Learning of adaptive behaviors requires the refinement of coordinated activity across multiple brain regions. However, how neural communications develop during learning remains poorly understood. Here, using two-photon calcium imaging, we simultaneously recorded the activity of layer 2/3 excitatory neurons in eight regions of the mouse dorsal cortex during learning of a delayed-response task. Across learning, while global functional connectivity became sparser, there emerged a subnetwork comprising of neurons in the anterior lateral motor cortex (ALM) and posterior parietal cortex (PPC). Neurons in this subnetwork shared a similar choice code during action preparation and formed recurrent functional connectivity across learning. Suppression of PPC activity disrupted choice selectivity in ALM and impaired task performance. Recurrent neural networks reconstructed from ALM activity revealed that PPC-ALM interactions rendered choice-related attractor dynamics more stable. Thus, learning constructs cortical network motifs by recruiting specific inter-areal communication channels to promote efficient and robust sensorimotor transformation.

Chronic rhinosinusitis (CRS) is increasingly recognized as a heterogeneous condition characterized by distinct inflammatory endotypes. In Western populations, CRS is mostly type 2 (T2) eosinophilic. In contrast, Asian cohorts show higher rates of non-T2 endotypes, posing unique challenges and limiting the applicability of Western treatment models. This expert commentary and scoping review explores endotype-driven care in CRS, synthesizes current research on Asian CRS cohorts, and examines existing gaps in our understanding, particularly in non-T2 CRS. Endotype-driven care improves treatment precision and minimizes therapeutic failure. However, most models remain largely Western-centric. Establishing Asia-specific criteria, accessible diagnostics, and therapies for non-T2 disease is essential.

Structural nasal obstruction is an important modifier of sleep-disordered breathing (SDB), but the specific impact of functional rhinoplasty on validated sleep-related outcomes has not been quantitatively synthesized. To systematically review and meta-analyze studies of adults with SDB undergoing functional rhinoplasty or septorhinoplasty, testing the hypothesis that surgery yields large improvements in nasal obstruction and modest improvements in sleep-related symptoms. PROSPERO-registered systematic review and random-effects meta-analysis conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020. PubMed, Embase and Cochrane Library were searched to September 2025 for studies reporting validated symptom scores before and after functional rhinoplasty or septorhinoplasty in adults with SDB. Standardized mean differences (SMDs) with Hartung–Knapp-adjusted confidence intervals were pooled; risk of bias and publication bias were formally assessed. Eight studies (27 cohorts; n = 1,192) met inclusion criteria. Surgery was associated with large improvement in nasal obstruction (Nasal Obstruction Symptom Evaluation SMD: −4.99; 95% CI: −9.12 to −0.85), moderate reductions in daytime sleepiness (Epworth Sleepiness Scale SMD: −1.09; 95% CI: −2.33 to 0.15) and global sleep disturbance (Pittsburgh Sleep Quality Index SMD: −0.74; 95% CI: −1.21 to −0.26), and modest gains in functional status (Functional Outcomes of Sleep Questionnaire-10 SMD: 0.41; 95% CI: 0.16–0.65). Heterogeneity was substantial for most outcomes and small-study effects were detected. Functional rhinoplasty and septorhinoplasty appear to improve nasal obstruction and sleep-related patient-reported outcomes in adults with SDB, supporting their role as adjunctive procedures in selected patients. High heterogeneity and predominantly observational data highlight the need for larger, phenotype-driven studies to refine effect estimates and patient selection (PROSPERO registration number: CRD420251168358).

Background: Chronic rhinosinusitis (CRS) affects nearly 9% of the global population with a rising incidence over recent decades. Neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease pose significant global burden, and emerging evidence suggests pathophysiological links through shared bioenergetic dysfunction, peripheral-to-central inflammatory signaling, and altered nasal microbiota. This review evaluates the evidence for CRS as a potentially modifiable peripheral contributor to neurodegenerative disease progression. Methods: A systematic review was conducted using PubMed, Cochrane, Web of Science, Embase, and CENTRAL from January 2000 to July 2025. Search terms included “Chronic Rhinosinusitis,” “Neurodegeneration,” “Mild Cognitive Impairment,” “Alzheimer’s Disease,” “Parkinson’s Disease,” “Bioenergetics,” and “Microbiome.” Clinical and experimental studies exploring epidemiological links, mechanistic pathways, biomarkers, and therapeutic targets were included. Results: Twenty-one studies involving over 100,000 participants met the inclusion criteria. Existing meta-analytic evidence demonstrated significant associations between CRS and cognitive impairment, with patients scoring approximately 9% lower on global cognitive measures than controls. However, other large-scale cohort studies did not pinpoint an increased dementia incidence, suggesting CRS may contribute to early, potentially reversible cognitive decline without directly driving dementia onset. Neuroimaging studies revealed altered frontoparietal connectivity and orbitofrontal hyperactivity in CRS patients. Mechanistic studies support peripheral inflammatory cytokines disrupting the blood–brain barrier, autonomic dysfunction impairing mucociliary clearance, microbiome-driven amyloid cross-seeding, and compromised cerebrospinal fluid clearance via olfactory–cribriform pathways. Discussion: Evidence supports complex, bidirectional relationships between CRS and neurodegeneration characterized by convergent inflammatory, autonomic, and bioenergetic pathways. Therapeutic strategies targeting sinonasal inflammation, microbiome dysbiosis, and mitochondrial dysfunction represent promising intervention avenues. Recognizing CRS as a treatable factor in neurodegenerative risk stratification may enable earlier diagnosis and prevention strategies.