@article{MTMT:34822010, title = {A demencia viselkedési és pszichés tüneteinek kezelése a háziorvosi gyakorlatban.}, url = {https://m2.mtmt.hu/api/publication/34822010}, author = {Hidasi, Zoltán and Fullajtár, Máté}, journal-iso = {HÁZIORVOS TOVÁBBKÉPZŐ SZEMLE}, journal = {HÁZIORVOS TOVÁBBKÉPZŐ SZEMLE}, volume = {29}, unique-id = {34822010}, issn = {1219-8641}, year = {2024}, pages = {124-128}, orcid-numbers = {Hidasi, Zoltán/0000-0002-7798-0145; Fullajtár, Máté/0000-0003-4786-2735} } @article{MTMT:34814536, title = {Motor dominance and movement-outcome congruency influence the electrophysiological correlates of sensory attenuation for self-induced visual stimuli}, url = {https://m2.mtmt.hu/api/publication/34814536}, author = {Balla, V.R. and Kilencz, Tünde and Szalóki, S. and Dalos, V.D. and Partanen, E. and Csifcsák, G.}, doi = {10.1016/j.ijpsycho.2024.112344}, journal-iso = {INT J PSYCHOPHYSIOL}, journal = {INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY}, volume = {200}, unique-id = {34814536}, issn = {0167-8760}, year = {2024}, eissn = {1872-7697} } @article{MTMT:34804337, title = {Theta-burst rTMS in schizophrenia to ameliorate negative and cognitive symptoms: study protocol for a double-blind, sham-controlled, randomized clinical trial}, url = {https://m2.mtmt.hu/api/publication/34804337}, author = {Csukly, Gábor and Orbán-Szigeti, Boglárka and Suri, Karolin Mária and Zsigmond, Réka Ildikó and Hermán, Levente and Simon, Viktória and Kabaji, Anita and Bata, Barnabás and Hársfalvi, Péter and Vass, Edit and Csibri, Éva and Farkas, Kinga and Réthelyi, János}, doi = {10.1186/s13063-024-08106-9}, journal-iso = {TRIALS}, journal = {TRIALS}, volume = {25}, unique-id = {34804337}, issn = {1745-6215}, year = {2024}, eissn = {1745-6215}, orcid-numbers = {Csukly, Gábor/0000-0002-5006-9407; Orbán-Szigeti, Boglárka/0000-0001-9744-4393; Zsigmond, Réka Ildikó/0000-0002-7019-6761; Hermán, Levente/0000-0002-1376-5366; Vass, Edit/0000-0002-8858-7277; Farkas, Kinga/0000-0002-1125-3957; Réthelyi, János/0000-0002-3641-012X} } @article{MTMT:34804106, title = {MicroRNA-Mediated Suppression of Glial Cell Line-Derived Neurotrophic Factor Expression Is Modulated by a Schizophrenia-Associated Non-Coding Polymorphism}, url = {https://m2.mtmt.hu/api/publication/34804106}, author = {Keszler, Gergely and Vékony, Bálint and Elek, Zsuzsanna and Nemoda, Zsófia and Angyal, Nóra and Bánlaki, Zsófia and Kovács-Nagy, Réka and Rónai, Zsolt and Réthelyi, János}, doi = {10.3390/ijms25084477}, journal-iso = {INT J MOL SCI}, journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, volume = {25}, unique-id = {34804106}, issn = {1661-6596}, abstract = {Plasma levels of glial cell line-derived neurotrophic factor (GDNF), a pivotal regulator of differentiation and survival of dopaminergic neurons, are reportedly decreased in schizophrenia. To explore the involvement of GDNF in the pathogenesis of the disease, a case–control association analysis was performed between five non-coding single nucleotide polymorphisms (SNP) across the GDNF gene and schizophrenia. Of them, the ‘G’ allele of the rs11111 SNP located in the 3′ untranslated region (3′-UTR) of the gene was found to associate with schizophrenia. In silico analysis revealed that the rs11111 ‘G’ allele might create binding sites for three microRNA (miRNA) species. To explore the significance of this polymorphism, transient co-transfection assays were performed in human embryonic kidney 293T (HEK293T) cells with a luciferase reporter construct harboring either the ‘A’ or ‘G’ allele of the 3′-UTR of GDNF in combination with the hsa-miR-1185-1-3p pre-miRNA. It was demonstrated that in the presence of the rs11111 ‘G’ (but not the ‘A’) allele, hsa-miR-1185-2-3p repressed luciferase activity in a dose-dependent manner. Deletion of the miRNA binding site or its substitution with the complementary sequence abrogated the modulatory effect. Our results imply that the rs11111 ‘G’ allele occurring more frequently in patients with schizophrenia might downregulate GDNF expression in a miRNA-dependent fashion.}, year = {2024}, eissn = {1422-0067}, orcid-numbers = {Vékony, Bálint/0000-0002-6814-7311; Nemoda, Zsófia/0000-0002-9550-7730; Bánlaki, Zsófia/0000-0002-3815-422X; Rónai, Zsolt/0000-0002-0909-7932; Réthelyi, János/0000-0002-3641-012X} } @CONFERENCE{MTMT:34802983, title = {SYMPTOM NETWORK DIFFERENCES BETWEEN SCHIZOPHRENIA AND AUTISM SPECTRUM DISORDER: A NETWORK ANALYSIS}, url = {https://m2.mtmt.hu/api/publication/34802983}, author = {Holka, Szilárd and Sörnyei, Dániel Tibor and Ágota, Vass and Kinga, Farkas}, booktitle = {Responding to Challenges in a Changing World}, unique-id = {34802983}, year = {2024}, pages = {875}, orcid-numbers = {Holka, Szilárd/0009-0000-8505-8153; Sörnyei, Dániel Tibor/0009-0005-6701-409X} } @article{MTMT:34797928, title = {Risk of conversion to mild cognitive impairment or dementia among subjects with amyloid and tau pathology : a systematic review and meta-analysis}, url = {https://m2.mtmt.hu/api/publication/34797928}, author = {Huszár, Zsolt and Engh, Marie Anne and Pavlekovics, Márk and Sato, Tomoya and Steenkamp, Yalea and Hanseeuw, Bernard and Terebessy, Tamás and Molnár, Zsolt and Hegyi, Péter and Csukly, Gábor}, doi = {10.1186/s13195-024-01455-2}, journal-iso = {ALZHEIMERS RES THER}, journal = {ALZHEIMERS RESEARCH & THERAPY}, volume = {16}, unique-id = {34797928}, issn = {1758-9193}, abstract = {Measurement of beta-amyloid (Aβ) and phosphorylated tau (p-tau) levels offers the potential for early detection of neurocognitive impairment. Still, the probability of developing a clinical syndrome in the presence of these protein changes (A+ and T+) remains unclear. By performing a systematic review and meta-analysis, we investigated the risk of mild cognitive impairment (MCI) or dementia in the non-demented population with A+ and A- alone and in combination with T+ and T- as confirmed by PET or cerebrospinal fluid examination.A systematic search of prospective and retrospective studies investigating the association of Aβ and p-tau with cognitive decline was performed in three databases (MEDLINE via PubMed, EMBASE, and CENTRAL) on January 9, 2024. The risk of bias was assessed using the Cochrane QUIPS tool. Odds ratios (OR) and Hazard Ratios (HR) were pooled using a random-effects model. The effect of neurodegeneration was not studied due to its non-specific nature.A total of 18,162 records were found, and at the end of the selection process, data from 36 cohorts were pooled (n= 7,793). Compared to the unexposed group, the odds ratio (OR) for conversion to dementia in A+ MCI patients was 5.18 [95% CI 3.93; 6.81]. In A+ CU subjects, the OR for conversion to MCI or dementia was 5.79 [95% CI 2.88; 11.64]. Cerebrospinal fluid Aβ42 or Aβ42/40 analysis and amyloid PET imaging showed consistent results. The OR for conversion in A+T+ MCI subjects (11.60 [95% CI 7.96; 16.91]) was significantly higher than in A+T- subjects (2.73 [95% CI 1.65; 4.52]). The OR for A-T+ MCI subjects was non-significant (1.47 [95% CI 0.55; 3.92]). CU subjects with A+T+ status had a significantly higher OR for conversion (13.46 [95% CI 3.69; 49.11]) than A+T- subjects (2.04 [95% CI 0.70; 5.97]). Meta-regression showed that the ORs for Aβ exposure decreased with age in MCI. (beta = -0.04 [95% CI -0.03 to -0.083]).Identifying Aβ-positive individuals, irrespective of the measurement technique employed (CSF or PET), enables the detection of the most at-risk population before disease onset, or at least at a mild stage. The inclusion of tau status in addition to Aβ, especially in A+T+ cases, further refines the risk assessment. Notably, the higher odds ratio associated with Aβ decreases with age.The study was registered in PROSPERO (ID: CRD42021288100).}, keywords = {DEMENTIA; Alzheimer's disease; beta-Amyloid; MILD COGNITIVE IMPAIRMENT; PHOSPHORYLATED TAU}, year = {2024}, eissn = {1758-9193}, orcid-numbers = {Engh, Marie Anne/0000-0003-4269-5130; Terebessy, Tamás/0000-0002-7494-6064; Hegyi, Péter/0000-0003-0399-7259; Csukly, Gábor/0000-0002-5006-9407} } @article{MTMT:34779723, title = {Olfactory genes affect major depression in highly educated, emotionally stable, lean women: a bridge between animal models and precision medicine}, url = {https://m2.mtmt.hu/api/publication/34779723}, author = {Eszlári, Nóra and Hullám, Gábor István and Gál, Zsófia and Török, Dóra and Nagy, Tamás and Millinghoffer, András Dániel and Baksa, Dániel and Gonda, Xénia and Antal, Péter and Bagdy, György and Juhász, Gabriella}, doi = {10.1038/s41398-024-02867-2}, journal-iso = {TRANSL PSYCHIAT}, journal = {TRANSLATIONAL PSYCHIATRY}, volume = {14}, unique-id = {34779723}, issn = {2158-3188}, abstract = {Most current approaches to establish subgroups of depressed patients for precision medicine aim to rely on biomarkers that require highly specialized assessment. Our present aim was to stratify participants of the UK Biobank cohort based on three readily measurable common independent risk factors, and to investigate depression genomics in each group to discover common and separate biological etiology. Two-step cluster analysis was run separately in males ( n = 149,879) and females ( n = 174,572), with neuroticism (a tendency to experience negative emotions), body fat percentage, and years spent in education as input variables. Genome-wide association analyses were implemented within each of the resulting clusters, for the lifetime occurrence of either a depressive episode or recurrent depressive disorder as the outcome. Variant-based, gene-based, gene set-based, and tissue-specific gene expression test were applied. Phenotypically distinct clusters with high genetic intercorrelations in depression genomics were found. A two-cluster solution was the best model in each sex with some differences including the less important role of neuroticism in males. In females, in case of a protective pattern of low neuroticism, low body fat percentage, and high level of education, depression was associated with pathways related to olfactory function. While also in females but in a risk pattern of high neuroticism, high body fat percentage, and less years spent in education, depression showed association with complement system genes. Our results, on one hand, indicate that alteration of olfactory pathways, that can be paralleled to the well-known rodent depression models of olfactory bulbectomy, might be a novel target towards precision psychiatry in females with less other risk factors for depression. On the other hand, our results in multi-risk females may provide a special case of immunometabolic depression.}, year = {2024}, eissn = {2158-3188}, orcid-numbers = {Eszlári, Nóra/0000-0003-4913-028X; Hullám, Gábor István/0000-0002-4765-2351; Gál, Zsófia/0000-0002-9441-1497; Török, Dóra/0000-0001-9213-4345; Nagy, Tamás/0000-0002-0137-4341; Baksa, Dániel/0000-0002-7826-9179; Gonda, Xénia/0000-0001-9015-4203; Bagdy, György/0000-0001-8141-3410; Juhász, Gabriella/0000-0002-5975-4267} } @article{MTMT:34774958, title = {Low Functional network integrity in cognitively unimpaired and MCI subjects with depressive symptoms. results from a multi-center fMRI study.}, url = {https://m2.mtmt.hu/api/publication/34774958}, author = {Csukly, Gábor and Tombor, László and Hidasi, Zoltán and Csibri, Eva and Fullajtár, Máté and Huszár, Zsolt and Koszovácz, Vanda and Lányi, Orsolya and Vass, Edit and Koleszár, Boróka and Kóbor, István and Farkas, Katalin and Rosenfeld, Viktória and Berente, Dalida Borbála and Bolla, Gergő Levente and Kiss, Mate and Kamondi, Anita and Horváth, András Attila}, doi = {10.1038/s41398-024-02891-2}, journal-iso = {TRANSL PSYCHIAT}, journal = {TRANSLATIONAL PSYCHIATRY}, volume = {14}, unique-id = {34774958}, issn = {2158-3188}, abstract = {Evidence suggests that depressive symptomatology is a consequence of network dysfunction rather than lesion pathology. We studied whole-brain functional connectivity using a Minimum Spanning Tree as a graph-theoretical approach. Furthermore, we examined functional connectivity in the Default Mode Network, the Frontolimbic Network (FLN), the Salience Network, and the Cognitive Control Network. All 183 elderly subjects underwent a comprehensive neuropsychological evaluation and a 3 Tesla brain MRI scan. To assess the potential presence of depressive symptoms, the 13-item version of the Beck Depression Inventory (BDI) or the Geriatric Depression Scale (GDS) was utilized. Participants were assigned into three groups based on their cognitive status: amnestic mild cognitive impairment (MCI), non-amnestic MCI, and healthy controls. Regarding affective symptoms, subjects were categorized into depressed and non-depressed groups. An increased mean eccentricity and network diameter were found in patients with depressive symptoms relative to non-depressed ones, and both measures showed correlations with depressive symptom severity. In patients with depressive symptoms, a functional hypoconnectivity was detected between the Anterior Cingulate Cortex (ACC) and the right amygdala in the FLN, which impairment correlated with depressive symptom severity. While no structural difference was found in subjects with depressive symptoms, the volume of the hippocampus and the thickness of the precuneus and the entorhinal cortex were decreased in subjects with MCI, especially in amnestic MCI. The increase in eccentricity and diameter indicates a more path-like functional network configuration that may lead to an impaired functional integration in depression, a possible cause of depressive symptomatology in the elderly.}, year = {2024}, eissn = {2158-3188}, orcid-numbers = {Csukly, Gábor/0000-0002-5006-9407; Tombor, László/0000-0001-9410-5732; Hidasi, Zoltán/0000-0002-7798-0145; Fullajtár, Máté/0000-0003-4786-2735; Koszovácz, Vanda/0000-0003-0668-0185; Vass, Edit/0000-0002-8858-7277; Kóbor, István/0000-0002-9123-5766; Rosenfeld, Viktória/0009-0001-3599-7803; Kamondi, Anita/0000-0001-9860-730X} } @article{MTMT:34772475, title = {A pszichiátria önazonossága a XXI. században}, url = {https://m2.mtmt.hu/api/publication/34772475}, author = {Tringer, László}, journal-iso = {PSYCHIATRIA HUNG}, journal = {PSYCHIATRIA HUNGARICA}, volume = {39}, unique-id = {34772475}, issn = {0237-7896}, year = {2024}, pages = {4-9}, orcid-numbers = {Tringer, László/0000-0002-6233-3359} } @article{MTMT:34755225, title = {Amygdala Volume is Associated with ADHD Risk and Severity Beyond Comorbidities in Adolescents: Clinical Testing of Brain Chart Reference Standards}, url = {https://m2.mtmt.hu/api/publication/34755225}, author = {Nárai, Ádám and Hermann, P. and Rádosi, Alexandra and Vakli, P. and Weiss, Béla and Réthelyi, János and Bunford, N. and Vidnyánszky, Z.}, doi = {10.1007/s10802-024-01190-0}, journal-iso = {RES CHILD ADOLES PSY}, journal = {RESEARCH ON CHILD AND ADOLESCENT PSYCHOPATHOLOGY}, unique-id = {34755225}, issn = {2730-7166}, abstract = {Understanding atypicalities in ADHD brain correlates is a step towards better understanding ADHD etiology. Efforts to map atypicalities at the level of brain structure have been hindered by the absence of normative reference standards. Recent publication of brain charts allows for assessment of individual variation relative to age- and sex-adjusted reference standards and thus estimation not only of case-control differences but also of intraindividual prediction. Methods. Aim was to examine, whether brain charts can be applied in a sample of adolescents (N = 140, 38% female) to determine whether atypical brain subcortical and total volumes are associated with ADHD at-risk status and severity of parent-rated symptoms, accounting for self-rated anxiety and depression, and parent-rated oppositional defiant disorder (ODD) as well as motion. Results. Smaller bilateral amygdala volume was associated with ADHD at-risk status, beyond effects of comorbidities and motion, and smaller bilateral amygdala volume was associated with inattention and hyperactivity/impulsivity, beyond effects of comorbidities except for ODD symptoms, and motion. Conclusions. Individual differences in amygdala volume meaningfully add to estimating ADHD risk and severity. Conceptually, amygdalar involvement is consistent with behavioral and functional imaging data on atypical reinforcement sensitivity as a marker of ADHD-related risk. Methodologically, results show that brain chart reference standards can be applied to address clinically informative, focused and specific questions. © The Author(s) 2024.}, keywords = {Adolescent; MRI; ADHD; normative modeling; Brain Chart}, year = {2024}, eissn = {2730-7174}, orcid-numbers = {Nárai, Ádám/0000-0001-5972-6509; Rádosi, Alexandra/0000-0003-1004-6611; Weiss, Béla/0000-0003-1031-0283; Réthelyi, János/0000-0002-3641-012X} }