Response trajectories of gambling severity after cognitive behavioral therapy in young-adult pathological gamblers

Background and aims: the significant increase in the prevalence of gambling disorder (GD) among young adults in recent years has attracted interest in determining therapeutic efficiency in this sector of the population. The aim of this work was to estimate the response trajectories of gambling severity during the six-month follow-up after a cognitive behavioral therapy (CBT) program in young adult patients and to identify the main variables associated with each trajectory. Methods: the sample included n = 192 patients, aged 19-35 years old, seeking treatment for GD. Response trajectories were identified through latent class growth analysis. Results: three trajectories emerged: T1 (n = 118, 61.5%), composed of patients with severe GD at pre-treatment and good evolution to recovery; T2 (n = 62, 32.3%), with patients with moderate-high GD affectation at baseline and good evolution to recovery; and T3 (n = 12, 6.3%), with participants with severe baseline GD severity and poor evolution after CBT (Abbott, 2019). The highest risk of poor therapeutic outcomes was related to lower social index positions, high emotional distress, high scores in harm avoidance and low scores in self-directedness. Discussion and conclusions: differences in the response trajectories at short-term follow-up after CBT reveal heterogeneity in the samples including young and young-adult GD patients. Patients' phenotype at baseline should be considered when developing efficient, person-centered intervention programs, which should comprise strategies aimed at increasing emotional regulation capacities, self-esteem and self-efficacy, with the aim of avoiding relapses in the medium-long term after therapy

Search for dark matter produced in association with bottom or top quarks in √s = 13 TeV pp collisions with the ATLAS detector

A search for weakly interacting massive particle dark matter produced in association with bottom or top quarks is presented. Final states containing third-generation quarks and miss- ing transverse momentum are considered. The analysis uses 36.1 fb−1 of proton–proton collision data recorded by the ATLAS experiment at √s = 13 TeV in 2015 and 2016. No significant excess of events above the estimated backgrounds is observed. The results are in- terpreted in the framework of simplified models of spin-0 dark-matter mediators. For colour- neutral spin-0 mediators produced in association with top quarks and decaying into a pair of dark-matter particles, mediator masses below 50 GeV are excluded assuming a dark-matter candidate mass of 1 GeV and unitary couplings. For scalar and pseudoscalar mediators produced in association with bottom quarks, the search sets limits on the production cross- section of 300 times the predicted rate for mediators with masses between 10 and 50 GeV and assuming a dark-matter mass of 1 GeV and unitary coupling. Constraints on colour- charged scalar simplified models are also presented. Assuming a dark-matter particle mass of 35 GeV, mediator particles with mass below 1.1 TeV are excluded for couplings yielding a dark-matter relic density consistent with measurements

Multiancestry analysis of the HLA locus in Alzheimer’s and Parkinson’s diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes

Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson’s disease (PD) and Alzheimer’s disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1*04:07, and intermediary with HLA-DRB1*04:01 and HLA-DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased Aβ42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues