Bambini, V. | bioRxiv Science

bioRxiv2026

Challenging the right-hemisphere assumption in post-stroke pragmatics: largely comparable impairment profiles across lesion sides

Traditional views assume that pragmatic deficits after stroke, which compromise the interpretation of communicative intentions and non-literal meanings, follow damage to the right hemisphere (RHD), with left-hemisphere damage (LHD) primarily linked to aphasia and structural language impairment. To examine hemispheric contributions to post-stroke pragmatic profiles, we assessed 99 stroke patients (40 LHD, including 14 with aphasia of minimal-to-moderate severity; 59 RHD) and 60 healthy controls with the Assessment of Pragmatic Abilities and Cognitive Substrates (APACS). While stroke patients overall performed worse than controls, LHD and RHD profiles were largely comparable across three converging analyses: (1) permutation tests revealed no hemispheric differences except on the two tasks requiring expressive components (Interview and Figurative Language 2), which in turn lowered the composites (APACS Production and Total); (2) equivalence testing established equivalence for most measures, with only these same tasks and composites remaining inconclusive; and (3) unsupervised clustering did not group patients by lesion side. Theory of Mind was robustly associated with pragmatic performance in both groups, whereas structural language abilities related specifically to LHD performance and general cognition only to RHD. Excluding aphasic LHD patients strengthened the evidence for comparable profiles, indicating that aphasic LHD patients largely drove the residual differences. In conclusion, primary pragmatic impairment, especially in the receptive domain, emerged comparably after LHD and RHD, with the only residual LHD disadvantage limited to tasks demanding open verbal output. These findings challenge the assumption of right-hemispheric specialization for pragmatics, stressing the need for pragmatic assessment in all post-stroke patients.

neuroscience↗

bioRxiv2020

Expression and Pharmacological Inhibition of TrkB and EGFR in Glioblastoma

Background A member of the Trk family of neurotrophin receptors, tropomyosin receptor kinase B (TrkB, encoded by the NTRK2 gene) is an increasingly important target in various cancer types, including glioblastoma (GBM). EGFR is among the most frequently altered oncogenes in GBM, and EGFR inhibition has been tested as an experimental therapy. Functional interactions between EGFR and TrkB have been demonstrated. In the present study, we investigated the role of TrkB and EGFR, and their interactions, in GBM.Methods and Results Analyses of NTRK2 and EGFR gene expression from The Cancer Genome Atlas (TCGA) datasets showed an increase in NTRK2 expression in the proneural subtype of GBM, and a strong correlation between NTRK2 and EGFR expression in glioma CpG island methylator phenotype (G-CIMP+) samples. We showed that when TrkB and EGFR inhibitors were combined, the inhibitory effect on A172 human GBM cells was more pronounced than when either inhibitor was given alone. When U87MG GBM cells were xenografted into the flank of nude mice, tumor growth was delayed by treatment with TrkB and EGFR inhibitors, given alone or combined, only at specific time points. Intracranial GBM growth in mice was not significantly affected by drug treatments.Conclusions Our findings indicate that correlations between NTRK2 and EGFR expression occur in specific GBM subgroups. Also, our results using cultured cells suggest for the first time the potential of combining TrkB and EGFR inhibition for the treatment of GBM.Competing Interest StatementThe authors have declared no competing interest.View Full Text

cancer biology↗