upper respiratory tract infection; injection site reaction; lymphocytopenia; arthralgia; alemtuzumab; CD52 antigen; cell therapy; nervous system inflammation; thyroid cancer; randomized controlled trial (topic); teriflunomide; rhinopharyngitis; Epstein Barr virus infection; ocrelizumab; fingolimod; Rac1 protein; hypertransaminasemia; natalizumab; dimethyl fumarate; DISEASE-MODIFYING THERAPIES; siponimod; ozanimod; ofatumumab; dihydroorotate dehydrogenase; Bruton tyrosine kinase; Approved drugs; ponesimod; melanoma in situ; immunoglobulin M deficiency; malignant catarrhal fever; Future perspective; beta1b interferon; off-label treatments; autoimmune inflammatory demyelinating disorder; autoimmune inflammatory demyelinating disorder; disease modifying strategy},
	year = {2024},
	eissn = {1875-6190},
	pages = {1286-1326}
}

@article{MTMT:34740498,
	title = {Antioxidants, Hormetic Nutrition, and Autism},
	url = {https://m2.mtmt.hu/api/publication/34740498},
	author = {Modafferi, S. and Lupo, G. and Tomasello, M. and Rampulla, F. and Ontario, M. and Scuto, M. and Salinaro, A.T. and Arcidiacono, A. and Anfuso, C.D. and Legmouz, M. and Azzaoui, F.-Z. and Palmeri, A. and Spano', S. and Biamonte, F. and Cammilleri, G. and Fritsch, T. and Sidenkova, A. and Calabrese, E. and Wenzel, U. and Calabrese, V.},
	doi = {10.2174/1570159X21666230817085811},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34740498},
	issn = {1570-159X},
	abstract = {Autism spectrum disorder (ASD) includes a heterogeneous group of complex neurodevel-opmental disorders characterized by atypical behaviors with two core pathological manifestations: def-icits in social interaction/communication and repetitive behaviors, which are associated with disturbed redox homeostasis. Modulation of cellular resilience mechanisms induced by low levels of stressors represents a novel approach for the development of therapeutic strategies, and in this context, neuropro-tective effects of a wide range of polyphenol compounds have been demonstrated in several in vitro and in vivo studies and thoroughly reviewed. Mushrooms have been used in traditional medicine for many years and have been associated with a long list of therapeutic properties, including antitumor, immunomodulatory, antioxidant, antiviral, antibacterial, and hepatoprotective effects. Our recent studies have strikingly indicated the presence of polyphenols in nutritional mushrooms and demonstrated their protective effects in different models of neurodegenerative disorders in humans and rats. Alt-hough their therapeutic effects are exerted through multiple mechanisms, increasing attention is focus-ing on their capacity to induce endogenous defense systems by modulating cellular signaling processes such as nuclear factor erythroid 2 related factor 2 (Nrf2) and nuclear factor-kappa B (NF-κB) path-ways. Here we discuss the protective role of hormesis and its modulation by hormetic nutrients in ASD. © 2024 Bentham Science Publishers.},
	keywords = {PATHOPHYSIOLOGY; antioxidants; review; human; ANTIOXIDANT; nonhuman; autism; RNA Interference; NUTRITION; interleukin 6; Catalase; Tumor Necrosis Factor; Superoxide dismutase; reactive oxygen metabolite; nerve growth factor; heat shock protein 70; brain derived neurotrophic factor; Hormesis; Hormesis; sirtuin 1; oxidation reduction potential; Caenorhabditis elegans; interleukin 1beta; blood brain barrier; interleukin 8; heme oxygenase 1; interleukin 1; intestine flora; interleukin 18; mitochondrial membrane potential; brain derived neurotrophic factor receptor; glycogen synthase kinase 3beta; C. ELEGANS; Mushrooms; transcription factor Nrf2; lipoxin A; Omics; Pi3K/Akt signaling; Autism spectrum disorders; antioxidant responsive element; Brain-gut axis; FECAL MICROBIOTA TRANSPLANTATION; kelch like ECH associated protein 1; interleukin 37; Trametes versicolor; vitagenes; Hericium erinaceus; canonical Wnt signaling; Nrf2 signaling; Oxidative stress; NF kB signaling; redoxomics},
	year = {2024},
	eissn = {1875-6190},
	pages = {1156-1168}
}

@article{MTMT:34751506,
	title = {The Interplay between Meningeal Lymphatic Vessels and Neuroinflammation in Neurodegenerative Diseases},
	url = {https://m2.mtmt.hu/api/publication/34751506},
	author = {Chen, J. and Pan, Y. and Liu, Q. and Li, G. and Chen, G. and Li, W. and Zhao, W. and Wang, Q.},
	doi = {10.2174/1570159X21666221115150253},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34751506},
	issn = {1570-159X},
	year = {2024},
	eissn = {1875-6190},
	pages = {1016-1032}
}

@article{MTMT:34603630,
	title = {Deciphering the Metabolome under Stress: Insights from Rodent Models},
	url = {https://m2.mtmt.hu/api/publication/34603630},
	author = {Papageorgiou, Maria P. and Theodoridou, Daniela and Nussbaumer, Markus and Syrrou, Maria and Filiou, Michaela D.},
	doi = {10.2174/1570159X21666230713094843},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34603630},
	issn = {1570-159X},
	abstract = {Despite intensive research efforts to understand the molecular underpinnings of psychological stress and stress responses, the underlying molecular mechanisms remain largely elusive. Towards this direction, a plethora of stress rodent models have been established to investigate the effects of exposure to different stressors. To decipher affected molecular pathways in a holistic manner in these models, metabolomics approaches addressing altered, small molecule signatures upon stress exposure in a high-throughput, quantitative manner provide insightful information on stress-induced systemic changes in the brain. In this review, we discuss stress models in mice and rats, followed by mass spectrometry (MS) and nuclear magnetic resonance (NMR) metabolomics studies. We particularly focus on acute, chronic and early life stress paradigms, highlight how stress is assessed at the behavioral and molecular levels and focus on metabolomic outcomes in the brain and peripheral material such as plasma and serum. We then comment on common metabolomics patterns across different stress models and underline the need for unbiased -omics methodologies and follow-up studies of metabolomics outcomes to disentangle the complex pathobiology of stress and pertinent psychopathologies.},
	keywords = {MICE; Mass spectrometry; RESTRAINT STRESS; metabolomics; Chronic stress; acute stress; early life stress; Social defeat},
	year = {2024},
	eissn = {1875-6190},
	pages = {884-903}
}

@article{MTMT:34589005,
	title = {Neurotensin and Neurotensin Receptors in Stress-related Disorders: Pathophysiology & Novel Drug Targets},
	url = {https://m2.mtmt.hu/api/publication/34589005},
	author = {Kyriatzis, Grigorios and Khrestchatisky, Michel and Ferhat, Lotfi and Chatzaki, Ekaterini Alexiou},
	doi = {10.2174/1570159X21666230803101629},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34589005},
	issn = {1570-159X},
	abstract = {Neurotensin (NT) is a 13-amino acid neuropeptide widely distributed in the CNS that has been involved in the pathophysiology of many neural and psychiatric disorders. There are three known neurotensin receptors (NTSRs), which mediate multiple actions, and form the neurotensinergic system in conjunction with NT. NTSR1 is the main mediator of NT, displaying effects in both the CNS and the periphery, while NTSR2 is mainly expressed in the brain and NTSR3 has a broader expression pattern. In this review, we bring together up-to-date studies showing an involvement of the neurotensinergic system in different aspects of the stress response and the main stress-related disorders, such as depression and anxiety, post-traumatic stress disorder (PTSD) and its associated symptoms, such as fear memory and maternal separation, ethanol addiction, and substance abuse. Emphasis is put on gene, mRNA, and protein alterations of NT and NTSRs, as well as behavioral and pharmacological studies, leading to evidence-based suggestions on the implicated regulating mechanisms as well as their therapeutic exploitation. Stress responses and anxiety involve mainly NTSR1, but also NTSR2 and NTSR3. NTSR1 and NTSR3 are primarily implicated in depression, while NTSR2 and secondarily NTSR1 in PTSD. NTSR1 is interrelated with substance and drug abuse and NTSR2 with fear memory, while all NTSRs seem to be implicated in ethanol consumption. Some of the actions of NT and NTSRs in these pathological settings may be driven through interactions between NT and corticotrophin releasing factor (CRF) in their regulatory contribution, as well as by NT's pro-inflammatory mediating actions.},
	keywords = {NEUROTENSIN; STRESS; DEPRESSION; anxiety; substance abuse; PTSD; fear memory; ethanol addiction},
	year = {2024},
	eissn = {1875-6190},
	pages = {916-934}
}

@article{MTMT:34584953,
	title = {The HPA Axis as Target for Depression},
	url = {https://m2.mtmt.hu/api/publication/34584953},
	author = {Menke, Andreas},
	doi = {10.2174/1570159X21666230811141557},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34584953},
	issn = {1570-159X},
	abstract = {Major depressive disorder (MDD) is a stress-related mental disorder with a lifetime prevalence of 20% and, thus, is one of the most prevalent mental health disorders worldwide. Many studies with a large number of patients support the notion that abnormalities of the hypothalamus-pituitary-adrenal (HPA) axis are crucial for the development of MDD. Therefore, a number of strategies and drugs have been investigated to target different components of the HPA axis: 1) corticotrophin-releasing hormone (CRH) 1 receptor antagonists; 2) vasopressin V1B receptor antagonists, 3) glucocorticoid receptor antagonists, and 4) FKBP5 antagonists. Until now, V1B receptor antagonists and GR antagonists have provided the most promising results. Preclinical data also support antagonists of FKBP5, which seem to be partly responsible for the effects exerted by ketamine. However, as HPA axis alterations occur only in a subset of patients, specific treatment approaches that target only single components of the HPA axis will be effective only in this subset of patients. Companion tests that measure the function of the HPA axis and identify patients with an impaired HPA axis, such as the dexamethasone-corticotrophin-releasing hormone (dex-CRH) test or the molecular dexamethasone-suppression (mDST) test, may match the patient with an effective treatment to enable patient-tailored treatments in terms of a precision medicine approach.},
	keywords = {GLUCOCORTICOID RECEPTOR; VASOPRESSIN; STRESS; DEPRESSION; Biomarkers; HPA axis; Antidepressants; V-1B RECEPTOR ANTAGONIST; Precision Medicine; FKBP5; CRH1; SSR149415},
	year = {2024},
	eissn = {1875-6190},
	pages = {904-915}
}

@article{MTMT:34567009,
	title = {Epigenetics of Fear, Anxiety and Stress – Focus on Histone Modifications},
	url = {https://m2.mtmt.hu/api/publication/34567009},
	author = {Ell, M.A. and Schiele, M.A. and Iovino, N. and Domschke, K.},
	doi = {10.2174/1570159X21666230322154158},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34567009},
	issn = {1570-159X},
	abstract = {Fear-, anxiety-and stress-related disorders are among the most frequent mental disorders. Given substantial rates of insufficient treatment response and often a chronic course, a better understanding of the pathomechanisms of fear-, anxiety-and stress-related disorders is urgently warranted. Epigenetic mechanisms such as histone modifications-positioned at the interface between the biolog-ical and the environmental level in the complex pathogenesis of mental disorders-might be highly in-formative in this context. The current state of knowledge on histone modifications, chromatin-related pharmacology and animal models modified for genes involved in the histone-related epigenetic machinery will be reviewed with respect to fear-, anxiety-and stress-related states. Relevant studies, pub-lished until 30th June 2022, were identified using a multi-step systematic literature search of the Pub-Med and Web of Science databases. Animal studies point towards histone modifications (e.g., H3K4me3, H3K9me1/2/3, H3K27me2/3, H3K9ac, H3K14ac and H4K5ac) to be dynamically and mostly brain region-, task-and time-dependently altered on a genome-wide level or gene-specifically (e.g., Bdnf) in models of fear conditioning, retrieval and extinction, acute and (sub-)chronic stress. Singular and underpowered studies on histone modifications in human fear-, anxiety-or stress-related phenotypes are currently restricted to the phenotype of PTSD. Provided consistent validation in human phenotypes, epigenetic biomarkers might ultimately inform indicated preventive interventions as well as personalized treatment approaches, and could inspire future innovative pharmacological treatment options targeting the epigenetic machinery improving treatment response in fear-, anxiety-and stress-related disorders. © 2024 Bentham Science Publishers.},
	keywords = {STRESS; Chromatin; anxiety; Histone; BDNF; fear; epigenetics; HDAC},
	year = {2024},
	eissn = {1875-6190},
	pages = {843-865}
}

@article{MTMT:34573632,
	title = {Interaction of Brain-derived Neurotrophic Factor, Exercise, and Fear Extinction: Implications for Post-traumatic Stress Disorder},
	url = {https://m2.mtmt.hu/api/publication/34573632},
	author = {Antolasic, E.J. and Jaehne, E.J. and van, den Buuse M.},
	doi = {10.2174/1570159X21666230724101321},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34573632},
	issn = {1570-159X},
	abstract = {Brain-Derived Neurotrophic Factor (BDNF) plays an important role in brain development, neural plasticity, and learning and memory. The Val66Met single-nucleotide polymorphism is a com-mon genetic variant that results in deficient activity-dependent release of BDNF. This polymorphism and its impact on fear conditioning and extinction, as well as on symptoms of post-traumatic stress disorder (PTSD), have been of increasing research interest over the last two decades. More recently, it has been demonstrated that regular physical activity may ameliorate impairments in fear extinction and alleviate symptoms in individuals with PTSD via an action on BDNF levels and that there are differential responses to exercise between the Val66Met genotypes. This narrative literature review first de-scribes the theoretical underpinnings of the development and persistence of intrusive and hypervigi-lance symptoms commonly seen in PTSD and their treatment. It then discusses recent literature on the involvement of BDNF and the Val66Met polymorphism in fear conditioning and extinction and its involvement in PTSD diagnosis and severity. Finally, it investigates research on the impact of physical activity on BDNF secretion, the differences between the Val66Met genotypes, and the effect on fear extinction learning and memory and symptoms of PTSD. © 2024 Bentham Science Publishers.},
	keywords = {STRESS; Exercise; Brain-Derived Neurotrophic Factor; Anxiety Disorders; Post-Traumatic Stress Disorder; Val66Met},
	year = {2024},
	eissn = {1875-6190},
	pages = {543-556}
}

@article{MTMT:34619131,
	title = {The Translational Future of Stress Neurobiology and Psychosis Vulnerability: A Review of the Evidence},
	url = {https://m2.mtmt.hu/api/publication/34619131},
	author = {Cullen, Alexis E. and Labad, Javier and Oliver, Dominic and Al-Diwani, Adam and Minichino, Amedeo and Fusar-Poli, Paolo},
	doi = {10.2174/1570159X21666230322145049},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34619131},
	issn = {1570-159X},
	abstract = {Psychosocial stress is a well-established risk factor for psychosis, yet the neurobiological mechanisms underlying this relationship have yet to be fully elucidated. Much of the research in this field has investigated hypothalamic-pituitary-adrenal (HPA) axis function and immuno-inflammatory processes among individuals with established psychotic disorders. However, as such studies are limited in their ability to provide knowledge that can be used to develop preventative interventions, it is important to shift the focus to individuals with increased vulnerability for psychosis (i.e., high-risk groups). In the present article, we provide an overview of the current methods for identifying individuals at high-risk for psychosis and review the psychosocial stressors that have been most consistently associated with psychosis risk. We then describe a network of interacting physiological systems that are hypothesised to mediate the relationship between psychosocial stress and the manifestation of psychotic illness and critically review evidence that abnormalities within these systems characterise high-risk populations. We found that studies of high-risk groups have yielded highly variable findings, likely due to (i) the heterogeneity both within and across high-risk samples, (ii) the diversity of psychosocial stressors implicated in psychosis, and (iii) that most studies examine single markers of isolated neurobiological systems. We propose that to move the field forward, we require well-designed, large-scale translational studies that integrate multi-domain, putative stress-related biomarkers to determine their prognostic value in high-risk samples. We advocate that such investigations are highly warranted, given that psychosocial stress is undoubtedly a relevant risk factor for psychotic disorders.},
	keywords = {SCHIZOPHRENIA; Cytokines; CORTISOL; clinical high-risk; Precision psychiatry; gut-microbiome},
	year = {2024},
	eissn = {1875-6190},
	pages = {350-377}
}

@article{MTMT:34610061,
	title = {Stress, Environment and Early Psychosis},
	url = {https://m2.mtmt.hu/api/publication/34610061},
	author = {Xenaki, Lida-Alkisti and Dimitrakopoulos, Stefanos and Selakovic, Mirjana and Stefanis, Nikos},
	doi = {10.2174/1570159X21666230817153631},
	journal-iso = {CURR NEUROPHARMACOL},
	journal = {CURRENT NEUROPHARMACOLOGY},
	volume = {22},
	unique-id = {34610061},
	issn = {1570-159X},
	abstract = {Existing literature provides extended evidence of the close relationship between stress dysregulation, environmental insults, and psychosis onset. Early stress can sensitize genetically vulnerable individuals to future stress, modifying their risk for developing psychotic phenomena. Neurobiological substrate of the aberrant stress response to hypothalamic-pituitary-adrenal axis dysregulation, disrupted inflammation processes, oxidative stress increase, gut dysbiosis, and altered brain signaling, provides mechanistic links between environmental risk factors and the development of psychotic symptoms. Early-life and later-life exposures may act directly, accumulatively, and repeatedly during critical neurodevelopmental time windows. Environmental hazards, such as pre- and perinatal complications, traumatic experiences, psychosocial stressors, and cannabis use might negatively intervene with brain developmental trajectories and disturb the balance of important stress systems, which act together with recent life events to push the individual over the threshold for the manifestation of psychosis. The current review presents the dynamic and complex relationship between stress, environment, and psychosis onset, attempting to provide an insight into potentially modifiable factors, enhancing resilience and possibly influencing individual psychosis liability.},
	keywords = {STRESS; Environment; first-episode psychosis; Hypothalamic-pituitary-adrenal; psychosocial stressors; Psychosis onset},
	year = {2024},
	eissn = {1875-6190},
	pages = {437-460}
}