搜索结果：Memory & cognition

Migraine attacks are frequently accompanied by patient-reported "subjective" cognitive symptoms, but objective findings have been inconsistent. We used high-frequency, smartphone-based cognitive testing to assess within-person changes in subjective and objective cognition across migraine phases using daily diaries. Adults with migraine were recruited through social media. Eligible participants met ICHD-3 migraine criteria and had 3 to 22 monthly headache days. For 30 days, they completed daily smartphone-based reports on headache features, cognitive symptoms, and three smartphone-based objective cognitive tasks. Objective tests included Symbol Search (processing speed/visual search), Color Dots (visual working memory/attention), and Grid Memory (visuospatial working memory). Primary analyses contrasted assessments on current headache days (ictal) versus days with no headache (nonictal). When possible, non-ictal days were subclassified using information from adjacent days as pre-ictal, post-ictal, and interictal days. Outcomes included subjective cognition, reaction time (mean across correctly scored trials), accuracy, and a speed-accuracy composite (Reaction Time/Accuracy). Mixed-effects models adjusted for age, sex, and practice effects. The 139 eligible participants (84.9% female; mean age 38.2 years) contributed 3,014 person-days for ictal versus nonictal comparisons (2,097 nonictal; 917 ictal); for 1,828 person-days precise phase classification was possible. Subjective cognitive symptoms were worse on ictal days, with higher odds of more severe brain fog (OR=3.39, 95% CI 2.70-4.27) and task forgetting (OR=2.82, 95% CI 2.29-3.49). In adjusted models, reaction times were slower on ictal days for Symbol Search (reaction time ratio =1.043, 95% CI 1.028-1.059) and Color Dots (ratio=1.015, 95% CI 1.003-1.026) but not Grid Memory (reaction time ratio =1.006, 95% CI 0.985-1.028). Grid Memory accuracy was lower on ictal days (OR=0.867, 95% CI 0.823-0.914). In analyses based on phase, most nonictal phases showed faster reaction time and lower subjective symptom burden relative to ictal days, with limited differentiation among preictal, postictal, and interictal periods. In persons with migraine, daily smartphone assessments revealed subjective cognitive impairment on ictal vs nonictal days in brain fog and forgetfulness. Objective testing revealed slowing in processing speed and attention and modest differences in the accuracy of working-memory. High-frequency digital cognition appears feasible and may provide scalable functional endpoints for real-world monitoring and treatment evaluation.

This study aimed to explore the relationships between physical disorders (visual impairment, hearing impairment, and chewing impairment) and depression among older adults in nursing homes in one city of China, and to examine the parallel mediating roles of activities of daily living (ADLs) and cognition. The study conducted a cross-sectional study involving 591 older adults from 50 nursing homes in China. Participants provided informations on their vision, hearing, and chewing. Cognition was assessed using tests of memory and thinking skills. ADLs were evaluated through measures of daily task performance, and depression was assessed by epidemiologic studies depression scale. Multiple linear regression analysis and PROCESS macro were used for data analysis. The overall detection rate of depression was 28.43%, and significant correlations were observed among physical disorders, ADLs, cognition, and depression (p&#x2009;<&#x2009;0.05). Mediation analysis revealed that hearing impairment not only had a direct effect on depression (&#x3b2;&#x2009;=&#x2009;2.298, p&#x2009;<&#x2009;0.001) but also significant indirect effects mediated through ADLs (&#x3b2;&#x2009;=&#x2009;0.630, p&#x2009;<&#x2009;0.01) and cognition (&#x3b2;&#x2009;=&#x2009;0.666, p&#x2009;<&#x2009;0.001). The total indirect effect accounted for 36.06% of the total effect. Similarly, the effects of visual impairment on depression were mediated by ADLs (&#x3b2;&#x2009;=&#x2009;0.301, p&#x2009;<&#x2009;0.05) and cognition (&#x3b2;&#x2009;=&#x2009;0.380, p&#x2009;<&#x2009;0.01), with the mediation effect accounting for 68.10%. In contrast, chewing impairment showed a direct effect on depression (&#x3b2;&#x2009;=&#x2009;1.354, p&#x2009;<&#x2009;0.01), but no significant mediation was found through ADLs and cognition. Our findings indicated that hearing and visual impairments were associated with an increased risk of depression, with these effects operating both indirectly through ADLs and cognition. These findings highlight the necessity of comprehensive geriatric care approaches that integrating sensory rehabilitation with interventions with ADLs and cognitive support.

Sleep-dependent memory consolidation differs by sex and maybe disrupted by Alzheimer's disease (AD) risk. Whether sex moderates associations between apolipoprotein E &#x3b5;4 ( APOE &#x3b5;4 ) status, non-rapid eye movement (NREM) sleep, and memory remains unclear. Eighty cognitively unimpaired older adults completed a word-pair memory task with encoding and immediate testing occurring prior to overnight polysomnography with high-density electroencephalography (hdEEG) and delayed recall occurring after sleep. Sleep-memory associations were examined as a function of sex and APOE &#x3b5;4 status. In this sample, a sex&#xd7; APOE &#x3b5;4 interaction was associated with overnight memory retention, with female carriers exhibiting less overnight forgetting than female non-carriers and male &#x3b5;4 carriers. NREM sleep differed by sex and APOE &#x3b5;4 status and was associated with memory retention in &#x3b5;4 carriers. These findings indicate sex-specific, sleep-dependent memory mechanisms associated with genetic AD risk, highlighting sleep as a potential early target for intervention, pending replication in larger samples.

The increasing potency of cannabis and the growing prevalence of chronic, high-dose use have raised concerns about its potential neurotoxic effects on cognitive functions, particularly memory. While low-dose cannabinoids have demonstrated therapeutic benefits, the molecular basis of memory impairment under high-dose exposure remains insufficiently clarified. This narrative review aims to elucidate the molecular mechanisms underlying memory impairment associated with chronic, high-dose &#x394;9-tetrahydrocannabinol (&#x394;9-THC) and cannabis exposure, and to distinguish these effects from the beneficial outcomes observed at lower doses. A narrative review methodology was employed to synthesize evidence from both human studies and murine models, focusing on molecular, cellular, and neurobiological pathways involved in memory dysfunction. Chronic high-dose activation of the endocannabinoid system (ECS) induces acascade of adverse molecular events, including neuroinflammation, oxidative stress, and activation of apoptotic pathways. Significant dysregulation of key neurotransmitter systems was also observed. Importantly, high-dose &#x394;9-THC disrupts neuroplasticity by impairing hippocampal neurogenesis, synaptogenesis, and dendritic remodeling, thereby compromising mechanisms essential for memory formation and consolidation. Adolescents and elderly individuals were identified as particularly vulnerable populations. Chronic exposure to highdose &#x394;9-THC is strongly associated with memory impairment through interconnected molecular pathways. These findings provide a mechanistic framework linking cannabis exposure to cognitive deficits and highlight the need for longitudinal human studies and the development of targeted therapeutic interventions.

Working memory impairments are a common late effect in survivors of childhood acute lymphoblastic leukaemia, yet the structural network substrates of these difficulties remain poorly defined. Existing connectomic studies often rely on whole-brain parcellations, overlooking working memory-associated circuitry and multiscale organization. We developed a multiscale structural connectivity framework to investigate working memory-associated networks using diffusion MRI and performed a cross-sectional study with 70 acute lymphoblastic leukaemia survivors and 70 age and sex matched healthy controls. Working memory-relevant regions were identified based on functional activation patterns, and structural connectomes were constructed at two spatial scales: a fine-scale 76-node network and a coarser 24-node network derived from spatially contiguous, architecturally and functionally coherent regional groupings, as defined in the multimodal parcellation atlas of Human Connectome Project. Graph theoretical metrics, clustering coefficient, Eigenvector centrality, local assortativity and participation coefficient were computed to assess local network topology. Group comparisons were conducted with false discovery rate correction for multiple comparisons. Compared to healthy controls, survivors exhibited marked topological shifts. Specifically, clustering and assortativity were increased in the caudate, putamen and thalamus but decreased in the frontoparietal cortex. In contrast, centrality and participation showed the opposite pattern, signalling subcortical segregation and cortical hyperintegration. These effects were consistent across both spatial scales. Additional findings included scale-specific effects unique to the fine scale, as well as heterogeneous fine-scale patterns that resolved into consistent regional changes at the coarse scale. All effects remained significant after false discovery rate correction, highlighting the robustness of the network reorganization. Our framework combining a targeted working memory network with multiscale connectomic analysis proves its worth by revealing structural changes of working memory circuitry in survivors compared to healthy controls. The results show a broad reorganization, with weakened cortical networks and strengthened subcortical circuits, possibly as a form of compensation. These insights sharpen our understanding of treatment-related structural network alterations and point to new targets for future studies of cognitive outcomes and rehabilitation.

Deficits in hippocampal-dependent memory tasks following lipopolysaccharide (LPS) administration are frequently reported. However, prior work has predominantly been conducted with males. Given recent reports showing sex-related differences in the cognitive effects of an acute LPS challenge, the present study evaluated whether sex differences in spatial learning and memory exist. Adult female and male C57BL/6J mice were evaluated for spatial learning and memory in a hidden platform version of the water maze following administration of LPS (0.25 mg/kg) prior to the first day of training. Results showed that LPS impaired spatial memory in males but had no effect on memory in females. Females and males showed differential use of behavioral search strategies during the probe trial, which may contribute to the selective vulnerability seen in males. Assessment of hippocampal and splenic inflammatory markers showed similar LPS-induced expression across the sexes, indicating that cytokine induction does not produce comparable cognitive deficits in males and females. However, males showed higher hippocampal expression of the interleukin type 1 receptor accessory proteins (AcP and AcPb) relative to females that may alter the impact of inflammation on the hippocampus. Ultimately, these data extend recent findings of sex-dependent effects of LPS on cognition to the water maze and emphasize the importance of reporting and comparing subjects' biological sex.

Successful working memory of previous locations is critical for optimal navigation of the environment in primates. However, it remains unclear how successful working memory influences the statistics of sensory-motor probing (e.g., whisking, sniffing, saccading). This study addresses this gap by investigating the coupling between saccadic eye movements and neural oscillations in the frontal eye field. We demonstrate that the influence of working memory on saccadic behaviors involves a distinct coupling to beta rhythms. Analyzing local field potentials (LFPs) and saccadic patterns in rhesus monkeys performing a visual foraging task, we find that prior memory of visual targets is followed by a significant reduction of the synchronization of saccades with beta oscillations. This reduction suggests that working memory refines saccadic strategies by dynamically modulating neural synchronization, thereby optimizing visual search efficiency. Our findings elucidate a fundamental mechanism through which memory may affect sensory-motor integration, highlighting the pivotal role of neural oscillatory adjustments in enhancing the cognitive processes that govern strategic eye movements and perception.

Chronic brain demyelination and neurodegeneration are hallmarks of progressive multiple sclerosis (MS) that underlie cognitive impairments. Neural precursor cells (NPCs) in the hippocampus support cognition through neurogenesis. With MS chronicity, neurogenesis declines leading to memory impairments. The mechanisms that drive NPC quiescence in MS are largely unknown. Here, we link downregulation of neuregulin-1 (NRG-1) to diminished self-renewal, activity and neurogenesis of NPCs, and hippocampal neurodegeneration and memory decline in mice with chronic demyelination. NRG-1 is a key signaling protein for neural differentiation and function that we previously reported its dysregulation in chronic active lesions of human secondary progressive MS (SPMS). We show that NRG-1 restoration reactivates NPCs and foster hippocampal repair by supporting neurogenesis, neuronal complexity, synaptogenesis, and remyelination that reverse memory impairments. Compared with Siponimod, a current disease modifying therapy for SPMS, NRG-1 achieved greater and multifaceted reparative effects, highlighting its potential as a regenerative therapy for progressive MS.

Aging in adults is associated with a decline in speech-in-noise (SiN) recognition, yet the neural mechanisms driving this decline remain insufficiently characterized. Most neural evidence on age-related SiN performance has relied on correlational approaches that describe how SiN ability is related to age, but it is not yet clear how changes in specific brain structures mediate this relationship. Moreover, it remains unclear how such mediation manifests when hearing sensitivity is clinically normal. The present study applied a brain-wide, region-level mediation framework to identify the neural pathways through which regional brain atrophy mediates age effects on SiN performance. We studied data from 208 adults (aged 20-80 years; M&#x202f;=&#x202f;49.5, SD&#x202f;=&#x202f;19.6) who participated in the Aging Brain Cohort (ABC) Study at the University of South Carolina. Participants completed pure-tone audiometry (PTA) test, the Words-in-Noise (WIN) test, and underwent high-resolution structural MRI. Regional gray- and white-matter volumes were derived using the Johns Hopkins University atlas, and mediation was assessed using the graphical Brain Association Tool (gBAT) to systematically examine how reduced brain volume mediates age-WIN recognition link. A secondary analysis examined mediation effects in a subgroup of 150 participants with clinically normal hearing sensitivity. Behavioral results showed that each additional decade of life was associated with approximately 1.3 dB SNR increase in WIN thresholds. Whole-brain mediation analyses showed that age-related atrophy in regions supporting selective attention, error monitoring, working memory, motor control, and multimodal cue integration mediated age-associated declines in SiN recognition. These neural mediation effects persisted, though with reduced magnitude, in the subgroup with clinically normal hearing sensitivity. The results identify brain structural mechanisms underlying SiN difficulties and emphasize that age-related changes in brain structure impair SiN performance even when audibility remains intact.

The associations between adult lead exposure and late-life cognition are largely unknown. In two cohorts, Kaiser Healthy Aging and Diverse Life Experiences (KHANDLE, n&#xa0;=&#xa0;1638) and Study of Healthy Aging in African Americans (STAR, n&#xa0;=&#xa0;741), we assessed residential proximity to lead-releasing facilities for association with domain-specific cognition 2 years later. Linear regression models adjusted for age, sex, race/ethnicity, income, education, marital status, smoking status, and alcohol consumption. We meta-analyzed across cohorts. Average age was 76.1 (KHANDLE), 68.8 years (STAR); average residential distance to a lead facility was 8.2&#xa0;km (KHANDLE), 3.6&#xa0;km (STAR). In meta-analysis,&#xa0;for every 5&#xa0;km closer a residence was located to a lead-releasing facility, episodic memory scores 2 years later were -0.05&#xa0;(95% confidence interval: -0.08, -0.02) standard deviation lower. Residential proximity to a lead-releasing facility was associated with poorer cognition 2 years later among adults in two cohorts.

Oxytocin plays an important and well-known role in promoting social interaction in maternal, sexual and interpersonal behaviors. In addition, it has been increasingly linked to the modulation of pain, fear and cognitive processes such as attention and memory, which seems to be supported by the presence of oxytocin receptors in various brain areas. With this in mind, this study aims to investigate the effects of inhaled oxytocin on fear, pain perception and aversive memory in humans, as well as the relationship between them. The study involved 65 healthy female volunteers who were randomly assigned to receive either intranasal oxytocin (40&#xa0;IU) or a placebo. The participants were divided into two experimental designs, A and B, with within-subject comparisons conducted. Its effects on pain were investigated by means of the Cold Pressor Test, keeping records of pain threshold and tolerance, as well as of its intensity using the Visual Analog Scale (VAS) and its classification using the McGill Pain Questionnaire. The effects on fear were investigated using the Trauma Film Paradigm, with the intensity of fear measured by means of the VAS, as well as aversion, attention and immersion in the film. A questionnaire was deployed to assess aversive declarative memory at different intervals. Intrusive aversive memories were analyzed by means of quantitative and qualitative records taken over 7&#xa0;days. Our results showed that oxytocin increased dislike of pain when the painful stimulus occurred in an aversive context, which may have contributed to a negative mood state. In addition, oxytocin attenuated intrusive memories in such a way as to reduce their frequency and the suffering they caused. Altogether, the results suggest that intranasal oxytocin can modulate the subjective perception of pain, fear and aversive memory in humans, depending on the context in which the stimuli occur and their biopsychosocial relevance.

Environmental sound recognition (ESR) enables listeners to interpret complex acoustic environments, yet the frequency regions that support recognition are poorly understood. This study used deep learning to model ESR in competing speech and estimate frequency band-importance functions (BIFs) underlying recognition performance. Trial-level responses were collected from 46 listeners who identified 25 everyday sounds mixed with speech across a wide range of target-to-masker ratios. Two model variants were evaluated: one trained to mimic human performance, which was trained on soft labels derived from listener responses, and one trained for maximum accuracy, which was trained on ground-truth correct sound labels, enabling a direct comparison between perceptually driven and task-optimal band-importance patterns. The human-trained model closely reproduced key features of human performance, whereas the ground-truth-trained model exceeded human accuracy and showed highly reliable performance across cross-validation folds. BIFs were estimated by bandstop filtering the target signal and quantifying the resulting drop in recognition accuracy. Both model variants yielded reproducible BIFs with five prominent peaks (&#x223c;0.43, 0.77, 1.46, 2.6, and 9.7&#x2009;kHz), largely driven by subsets of sounds having sharply tuned spectral dependence. This convergence across training objectives suggests that human performance closely reflects the task-optimal frequencies for segregating environmental sounds from speech maskers.

Working memory (WM) impairments affect a subset of multiple sclerosis (MS) patients even during early disease stages, yet the specific cognitive subprocesses and neural mechanisms underlying these deficits remain unclear. Using a multimodal neuroimaging approach combining high-density event-related potentials and structural MRI, we examined the temporal dynamics and structural correlates of WM dysfunction in recently diagnosed MS patients with less than six years of disease duration and minimal clinical disability. Thirty-four MS patients and 19 age-matched healthy controls performed a visuo-verbal WM task during high-density EEG recording and received complete neuropsychological and structural brain imaging evaluation. Behavioral analysis revealed significant WM impairment in a subgroup of MS patients. Electrophysiological findings showed markedly reduced P3 amplitudes during the encoding phase in impaired MS patients, suggesting weaker memory trace formation. Source localization analysis demonstrated aberrant frontoparietal activation patterns, with enhanced frontal engagement and attenuated posterior cortical activity in MS patients showing WM deficits. Structural neuroimaging revealed significant thalamic volume loss and cortical thinning in the right superior parietal and lingual gyri in memory impaired MS patients, regions central to visuospatial processing. Critically, gray matter alterations correlated significantly with electrophysiological markers and behavioral WM performance. These findings establish that early WM impairment in MS reflects disrupted encoding processes through abnormal frontoparietal network dynamics and selective structural degenerative changes. This integrated analysis clarifies the mechanistic basis of cognitive dysfunction in early MS and identifies neurobiological substrates amenable to targeted cognitive rehabilitation, with implications for early detection and intervention strategies to prevent accelerated cognitive decline.

Recently, research has focused on understanding the assessment and management of Parkinson's Disease Mild Cognitive Impairment (PD-MCI) (Svenningsson et&#xa0;al., 2012). The primary aim of this two-phase study was to develop a novel cognitive assessment tool, Par-Cog (Parkinson's Cognition) designed to evaluate PD-MCI. In Phase 1, 20 experts(including Neurologists, Geriatricians, Neuropsychologists, and PD Nurses) were recruited via social media and anonymously completed a survey on Qualtrics, providing feedback on the acceptability and validity of the Par-Cog. The qualitative data were analyzed using the content analysis method proposed by Elo & Kyng&#xe4;s, 2008, while descriptive statistics analyzed the quantitative data. Phase 2 included 100 cognitively healthy participants from the British Isles, aged between 50 and 79&#x2009;years, who were randomly assigned to either Group A or Group B (alternating, consecutive order for completing the Par-Cog and Addenbrookes, ACE-III) using Zoom. In Phase 1, the Par-Cog demonstrated strong face and content validity, with high acceptability reported by experts, particularly Neuropsychologists. In Phase 2, the total and 5 domain Par-Cog scores were normally distributed, showing no floor effects. Significant ceiling effects were found for language and visuospatial scores. Mean-based percentiles were calculated, with Pearson's correlation and regression analyses revealing significant relationships between age and education with Par-Cog scores (p <.05) except for visuospatial scores. Significant correlations were found between ACE-III and Par-Cog attention, memory, and executive functioning scores (convergent validity, p < .05). Bland Altman plots indicated good agreement between Par-Cog and ACE-III scores, and the internal consistency for Par-Cog total (&#x3b1;&#x2009;=&#x2009;0.70), memory (&#x3b1; = .60) and executive functioning (&#x3b1;&#x2009;=&#x2009;0.82) scores were deemed acceptable. The administration of the test did not statistically influence Par-Cog scores (M =.51, 95% CI [-5.78, 4.74], t(98)= -1.95, p= .835). Although the Par-Cog is still in the early stages of development, this study indicates that it serves as an effective remote assessment tool for evaluating PD-MCI, with constructs of acceptability, validity and reliability examined.

Population aging is associated with progressive declines in physical and cognitive function driven by chronic low-grade inflammation and dysregulation of interconnected biological systems. Within the geroscience framework, we tested whether chronic swimming initiated in late midlife attenuates age-related deficits by modulating body composition, systemic and hippocampal inflammation, episodic-like memory and gut microbiota composition. Male C57BL/6 mice were trained for 8 weeks starting at 14 months; age-matched controls remained sedentary. Swimming reduced weight gain and epididymal fat mass and progressively improved muscle strength and endurance. Exercised mice showed enhanced short-term spatial discrimination and long-term associative recognition in object location and object-in-place tasks without changes in locomotion or anxiety-like behavior. These cognitive benefits coincided with reduced circulating pro-inflammatory cytokines and a hippocampal shift toward a neuroprotective profile, with down-regulation of inflammatory and glial activation markers and up-regulation of brain-derived neurotrophic factor (BDNF). Muscle performance correlated positively with hippocampus-dependent memory, linking physical resilience to cognitive outcomes. In parallel, 16S rRNA gene sequencing revealed an exercise-induced remodeling of the gut microbiota, characterized by significant changes in community structure and coordinated shifts in the relative abundance of shared taxa. Exercise enriched genera associated with metabolic homeostasis and anti-inflammatory functions, including Akkermansia, Odoribacter and Alistipes, while reducing taxa more prevalent in sedentary animals, such as Romboutsia. Collectively, these findings demonstrate that moderate-intensity swimming initiated during late middle age concurrently improves physical performance, cognitive resilience, inflammatory status and gut microbiota composition, supporting exercise as a multi-system intervention associated with coordinated adaptations across the muscle-gut-brain axis during aging.

To investigate changed levels of serum astrocytic biomarkers, including glial cell line-derived neurotrophic factor (GDNF), aldehyde dehydrogenase (ALDH) and connexin-26, and the correlations with depression subtypes, cognitive dysfunction and electroencephalogram measures in patients with depression disorder (DD). Seventy-three patients and 46 healthy subjects (HC) were enrolled. Questionnaires, Nine Box Maze Test (NBMT) were used to assess sleep and neuropsychology. Serum biomarkers were evaluated with enzyme-linked immunosorbent assay. Partial subjects (45 DD and 10 HC) completed polysomnography. Compared to the HC, the patients had lower levels of GDNF, ALDH and connexin-26, and increased errors in NBMT tasks, including spatial/object working memory (SWM/OWM) and spatial/object reference memory (SRM/ORM). The connexin-26 concentration was higher in recurrent depression relative to dysthymia and bipolar depression; and GDNF concentrations was higher in the first episode depression compared to the recurrent depression and bipolar depression, with the lowest concentration in dysthymia. Partial correlation analysis for patients showed that the GDNF positively associated with N3% and power of delta wave; ALDH positively associated with MMSE score and OWM error; and connexin-26 negatively correlated with ORM and SRM errors. Depressive patients had decreased serum levels of GDNF, ALDH and CX26, with subtype-specific difference in GDNF and CX26, which were associated with impaired cognition and slow wave power of electroencephalogram.

Gold nanoparticles (AuNPs) emerge as promising neuromodulatory biomaterials due to their tunable optical properties, biocompatibility, and ability to cross the blood-brain barrier. Here, we investigated the behavioral and neuroprotective effects of citrate-stabilized AuNPs (~ 19&#xa0;nm) coated with PEG3350 and irradiated under white (AuWL+PEG) or green light (AuGL+PEG), compared with non-irradiated PEGylated AuNPs (AuNP+PEG). Comprehensive physicochemical analyses demonstrated that green-light irradiation enhanced surface plasmon resonance (SPR) activity, improved PEG adsorption, and yielded superior colloidal stability relative to white-light irradiation. In vivo evaluation in Wistar rats revealed that AuGL+PEG produced robust anxiolytic-like effects in the elevated plus maze, significantly enhanced spatial working memory in the Y-maze, and improved performance in the radial arm maze, approaching the efficacy of donepezil. In the forced swimming test, AuGL+PEG also produced the most favorable antidepressant-like profile, reducing immobility without locomotor confounds. Biochemically, AuGL+PEG markedly enhanced antioxidant capacity, increasing SOD, CAT, GPX, and GSH levels while reducing lipid peroxidation (MDA), consistent with restored redox homeostasis. Acetylcholinesterase inhibition was significantly greater in irradiated groups, supporting improved cholinergic signaling. Toxicological evaluation indicated no major systemic or hematological toxicity at the administered doses. Collectively, the findings demonstrate that light-engineered PEGylated AuNPs, particularly those activated with green light, exhibit potent neuroprotective and cognition-enhancing effects mediated by plasmonic surface optimization, antioxidant defense reinforcement, and cholinergic modulation. These results identify AuGL+PEG as a promising candidate nanomaterial for future applications in neuromodulation, cognitive enhancement, and the treatment of neurodegenerative diseases.

Resting-state functional connectivity (RSFC) contains participant-specific patterns that can support differentiation among individuals within a cohort. This paper proposed computational approaches for determining the differential identifiability of nodes within the RSFC from the Human Connectome Project (HCP) and Leipzig Mind-Brain-Body (LEMON) datasets, and defined fingerprint-like nodes to explore individual brain functional fingerprint recognition and cognitive prediction. In addition, the predictions of fluid intelligence and working memory were explored. Experiments revealed that fingerprint-like nodes achieved higher recognition rates than whole-brain functional connectivity nodes, with individual recognition rates of at least 95.6% and 99.5% in the HCP and LEMON datasets, respectively. These nodes showed variability across brain atlases and datasets but consistent distribution within functional networks. Predictive models using these nodes also improved fluid intelligence and working memory predictions. Compared with existing methods, the proposed approaches define fingerprint-like nodes and systematically reveal their spatial distribution characteristics and contribution weights to individual functional fingerprint recognition at the node level. Although the VAN and DAN contribute less to individual identification of functional fingerprints compared to the FPN and DMN, our experiments find there are nodes within these networks that significantly impact individual identification. The fingerprint-like nodes performed well in both individual brain functional fingerprint identification and cognitive prediction. These approaches would contribute to a deeper understanding of the neural mechanisms of RSFC organization and function, as well as the mechanisms of RSFC in individual recognition and cognitive prediction.

Becoming a parent is a significant life transition, leading to extensive change and uncertainty in one's daily environment. Parenthood is often thought to have adverse consequences across multiple cognitive domains, such as memory, a phenomenon known colloquially as 'baby brain'. Evidence supporting an objective cognitive decline in the postpartum period is unconvincing, and it is unknown whether fathers experience similar changes in cognitive function. Here we examine cognitive differences in birthgiving mothers and non-birthgiving fathers up to two years postpartum. Four hundred participants (300 parents and 100 non-parents) completed a cognitive battery assessing executive function, working and episodic memory, processing speed and subjective memory. Parents showed similar performance to non-parent controls on all objective cognition measures, and we found evidence for no differences in cognitive performance between mothers and fathers, suggesting the absence of so-called "baby brain" effects. Significant group differences in subjective memory were driven by a self-promotion bias, where male non-fathers reported better subjective memory than all other groups. A commonly shown phenomenon in males, this self-promotion bias appeared to be lost in fathers, an effect driven by lack of sleep. Strikingly, there was no effect of time postpartum on any cognitive measure. Therefore, these results challenge the societal 'baby brain' stereotype, and provide a new foundation to support family units together irrespective of birth-giving status.