@article{MTMT:34417253, title = {Personality traits and psychological complaints under patients suffering from headaches}, url = {https://m2.mtmt.hu/api/publication/34417253}, author = {Hal, Melinda and Hal, Viktor and Vécsei, László and Balog, Anna and Majláth, Zsófia and Tajti, János and Ertsey, Csaba and Bozsik, György and Zsombók, Terézia Ibolya and Purebl, György}, doi = {10.18071/isz.76.0385}, journal-iso = {IDEGGYOGY SZEMLE}, journal = {IDEGGYOGYASZATI SZEMLE / CLINICAL NEUROSCIENCE}, volume = {76}, unique-id = {34417253}, issn = {0019-1442}, abstract = {Background and purpose – Although headaches are often comorbid with psychological symptoms, the underlying psychological processes, e.g. the role of personality dimensions as headache determinants remains unclear. Studies found associations between headaches and various personality traits; according to the Big Five model of personality, persons suffering from headaches exhibit a higher rate in neuroticism, while a lower rate in extraversion, openness to experiences and positive emotions. This is the first study to clarify the associations among duration, intensity, and frequency of headaches and personality dimensions. Through this study we could get into the personality dimensions in the background of pain experience and that which personality dimensions bear a part in the behaviour of the persons, who suffered from headache, but do not seek treatment through this complaint. Methods – Treated (Group1) and untreated (Group2) headache patients and healthy controls (Group3) were investigated (total of 360 participants). The main headache components of intensity, duration, and frequency were used as dependent variables with personality dimensions in the Big Five concept investigated by the NEO-PI-R Personality Inventory. Results – Employing multiple regression analysis, facets of personality described 14.7% of headache intensity, 10.9 % of duration, and 18.7 % of frequency variance. Group1 and Group2 reached significantly higher values on the dimension of anxiety, depression, and vulnerability to stress than Group3. Group1 showed a significantly higher value on trust personality dimension than Group3 and Group2. Group3 exhibited a significantly higher value in the trust dimension than Group2. Concerning vulnerability to stress, the highest value was yielded by the “treated and suffering from headaches” group and there was a significant difference also with the “untreated and suffering from headaches” group and with the control group. In this dimension, the “untreated and suffering from headaches” group’s point value was significantly higher than the control group’s (p<0.01, U=-4.501). Conclusion – Our study demonstrates that the three headache components are not independent from personality traits, and personality traits may interact with treatment seeking behavior even in the presence of significant headache complaints. The role of the personality traits are significant in the intensity, duration and frequency of headaches.}, year = {2023}, eissn = {2498-6208}, pages = {385-393}, orcid-numbers = {Vécsei, László/0000-0001-8037-3672; Tajti, János/0000-0003-0857-5266; Ertsey, Csaba/0000-0003-3288-1941; Bozsik, György/0000-0001-5865-1162; Zsombók, Terézia Ibolya/0000-0002-7535-0465; Purebl, György/0000-0002-9750-2001} } @{MTMT:33665496, title = {Neuroprotection by Kynurenine Metabolites}, url = {https://m2.mtmt.hu/api/publication/33665496}, author = {Majláth, Zsófia and Szalárdy, Levente and Zádori, Dénes and Klivényi, Péter and Fülöp, Ferenc and Toldi, József and Vécsei, László}, booktitle = {Handbook of Neurotoxicity}, doi = {10.1007/978-3-031-15080-7_165}, unique-id = {33665496}, year = {2023}, pages = {1067-1080}, orcid-numbers = {Szalárdy, Levente/0000-0002-1084-6195; Zádori, Dénes/0000-0003-0749-7980; Klivényi, Péter/0000-0002-5389-3266; Fülöp, Ferenc/0000-0003-1066-5287; Toldi, József/0000-0001-7355-0503; Vécsei, László/0000-0001-8037-3672} } @article{MTMT:31040417, title = {The effect of psychiatric comorbidities and stress-coping strategies on perceived quality of life in migraine.}, url = {https://m2.mtmt.hu/api/publication/31040417}, author = {Petrovics-Balog, Anna and Majláth, Zsófia and Lukács, Melinda and Holczer, Adrienn and Must, Anita and Tajti, János and Vécsei, László}, doi = {10.18071/isz.72.0397}, journal-iso = {IDEGGYOGY SZEMLE}, journal = {IDEGGYOGYASZATI SZEMLE / CLINICAL NEUROSCIENCE}, volume = {72}, unique-id = {31040417}, issn = {0019-1442}, abstract = {Migraine is one of the most disabling primary headache conditions. We aimed to detect hidden symptoms of anxiety and depression and to survey stress-coping mechanisms and related quality of life in a large migraine population without any known psychiatric comorbidity.123 migraine patients (MG) and 66 healthy subjects (HC) completed the Beck Depression Inventory-II (BDI-II), the State and Trait Anxiety Inventory (S-STAI and T-STAI), the Stress and Coping Inventory (SCI) and the 36-Item Short Form Health Survey (SF-36).MG patients reached significantly higher scores on the BDI-II and the T-STAI yielding previously undetected anxiety and depression symptoms. Significant differences were present on the SCI: higher stress scores and lower coping levels suggested impaired stress-coping strategies in migraine. MG patients achieved significantly lower scores on most of SF-36 subscales indicating lower perceived quality of life. Significant correlations were found between BDI-II, T-STAI, SCI scores and subscales of the SF-36.Unrecognized symptoms of anxiety and depression, as well as less effective stress-coping strategies might be related to the lower perceived quality of life in migraine. The screening of these symptoms might lead to more focused and efficient therapeutic strategies. Addressing stress management techniques could improve quality of life on the long-term.}, keywords = {MIGRAINE; Quality of Life; Comorbidity; stress-coping}, year = {2019}, eissn = {2498-6208}, pages = {397-404}, orcid-numbers = {Tajti, János/0000-0003-0857-5266; Vécsei, László/0000-0001-8037-3672} } @article{MTMT:3371556, title = {Kynurenine system and multiple sclerosis, pathomechanism and drug targets with an emphasis on laquinimod}, url = {https://m2.mtmt.hu/api/publication/3371556}, author = {Majláth, Zsófia and Annus, Ádám and Vécsei, László}, doi = {10.2174/1389450117666161223125417}, journal-iso = {CURR DRUG TARGETS}, journal = {CURRENT DRUG TARGETS}, volume = {19}, unique-id = {3371556}, issn = {1389-4501}, abstract = {Multiple sclerosis is a common chronic, disabling autoimmune neurological disease affecting mainly young adults. In its pathomechanism, neurodegenerative and acute inflammatory characteristics are both involved. Disease-modifying therapies aim to reduce relapse-rate and slow down the deterioration in neurological functions. The currently available therapies fail to exert neuroprotective effects and most of them are associated with potentially toxic side-effects, therefore, ongoing research aims to develop novel drug candidates to cover these therapeutic gaps. The kynurenine pathway has been implicated in both the physiological processes of the central nervous system and in the pathomechanism of several neurological disorders as well. Alterations of the kynurenine pathway metabolites have been detected in multiple sclerosis and a number of potential therapeutic targets related to this metabolic route have been already identified. Laquinimod is a quinoline carboxamide showing structural similarities with kynurenic acid, which proved to have beneficial effects on reduction of brain atrophy and disability progression. The kynurenine pathway is therefore a promising target for the development of future drugs for the treatment of autoimmune diseases such as multiple sclerosis.}, keywords = {IN-VITRO; CEREBROSPINAL-FLUID; NEUROTROPHIC FACTOR; T-CELLS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE SCLEROSIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; QUINOLINIC ACID; neuroprotection; neuroinflammation; kynurenine system; TRYPTOPHAN-METABOLISM; laquinimod; THERAPEUTIC STRATEGIES; ORAL LAQUINIMOD}, year = {2018}, eissn = {1873-5592}, pages = {805-814}, orcid-numbers = {Annus, Ádám/0000-0003-0498-6578; Vécsei, László/0000-0001-8037-3672} } @{MTMT:31890251, title = {Sustained release nanocomposite, a process for producing the same and use thereof}, url = {https://m2.mtmt.hu/api/publication/31890251}, author = {Dékány, Imre and Krizbai, István and Majláth, Zsófia and Toldi, József and Varga, Noémi and Vécsei, László}, unique-id = {31890251}, year = {2017}, orcid-numbers = {Dékány, Imre/0000-0001-5472-5355; Toldi, József/0000-0001-7355-0503; Vécsei, László/0000-0001-8037-3672} } @{MTMT:3277014, title = {Neurológiai betegségek klinikai vonatkozásai}, url = {https://m2.mtmt.hu/api/publication/3277014}, author = {Tajti, János and Szok, Délia and Vécsei, László and Vörös, Erika Sarolta and Gárdián, Gabriella and Majláth, Zsófia}, booktitle = {Neurológia a betegágynál}, unique-id = {3277014}, year = {2017}, pages = {77-146}, orcid-numbers = {Tajti, János/0000-0003-0857-5266; Vécsei, László/0000-0001-8037-3672} } @article{MTMT:3253312, title = {Treatment possibilities for psychosis in parkinson's disease with an emphasis on the newly approved drug: pimavanserin}, url = {https://m2.mtmt.hu/api/publication/3253312}, author = {Majláth, Zsófia and Obál, Izabella and Vécsei, László}, doi = {10.2174/1871527315666161006104347}, journal-iso = {CNS NEUROL DISORD-DR}, journal = {CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS}, volume = {16}, unique-id = {3253312}, issn = {1871-5273}, abstract = {Parkinson's disease (PD) is a progressive neurodegenerative disorder with prominent motor and non-motor symptoms. Psychosis develops in over 40% of PD patients and it is one of the most distressing symptoms for patients and caregivers alike. Until recently, atypical antipsychotics, clozapine and quetiapine were used to treat psychotic symptoms, but treatment was associated with substantial concerns for side-effects of clozapine and unfounded efficacy for quetiapine. Extensive research has shown that the antipsychotic effect of these drugs could be attributed to serotonin 2a receptor (5-HT2A) triggered mechanisms. A selective 5-HT2A inverse agonist, pimavanserin, has been developed, investigated and has gained approval in April 2016 in the US for the treatment of hallucinations and delusions in PD. In this review we primarily focus on psychosis in PD, the current treatment possibilities and the new, emerging therapy, pimavanserin, a selective 5-HT2A inverse agonist. All articles were reviewed in this topic and indexed in PubMed with keywords: Parkinson's disease psychosis, serotonin 2a receptor inverse agonist, clozapine, quetiapine, pimavanserin.}, keywords = {CLOZAPINE; HEALTHY-VOLUNTEERS; quetiapine; Anxiety Disorders; INCREASED RISK; NONMOTOR SYMPTOMS; RETROSPECTIVE COHORT; ATYPICAL ANTIPSYCHOTIC-DRUGS; 5-HT2A RECEPTORS; VISUAL HALLUCINATIONS; DOPAMINE-D-2 RECEPTORS; RECEPTOR INVERSE AGONIST; serotonin 2a receptor inverse agonist; pimavanserin; Parkinson's disease psychosis}, year = {2017}, eissn = {1996-3181}, pages = {234-243}, orcid-numbers = {Vécsei, László/0000-0001-8037-3672} } @article{MTMT:3192890, title = {Excitotoxins, mitochondrial and redox disturbances in multiple sclerosis}, url = {https://m2.mtmt.hu/api/publication/3192890}, author = {Rajda, Cecília and Pukoli, Dániel and Bende, Zsuzsanna and Majláth, Zsófia and Vécsei, László}, doi = {10.3390/ijms18020353}, journal-iso = {INT J MOL SCI}, journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, volume = {18}, unique-id = {3192890}, issn = {1661-6596}, abstract = {Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). There is increasing evidence that MS is not only characterized by immune mediated inflammatory reactions, but also by neurodegenerative processes. There is cumulating evidence that neurodegenerative processes, for example mitochondrial dysfunction, oxidative stress, and glutamate (Glu) excitotoxicity, seem to play an important role in the pathogenesis of MS. The alteration of mitochondrial homeostasis leads to the formation of excitotoxins and redox disturbances. Mitochondrial dysfunction (energy disposal failure, apoptosis, etc.), redox disturbances (oxidative stress and enhanced reactive oxygen and nitrogen species production), and excitotoxicity (Glu mediated toxicity) may play an important role in the progression of the disease, causing axonal and neuronal damage. This review focuses on the mechanisms of mitochondrial dysfunction (including mitochondrial DNA (mtDNA) defects and mitochondrial structural/functional changes), oxidative stress (including reactive oxygen and nitric species), and excitotoxicity that are involved in MS and also discusses the potential targets and tools for therapeutic approaches in the future. © 2017 by the authors; licensee MDPI, Basel, Switzerland.}, keywords = {glutamate; Mitochondria; MULTIPLE SCLEROSIS; neurodegeneration; biomarker; excitotoxin; Oxidative stress}, year = {2017}, eissn = {1422-0067}, orcid-numbers = {Rajda, Cecília/0000-0002-0252-4778; Vécsei, László/0000-0001-8037-3672} } @{MTMT:2974963, title = {Hatóanyagoknak a központi idegrendszerben történő szabályozott leadására alkalmas nanokompozit, eljárás annak előállítására és alkalmazása}, url = {https://m2.mtmt.hu/api/publication/2974963}, author = {Dékány, Imre and Krizbai, I and Majláth, Zsófia and Toldi, J and Varga, N and Vécsei, László}, unique-id = {2974963}, year = {2017}, orcid-numbers = {Dékány, Imre/0000-0001-5472-5355; Vécsei, László/0000-0001-8037-3672} } @article{MTMT:3163235, title = {Corrigendum to “Migraine and neuropeptides” [Neuropeptides (2015) 19–30]}, url = {https://m2.mtmt.hu/api/publication/3163235}, author = {Tajti, János and Szok, Délia and Majláth, Zsófia and Tuka, Bernadett and Csáti, Anett and Vécsei, László}, doi = {10.1016/j.npep.2016.10.001}, journal-iso = {NEUROPEPTIDES}, journal = {NEUROPEPTIDES}, volume = {60}, unique-id = {3163235}, issn = {0143-4179}, keywords = {Endocrinology & Metabolism}, year = {2016}, eissn = {1532-2785}, pages = {91-91}, orcid-numbers = {Tajti, János/0000-0003-0857-5266; Tuka, Bernadett/0000-0002-1410-4666; Vécsei, László/0000-0001-8037-3672} }