Explore the vast range of titles available.

\"Using herself as a guinea pig, a science journalist explores 'neuroplasticity' to find out whether she can make meaningful, lasting changes to the way her brain works\"-- Provided by publisher.

Please confirm that an ethics committee approval has been applied for or granted: Not relevant (see information at the bottom of this page)Background and Aims Complex regional pain syndrome (CRPS) is characterized by being disproportionate to the triggering event; the associated characteristics are autonomic dysfunction, swelling of the zone of affection, and even changes in the skin, such as dystrophy and rigidity. The pathophysiology is still unknown; it has been mentioned as a multifactorial disorder, with an exaggerated immune response to the triggering event, abnormal vasomotor function, and even maladaptive neuroplasticity. This study aimed to evaluate the differently expressed genes (DEG) between 4 patients with complex regional pain syndrome vs. healthy controls and analyze the pathways intervening.MethodsMaterial/Methods: The gene expression dataset GSE47603 was downloaded from the GEO database, and DEG obtained. The highest up-regulated genes were examined in the String platform for the protein-protein interaction (PPI) network.ResultsResults: 60 primary genes up-regulated were identified according to the Log2-fold change statistics. The network for the 60 genes was sub-selected in clusters in STRING, obtaining a network of 20 nodes, 24 edges, and a PPI enrichment p-value of 3.73e-11. The principal intervening pathways were mitochondrial ATP synthesis, the electron transport chain, and lysosome vesicle biogenesis.Abstract #35904 Figure 1Meandiff plot of genes expressed in CRPS Vs controls[Figure omitted. See PDF]Abstract #35904 Figure 2CRPS cluster of 20 nodes, with the principal proteins involved in mitochondrial functions[Figure omitted. See PDF]ConclusionsWe found a relevant participation of mitochondrial metabolism in the PPI network that has not been mentioned before as a pain onset in CRPS, but at the same time presence of pain has been reported in patients with mitochondrial disease, the essential role that it could play in the sudden development of pain in CRPS needs to be further analyzed.

This is the incredible story and miraculous work of a remarkable woman. Though she began life severely learning disabled, she built herself a better brain and a brain training program that has helped thousands of others do the same.

Abstract Disclosure: D.A. Zieba: None. E.A. Oclon: None. A. Gurgul: None. I. Jasielczuk: None. T. Szmatola: None. Leptin resistance impairs hypothalamic signaling, altering neuronal gene expression and neuroplasticity and contributing to hypothalamic dysfunction. SMLA, a superactive mouse leptin antagonist, competes with wild-type leptin for receptor binding with 60-fold greater efficiency, offering a unique approach to modulating leptin signaling. This study examines the transcriptomic effects of leptin resistance and SMLA treatment in hypothalamic neurons. The adult-derived mHypoA-2/12 hypothalamic cell line was cultured in DMEM supplemented with 10% FBS and antibiotics. Cells were plated in 24-well plates at 1.5 × 10⁵ cells/well and maintained at 37°C with 5% CO₂. Experimental groups included Ctrl, BA (50.6 nM leptin, 31.25 µM antagonist), and CA (12.8 nM leptin, 31.25 µM antagonist). Cells were incubated for 24 hours before RNA isolation. Total RNA was extracted, quality-checked, and quantified. Libraries were prepared using QuantSeq 3’ mRNA-Seq, pooled, and sequenced (150 bp, single-end) to obtain at least 6 million reads per sample. Sequencing quality was assessed with FastQC, trimming, and filtering with Flexbar. Reads were mapped to the mouse GRC39 genome (STAR aligner) and counted with Htseq-count. Data normalization, clustering, and differential expression analysis were performed using DESeq2 on iDEP.96. Gene Ontology and KEGG pathway enrichment were analyzed with FDR < 0.05. Statistical analyses were performed in JASP using one-way ANOVA with Tukey post hoc or Kruskal-Wallis with Dunn post hoc as appropriate. RNA-seq validation by qPCR showed strong correlation (r > 0.85, p < 0.05). Leptin resistance led to significant gene changes critical for neuroplasticity and neuronal stress responses. Txnip decreased (logFC = −2.77, p < 7.19 × 10⁻¹⁰), while Hdac7 (logFC = +1.38, p < 1.29 × 10⁻⁸) and Ctnnbip1 (logFC = +1.69, p < 4.71 × 10⁻¹⁰) increased, suggesting potential disruptions in oxidative protection and synaptic remodeling. SMLA treatment reversed these changes, increasing Txnip (logFC = +1.48, p < 0.003) and reducing Hdac7 and Ctnnbip1 expression (logFC = −1.03 and −1.22, respectively). Additionally, Casp3 expression normalized with SMLA (logFC = +1.13, p < 1.22 × 10⁻⁵), potentially restoring synaptic pruning. Results suggest that SMLA may mitigate leptin resistance-induced disruptions in neuroplasticity. In summary, our findings demonstrate that leptin resistance alters key gene networks involved in neuroplasticity and stress responses in hypothalamic neurons. SMLA treatment reverses these molecular changes, restoring gene expression profiles linked to oxidative protection and synaptic remodeling. Understanding the mechanisms of leptin signaling modulation may provide a foundation for developing strategies to address leptin-related disorders. This research was financially supported by the grant no. UMO-2023/51/B/NZ9/00651. Presentation: Monday, July 14, 2025

\" The New York Times bestselling author of The Brain That Changes Itself presents astounding advances in the treatment of brain injury and illness. In The Brain That Changes Itself, Norman Doidge described the most important breakthrough in our understanding of the brain in four hundred years: the discovery that the brain can change its own structure and function in response to mental experience-what we call neuroplasticity. His revolutionary new book shows, for the first time, how the amazing process of neuroplastic healing really works. It describes natural, non-invasive avenues into the brain provided by the forms of energy around us-light, sound, vibration, movement-which pass through our senses and our bodies to awaken the brain's own healing capacities without producing unpleasant side effects. Doidge explores cases where patients alleviated years of chronic pain or recovered from debilitating strokes or accidents; children on the autistic spectrum or with learning disorders normalizing; symptoms of multiple sclerosis, Parkinson's disease, and cerebral palsy radically improved, and other near-miracle recoveries. And we learn how to vastly reduce the risk of dementia with simple approaches anyone can use. For centuries it was believed that the brain's complexity prevented recovery from damage or disease. The Brain's Way of Healing shows that this very sophistication is the source of a unique kind of healing. As he did so lucidly in The Brain That Changes Itself, Doidge uses stories to present cutting-edge science with practical real-world applications, and principles that everyone can apply to improve their brain's performance and health\"-- Provided by publisher.

IntroductionThere are currently no approved pharmacotherapies to treat cognitive impairment associated with schizophrenia (CIAS). Iclepertin (BI 425809) is a novel glycine transporter-1 inhibitor under development for treatment of CIAS. A previous study demonstrated pro-cognitive effects of iclepertin in patients with schizophrenia; however, concurrent cognitive stimulation could in theory enhance any pro-cognitive pharmacological effects on neuroplasticity. We present preliminary demographics and baseline data from a trial exploring the efficacy of iclepertin together with at-home computerized cognitive training (CCT).MethodsThis is an ongoing Phase II, double-blind, placebo-controlled, parallel-group trial in patients with schizophrenia on stable antipsychotic therapy across ~58 centers in 6 countries. Patients aged 18–50 years, compliant with CCT during the run-in period (completing ≥2 hours/week for 2 weeks), were randomized (1:1) to receive once-daily iclepertin 10 mg or placebo together with CCT for 12 weeks. Thereafter, minimum compliance for at-home CCT is 1 hour/week, with a target of ~30 hours across 3–5 sessions totaling 2.5 hours/week. Patients have been stratified to balance potential effects of age (18–40; 41–50 years). Primary endpoint is change from baseline (CfB) in neurocognitive composite T-score of the MATRICS Consensus Cognitive Battery (MCCB) at Week 12. Secondary endpoints include CfB in the Schizophrenia Cognition Rating Scale (SCoRS) total score, MCCB overall composite T-score, and Positive and Negative Syndrome Scale (PANSS) total scores. Novel exploratory endpoints include the Virtual Reality Functional Capacity Assessment Tool to assess daily functioning and the Balloon Effort Task to assess motivation in cognitive performance.ResultsOf the planned sample of 200 randomized patients, the overall treated population currently includes 183: 67% (n=122) are male; mean (standard deviation [SD]) age and time since first diagnosis are 38.2 (7.9) years and 13.5 (8.5) years. Overall, 49% (n=89) are White and 43% (n=79) are Black or African American; 80% (n=147) are from North America, 15% (n=28) from Europe, and 4% (n=8) from Australia/New Zealand. Mean (SD) baseline MCCB neurocognitive composite and overall T-scores (n=178) are 33.7 (11.9) and 32.5 (12.6). Mean (SD) baseline SCoRS total score (n=167) is 35.2 (8.7). Mean (SD) baseline PANSS total and negative symptom scale scores (n=183) are 64.7 (14.6) and 17.3 (5.4). Median (Q1, Q3) CCT compliance over the on-treatment period for patients who have completed or discontinued early is 2.00 (1.21, 2.51) hours/week.ConclusionThis trial is, to our knowledge, the largest of its kind combining daily pharmacotherapy for CIAS with at-home CCT. It will indicate whether iclepertin together with concurrent cognitive stimulation provides enhanced cognitive benefit, and whether any improvements in neurocognition can translate into improved measures of daily functioning in patients.FundingBoehringer Ingelheim International GmbH (NCT03859973/1346-0038)