ABSTRACT Purpose For more than 20 years, the goal of glioma surgery has been to remove as much tumor as possible without compromising patient safety. Many retrospective studies support that greater extent of resection is often associated with longer survival. However, three recent developments have challenged this traditional approach. First, the 2021 World Health Organization classification introduced a molecular approach to glioma diagnosis, which made tumor biology an additional consideration, alongside imaging, in setting surgical targets. Second, the IDH‐targeted therapies, particularly vorasidenib for IDH‐mutant low‐grade gliomas, have made residual disease a clinically meaningful variable rather than a surgical failure. Third, early phase locoregional chimeric antigen receptor (CAR) T‐cell trials have suggested that the resection cavity may be an important site for treatment delivery. These developments raise a question: should the goal of glioma surgery remain the same when targeted and locoregional therapies are available? In this review, we examine the evidence for extent of resection and discuss how newer therapies may affect surgical decision‐making. Methods A structured literature search of PubMed, Scopus, and Web of Science (inception to May 2026) was conducted, and evidence quality was graded narratively. Findings We argue that these therapies do not replace maximal safe resection but reshape its application in clinical practice. Surgical planning may increasingly need to consider tissue sampling and access for future therapies alongside tumor removal. We also highlight five key controversies and outline five priorities for future research. Conclusion Based on the available evidence, we propose an oncofunctional‐immunotherapeutic framework in which molecular subtype is considered before surgery, the resection cavity is seen as a potential therapeutic site, and preservation of neurological function remains essential for enabling further treatment. These elements are not yet integrated into a single clinical framework.
ABSTRACT Background Mild cognitive impairment (MCI) is associated with subtle deficits in cognitive‐motor integration and postural control; however, the cortical mechanisms underlying impaired cognitive–postural dual‐task performance remain unclear. This study aimed to investigate behavioral alterations, cortical activation patterns, and brain–behavior coupling characteristics during cognitive–postural dual‐tasking in older adults with MCI. Methods Fifty‐three community‐dwelling older adults were enrolled, including 26 individuals with MCI and 27 cognitively normal controls. Participants performed a verbal fluency task while maintaining upright standing under four dual‐task conditions combining visual availability (eyes open/closed) and support‐surface stability (stable/unstable). Postural performance was assessed using the anteroposterior stability index (API) and mediolateral stability index (MLI), while cognitive performance was evaluated using verbal fluency scores. Functional near‐infrared spectroscopy (fNIRS) was used to measure task‐related cortical activation in bilateral prefrontal, primary somatosensory, primary motor, and premotor cortices. Between‐group comparisons, partial correlation analyses, and regression‐based interaction analyses were conducted to examine alterations in brain–behavior relationships. Results Compared with cognitively normal controls, participants with MCI exhibited poorer postural stability under dual‐task conditions involving reduced visual input and/or unstable support surfaces. Reduced cortical activation was observed mainly in prefrontal regions during unstable support with eyes open and extended to sensorimotor‐related regions under combined visual deprivation and unstable support. Brain–behavior associations differed between groups. In cognitively normal older adults, increased cortical activation was generally associated with better behavioral performance. In contrast, individuals with MCI showed stronger associations between reduced activation of distributed prefrontal–sensorimotor regions and impaired postural performance, particularly under the eyes‐closed unstable‐support condition. Regression‐based interaction analysis further demonstrated a significant group‐dependent association between right prefrontal activation and mediolateral postural stability. Conclusions Older adults with MCI exhibit altered brain–behavior coupling during cognitive–postural dual‐task conditions involving sensory and postural constraints, characterized by altered relationships between prefrontal–sensorimotor cortical activation and behavioral performance. These findings provide new insights into the neural mechanisms underlying cognitive‐motor dysfunction in MCI and highlight abnormal brain–behavior coupling as a potential feature of early functional impairment.
ABSTRACT Purpose Artificial intelligence (AI) is increasingly applied to neuroimaging, electrophysiology, clinical text, and digitally measured behavior, but reported performance often exceeds the maturity of clinical evidence. Method We conducted a structured narrative review, informed by SANRA principles, of English‐language human studies, reviews, and regulatory sources identified in PubMed/MEDLINE and IEEE Xplore from January 2022 through July 2026; older landmark studies were retained when necessary for historical or methodological context. We applied a common translational‐evidence framework across six prespecified neurological domains to distinguish technical performance from external validation, prospective clinical evaluation, implementation, and demonstrated patient benefit. Evidence was appraised according to cohort representativeness, patient‐level data separation, external and prospective validation, calibration, clinical comparators, regulatory status, workflow integration, and patient‐level benefit. Finding Across stroke, dementia, Parkinson disease, epilepsy, multiple sclerosis, and neuro‐oncology, the strongest evidence concerns narrowly defined imaging and signal‐processing tasks. A cluster‐randomized stroke study demonstrated shorter thrombectomy workflow time, and several externally validated models show improved portability. In contrast, many high‐accuracy classification and segmentation studies remain retrospective, single‐dataset, internally validated, and uncalibrated. Multimodal learning, foundation models, federated learning, and large language models broaden capability but introduce additional risks related to dataset shift, bias, opacity, privacy, and automation. Conclusion Neuro‐AI should be judged by its intended clinical task and evidence maturity rather than headline accuracy. Multicenter external validation, prospective workflow evaluation, calibration, subgroup reporting, human‐factors testing, and post‐deployment surveillance are prerequisites for safe and equitable clinical use.
ABSTRACT Background Generalized anxiety disorder (GAD) and insufficient sleep frequently co‐occur during early adulthood, yet resting‐state electroencephalographic (EEG) evidence in this population remains limited. The present study aimed to characterize resting‐state EEG spectral power in young adults with GAD who also reported habitual short sleep, compared with healthy controls. Methods This exploratory case‐control study included 56 university students: 28 participants with GAD and self‐reported habitual short sleep and 28 healthy controls. Resting‐state EEG spectral power was quantified in the delta, theta, alpha, and beta bands. We retained unadjusted group comparisons for description and fitted age‐ and sex‐adjusted linear models for the primary inferential interpretation. Channel‐wise models likewise included group, age, and sex, with Benjamini–Hochberg FDR correction across the 30 channels within each frequency band. Results After adjustment for age and sex, group coefficients remained positive for delta (2.51, 95% CI: 0.20 to 4.82), theta (2.52, 95% CI: 0.29 to 4.74), alpha (2.46, 95% CI: –0.12 to 5.03), and beta power (2.14, 95% CI: 0.13 to 4.15), but none met the FDR threshold (adjusted FDR p = 0.0501, 0.0501, 0.0608, and 0.0501, respectively). In unadjusted analyses, delta, theta, and beta differences survived FDR correction (FDR p = 0.0480 for each), whereas alpha did not (FDR p = 0.0553). In adjusted channel‐wise analyses, 26 channel‐by‐band comparisons across 15 channels survived within‐band FDR correction; all occurred in delta or theta and were concentrated over posterior and centroparietal electrodes. Conclusions Whole‐scalp estimates were directionally higher in the GAD plus habitual short‐sleep group, but no age‐ and sex‐adjusted frequency‐band comparison survived FDR correction. Adjusted exploratory channel‐wise findings indicated a posterior and centroparietal concentration in delta and theta power. These estimates remain preliminary and do not permit attribution to GAD, habitual short sleep, or their interaction.
Abstract Background Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive motor and non‐motor symptoms. Insulin‐like Growth Factor‐1 (IGF‐1), a neuroprotective hormone, has been proposed as a potential biomarker in PD. Objectives This study aimed to evaluate differences in serum IGF‐1 levels between people with PD (PwPD) and healthy controls, and to assess associations with symptom severity. Methods We conducted a systematic search of PubMed, Embase, and Web of Science on December 7, 2024. Observational studies comparing serum IGF‐1 in PwPD and healthy controls, or assessing its associations with PD symptoms, were included. Study quality was evaluated using the Newcastle–Ottawa Scale. A random‐effects meta‐analysis pooled mean differences (MD) in IGF‐1 levels, and correlation coefficients were synthesized for motor symptoms. Non‐motor symptom associations were analyzed using effect direction plots. Results Eighteen studies with 2,480 participants (1,465 PwPD; 1,015 controls) were included. PwPD had significantly higher serum IGF‐1 levels than controls (MD: 21.3 ng/mL; 95CI: 11.49, 31.12; p < 0.001). Elevated IGF‐1 was consistent across early/late‐stage and drug‐naïve/treated PwPD, with no significant subgroup differences. Meta‐analysis of five studies (413 PwPD) showed an inverse correlation between IGF‐1 levels and motor symptom severity (r = −0.35; 95% CI: −0.53, −0.08; p < 0.01), although individual study findings were heterogeneous, and the certainty of evidence was low. Non‐motor symptoms also showed no consistent associations. Conclusions PwPD exhibit elevated serum IGF‐1 levels and may be inversely associated with motor symptom severity. IGF‐1's relationship with non‐motor symptoms remains unclear and requires further study. Longitudinal research is needed to determine IGF‐1's utility as a PD biomarker
