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Lee, J.-H.

Publications and source records attributed to Lee, J.-H..

At least 19 recordsLinked to original sources

Osmotic Coupling of Mechanics and Epigenetics Regulates Chromatin Phase Organization

Cells experience epigenetic, osmotic, and mechanical perturbations that reorganize chromatin, yet how these distinct cues are integrated into a common physical response of the nucleus remains unclear. Here, we identify nuclear hydration as a central state variable that links microenvironmental perturbations to chromatin phase organization and nuclear mechanics. We develop a non-equilibrium mesoscale model that couples chromatin elasticity, water transport, and epigenetic reaction-diffusion kinetics. In this framework, chromatin behaves as a deformable polymer that segregates into coexisting water-rich euchromatic and water-poor heterochromatic phases, whose compositions and morphologies are regulated by hydration-dependent swelling, elastic strain, and histone-mark interconversion. The model predicts that epigenetic perturbations, osmotic shocks, and volume-changing mechanical loads reorganize chromatin by shifting intranuclear water content, nuclear volume, and euchromatin-heterochromatin phase balance. It further predicts that anisotropic forces impose directional strain, driving heterochromatin elongation, alignment, and lamellar transitions. Quantitative comparisons with super-resolution imaging, AFM and chromatin-accessibility measurement - across pharmacological, osmotic, and mechanical perturbations including confinement and micropatterning - support these predictions. Together, our results establish a chemo-mechano-osmotic framework in which nuclear hydration integrates biochemical and biophysical cues to regulate chromatin organization across scales.

biophysics↗

Non3nExonFinder: transcript-aware identification of shared non-triplet coding exons

Selection of an appropriate coding exon is an important upstream step in exon deletion-based loss-of-function strategies, particularly for genes with multiple transcript isoforms. However, manual comparison of exon structures across multiple transcripts can be time-consuming and may overlook transcript-specific differences in exon boundaries and coding sequence (CDS) composition. Non3nExonFinder was developed as an interactive R/Shiny-based tool for identifying shared non-triplet coding exons across user-defined human or mouse NCBI RefSeq protein-coding transcripts. Non3nExonFinder evaluates exon/CDS annotations and coding contributions for each transcript, identifies common exons with identical genomic boundaries, and prioritizes candidates based on CDS-only status and coding-length divisibility by three. Non-triplet CDS-only exons that are internal in all selected transcripts are classified as high-confidence candidates. Independent reconstruction from the original RefSeq GTF files across 80 genes (40 human and 40 mouse), comprising 6,848 transcript-specific exon instances, showed complete concordance with Non3nExonFinder outputs, with exact recovery of all candidate sets. Non3nExonFinder provides a reproducible upstream framework for transcript-aware prioritization of exon-deletion targets.

bioinformatics↗

Spatial Logic Reconciles Gene-signature Methods in Triple Negative Breast Cancer

Triple-Negative Breast Cancer (TNBC) presents a significant clinical challenge due to its heterogeneity and lack of targeted treatment options, with chemotherapy and immunotherapy combinations currently serving as the main therapeutic strategy. Efforts to address TNBC heterogeneity have largely focused on classifying intrinsic cancer subtypes based on differential tumor mRNA expression, a strategy that has proven effective in hormone receptor-positive breast cancers but has yet to yield a clinically useful predictor of survival or treatment response in TNBC. We hypothesize that both the intrinsic characteristics of TNBC and the surrounding immune microenvironment influence treatment outcomes and that immune cell infiltration affects TNBC subtype classification and response variability. To explore this hypothesis, we compared the predictive and prognostic capabilities of cancer subtype-based (TNBC-type) gene signatures and immune cell deconvolution methods (CIBERSORT) within the same TNBC datasets. We found that immune cell abundance outperformed TNBC subtype-signatures and multicellular immune cell aggregates showed the highest performance of all. More specifically, aggregate immune cells associated with tertiary lymphoid structures and tumor associated macrophages/monocytes demonstrated statistically significant predictive value. These findings were confirmed in an independent cohort of 67 TNBC patients treated with neoadjuvant chemotherapy. Further, single-cell RNA sequencing analysis revealed that the predictive power of cancer-subtype could be partially explained by immune- and stromal features. Examination of single-cell resolution spatial transcriptomic data confirmed presence of TLS-like, TAM- and cancer-stromal niches within TNBC biopsy samples that were associated with treatment response. Overall, our results highlight that immune cell aggregates, which capture the spatial organization of the TME, outperform cell-type specific gene signatures in predicting TNBC outcomes. Our novel approach provides a robust framework for interpreting spatial relationships in bulk RNA-seq data, offering a pathway for reconciling past data with current advancements in spatial profiling technologies. This work paves the way for future studies to leverage the multi-cellular complexity of TNBC, enhancing diagnostic precision and facilitating the development of therapies that strategically modulate the tumor microenvironment for improved anti-cancer responses.

cancer biology↗

Disease Stage- and Risk-Associated RNA Editing Signatures in Acute Myeloid Leukemia and Their Utility for Peripheral Blood-Based Assessment

RNA editing is a widespread post-transcriptional regulatory mechanism, but its role in acute myeloid leukemia (AML) remains incompletely understood. We analyzed RNA editing in 59 paired diagnosis-relapse AML samples and eight age-matched healthy controls using a stringent discovery pipeline and beta-binomial regression framework accounting for overdispersion and repeated measurements. A total of 166,323 high-confidence RNA editing sites mapping to 5,917 genes were identified. Of tested sites, 1.2%-3.6% varied significantly by disease stage or ELN-2022 risk group. Disease stage-specific editing signatures distinguished healthy controls, diagnosis, and relapse samples, with relapse-associated signals validated in an independent AML cohort. ELN-2022 risk-specific editing signatures showed substantial overlap between intermediate- and adverse-risk groups. Cross-cohort analyses identified four bone marrow (BM) editing sites in TMEM165, COQ4, TIMM17A, and PLXDC2 reproducibly associated with relapse and one peripheral blood (PB) editing site in ABHD18 elevated in higher-risk ELN-2022 groups. Most editing sites were shared between BM and PB; only 2.1%-2.3% exhibited tissue-specific differences. Higher global editing levels were correlated with leukemic state, white blood cell count, and selected clinical features. These findings identify reproducible RNA editing signatures linked to AML disease stage and risk and support the use of RNA editing biomarkers for PB disease assessment.

bioinformatics↗

Mono-ADP-ribosylation-driven immunosuppression and cross-resistance to therapy through cancer cell intrinsic and extrinsic mechanisms

Mono-ADP-ribosylation (MARylation) is emerging as an important regulator of anti-cancer immunity and immunosuppressive tumor microenvironment (TME). Our previous studies showed that PARP11, one of several enzymes that facilitate MARylation, regulates the activities of intratumoral cytotoxic T lymphocytes (CTLs) and regulatory T cells (Tregs). Here, we demonstrate that stimuli such as adenosine, epinephrine, or glucagon-like peptide-1 (GLP1) induced PARP11 in cancer cells. Upregulation of PARP11 in cancer cells led to PARP11-mediated MARylation, ubiquitination, and accelerated degradation of MHC-I through the autophagy-lysosomal pathway. Induction of PARP11 protected cancer cells from killing by specific CTLs and stimulated tumor growth and progression. Genetic ablation of PARP11 attenuated MHC-I MARylation, ubiquitination, and interaction with autophagy receptors. Pharmacologic inhibition of PARP11 in pancreatic ductal adenocarcinoma (PDAC) cells restored their MHC-I levels, sensitized them to killing by CTLs, inhibited tumor growth, and impeded their initial resistance to chemotherapy and their acquired resistance to targeted therapy with RAS inhibitors. Moreover, inhibition of PARP11 prevented hyperprogressive disease in a mouse melanoma model treated with immune checkpoint inhibitors (ICBs), suggesting that PARP11 is a major therapeutically actionable driver of immunosuppression in tumors. SYNOPSISInduction of PARP11 in the tumor microenvironment mediates immunosuppression. This study reports that PARP11-driven MARylation and ubiquitination of MHC-I in cancer cells drives immune evasion, tumor growth and resistance to therapies.

cancer biology↗

Specialized outputs and behavioral contributions of Purkinje cell subtypes

Purkinje cells (PCs), the sole outputs of the cerebellar cortex, transform granule cell firing patterns into appropriate outputs to drive learning and behavior. Two major PC classes (typically defined by Aldoc expression) can be further subdivided into nine molecularly distinct PC subtypes, suggesting that each subtype might be specialized for distinct categories of cerebellar processing. This has been difficult to test due to limited tools to target PC subtypes. We therefore developed intersectional tools to target PC subtypes, specifically Kcng4+ PCs (primarily Aldoc-) and Gpr176+ PCs (Aldoc1). We mapped their distributions within the cerebellar cortex and quantitatively characterized their outputs onto different types of cerebellar nuclei (CbN) neurons. Although projections by PC subtypes defined by Kcng4 and Gpr176 are regionally segregated within the CbN, each PC subtype synapses onto many types of CbN neurons, and individual CbN neurons often receive convergent inputs from multiple PC subtypes. We also selectively silenced PC subtype outputs and found that silencing Kcng4+ PC outputs impaired motor behaviors while sparing emotional and social behaviors, whereas silencing Gpr176+ PC outputs selectively increased exploratory behavior and reduced anxiety without affecting motor and social behaviors. These findings demonstrate that molecularly defined PC subtypes differentially regulate specific behaviors and establish a versatile framework for uncovering how cerebellar circuits are specialized to control diverse behaviors.

neuroscience↗

The Paipu framework enables creation of a large-scale mammalian cancer transcriptomics atlas

A plethora of studies have identified shared molecular mechanisms involved in tumor development across humans and other mammalian species. While these two-species analyses advance understanding of human disease, extending them across many species would provide evolutionary insight into molecular mechanisms driving human cancers. However, this expansion requires knowledge transfer and harmonization across species. Genomic differences between species, including variation in genome annotation quality, have historically hindered multi-species large-scale atlas creation. To overcome these challenges, we present Paipu, a comprehensive pipeline designed to streamline querying, preprocessing, harmonization, and retrieval of large-scale RNA-seq data and associated metadata from the NCBI Sequence Read Archive (SRA). Paipu facilitates multi-species analysis by creating a harmonized atlas from user-defined search terms and species. It consists of three components: reference genome preparation, SRA metadata retrieval, and RNA-seq data processing. We apply Paipu to 188 cancer-related terms in 239 non-human mammalian species, creating a harmonized atlas of 3,484 RNA-seq samples spanning 17 species and 35 cancers. This pan-mammalian pan-cancer atlas enables myriad comparative genomics analyses that leverage genetic variation to better understand rare human cancers. As such, Paipu serves as a resource for cross-species cancer genomics and supports atlas creation for any set of species and search terms. Graphical Abstract

bioinformatics↗

The astrocyte-enriched gene Tmem44 regulates circadian protein translation in mouse astrocytes

Astrocytes contain cell-autonomous circadian clocks, but how astrocyte-enriched clock-controlled genes feed back onto the circadian clock remains poorly understood. Here, we identify transmembrane protein 44 (Tmem44) as an astrocyte-enriched circadian transcript whose protein product regulates clock protein abundance through translational control. Tmem44 mRNA oscillated in cultured mouse cortical astrocytes in a BMAL1-dependent manner, whereas TMEM44 protein was constitutively expressed and localized to the endoplasmic reticulum. Acute Tmem44 knockdown reduced BMAL1 and PER2 protein levels without altering their mRNA levels or degradation kinetics, and dampened the amplitude and advanced the phase of Per2-luciferase circadian rhythms. SUnSET assays revealed that Tmem44 knockdown decreased global nascent protein synthesis. Proximity labeling and co-immunoprecipitation further showed that TMEM44 associates with ribosomal proteins and ER-associated translational machinery. Importantly, global protein synthesis exhibited circadian oscillation in synchronized astrocytes, and this rhythmic translation was abolished by Tmem44 knockdown. These findings identify TMEM44 as an astrocyte-enriched, ER-resident translational regulator that supports rhythmic protein synthesis and sustains proper amplitude and phase of the astrocyte circadian clock.

neuroscience↗

Epigenetic control of S100A8/A9-driven monocytic inflammation licenses anti-leukemic functionality of immature NK cells during hematopoietic stem cell differentiation.

Inflammation is a key driver of hematopoietic dysfunction in myeloid malignancies, but its role in the context of hypomethylating therapy remains incompletely understood. Although 5-Azacytidine is used posttransplant in high-risk myelodysplastic syndrome (MDS), only 50% of patients show a clinical response. We provide evidence that inherent inflammatory properties of healthy donor CD34+ stem cells exist that are likely to contribute to the "response" seen in MDS patients. These are linked to epigenetic priming of the myeloid niche, resulting in S100A8/A9-driven inflammatory program that promotes functionality of immature NK cells. Using in vitro differentiation systems, multi-omic profiling, and a S100A9-/- mouse model, we find that 5-AzaC modulates inflammatory transcriptional programs through epigenetic rewiring of upstream regulatory elements. Loss of S100A9 disrupts myeloid differentiation, impairs NK cell maturation, and alters key developmental regulators including CEBPB, JUN, and NFIL3. In vivo, 5-AzaC restores these defects and primes NK cells in a time- and context-dependent manner. Re-analysis of the published Australian MDS/CMML cohort shows that "responders" display increased S100A8/A9 expression together with enhanced IFN-{gamma}, IL6-JAK-STAT3, and TNF signaling. These findings suggest that inflammatory myeloid programs may serve as predictive biomarkers and therapeutic targets to enhance NK cell-mediated graft-versus-leukemia activity posttransplant. SummaryO_LIWe provide compelling evidence that inherent properties of healthy donor CD34+ hematopoietic stem cells (SCs) exist that are likely to contribute to the "response" seen upon pre-emptive posttransplant 5-AzaC therapy of patients with high-risk myelodysplastic syndrome (MDS). C_LIO_LIThese properties are linked to a distinct form of epigenetic plasticity at upstream-located transcription factor (TF) binding sites. This may indirectly contribute to acute S100A8/A9-driven inflammation, which is demonstrable in distinct monocyte subsets and, importantly, also in NK cells thereby determining the characteristics of inflammatory monocyte-NK cell crosstalk. C_LIO_LIMice with a targeted deletion of S100A9 fail to upregulate CEBPB / JUN and NFIL3 which results in impaired myeloid priming and dysfunctional NK cell maturation, respectively. C_LIO_LIRe-analysis of the Australian MDS/CMML cohort confirms that MDS patients that "respond" to 5-AzaC exhibit activated IFN-{gamma}, IL6-JAK-STAT3, and TNF-signaling pathways in the context of upregulated S100A8/A9 after six months of treatment. C_LIO_LIOur study indicates that screening of healthy donors SCs for specific inflammatory markers in early developing monocytes could be used as a marker to predict which donor will have the potential of generating a S100A8/A9-driven inflammatory response. This may help identify patients with MDS as well as AML who are likely to benefit from low-dose, short-term 5-AzaC therapy as early as day 7 after transplantation, potentially resulting in increased graft-versus-leukemia (GvL) activity. C_LI

immunology↗

Pharmacological intervention targeting neuroimmune axis in the aging hypothalamus prevents age-associated physiological decline

Systemic physiological aging is largely driven by disrupted metabolic homeostasis, yet the central mechanisms of this metabolic dysfunction remain poorly defined. Here, we identify the hypothalamus as a critical hub driving systemic aging through neuroimmune-mediated mechanisms. Single-cell transcriptomic and immunohistochemical analyses revealed that aged hypothalami exhibit significant infiltration of CD8 T lymphocytes, beginning in middle age, with signatures of activation and tissue residency. These T cells intimately interact with tanycytes and microglia, promoting neuroinflammation and progressive tanycyte loss, a defining hallmark of hypothalamic aging. T cell receptor profiling revealed a substantial presence of invariant natural killer T (iNKT) and mucosal-associated invariant T (MAIT) cells, likely activated through cytokine-driven, antigen-independent mechanisms. In aged hypothalamus, microglia secrete chemokines CCL3 and CCL4, whose ectopic expression in young mice was sufficient to trigger persistent hypothalamic T cell infiltration and accelerated systemic aging. Circulating oxidized LDLs (OxLDLs) were identified as upstream inducers of this chemokine response. Notably, pharmacological blockade of the CCL3/4-CCR5 axis with Maraviroc and Cenicriviroc prevented T cell recruitment and ameliorated metabolic and physiological impairments. Given the clinical safety of CCR5 antagonists and individuals lacking functional CCR5 remain generally healthy throughout life, our findings highlight midlife CCL3/4-CCR5 inhibition as a translatable therapeutic target for delaying age-related decline and promoting healthspan.

neuroscience↗

The Role of Pavlovian Bias in Smoking Cessation Success and Neurocognitive Alterations During Nicotine Withdrawal

BackgroundInability to manage conflicts between multiple decision-making systems is associated with various mental disorders including addiction. The imbalance between the Pavlovian and instrumental systems may contribute to smoking cessation failure and relapse, as excessive Pavlovian motivation may override goal-directed quitting attempts. However, the exact role of the Pavlovian bias in smoking cessation and its neurocognitive mechanisms remain poorly understood. MethodsEighty-six smokers participated in a smoking cessation clinic, completing the well-established orthogonalized go-nogo task before and after the intervention. We applied computational modeling and functional magnetic resonance imaging (fMRI) analyses to investigate the role of Pavlovian bias and its neural correlates in predicting smoking cessation outcomes. ResultsComputational modeling revealed that higher levels of Pavlovian bias were associated with treatment failures. Importantly, Pavlovian bias significantly moderated the relationship between clinic participation rate and the likelihood of smoking cessation, suggesting that such bias can undermine motivational effort to quit. Furthermore, individuals who successfully quit smoking exhibited increased Pavlovian bias toward reward following cessation, indicating a potential cognitive mechanism underlying the relapse cycle. Complementary fMRI analyses demonstrated that Pavlovian bias influenced valence encoding in the ventromedial prefrontal cortex (vmPFC), suggesting altered decision-making neural circuits. ConclusionsPavlovian bias can be a critical risk factor of relapse in the smoking population, while this bias can be increased in response to nicotine abstinence. Moreover, the results highlight the roles of the vmPFC in decision-making under Pavlovian-instrumental conflict, providing insights into the neural underpinnings of relapse vulnerability. Understanding these mechanisms may guide targeted interventions to enhance smoking cessation outcomes.

neuroscience↗

Proximity proteomics reveals the molecular architecture of phytochrome B photobodies in Arabidopsis thaliana

The red/far-red light photoreceptor phytochrome B (phyB) forms light-induced subnuclear condensates, termed photobodies, that coordinate plant responses to light and temperature. Despite their central role in environmental signaling, the molecular composition of phyB photobodies during their early formation has remained unknown. Here, we established an in planta proximity labeling approach using miniTurbo-based biotinylation in Arabidopsis thaliana to capture proteins associated with phyB photobodies during early de-etiolation. Mass spectrometry identified 42 high-confidence proximal proteins, including 11 known core components and 31 previously unrecognized photobody-associated proteins. Among these, the co-chaperone HOP1 forms light-dependent nuclear condensates that partially co-localize with phyB photobodies. HOP1 condensates are smaller in the wild-type background than in phyB-overexpressing seedlings, and HOP1 overexpression enhanced cotyledon expansion under red light. These findings suggest that HOP1 contributes to photomorphogenesis by stabilizing phyB photobodies and sustaining active phyB signaling. Together, our results reveal that nascent large phyB photobodies function as dynamic hubs integrating chaperone-mediated protein quality control with transcriptional regulation, providing the first in planta proteomic framework for understanding photobody assembly and signaling in plants.

plant biology↗

Aggressive nitrogen assimilation during exponential growth in Chlamydomonas reinhardtii

Bioavailable nitrogen (N) is a key limiting factor for global biomass production. In dynamic environments, organisms must employ effective nitrogen use strategies (NUS) to capitalize on episodic N availability. The recent discovery of intracellular guanine crystals in diverse algal species has prompted questions about their roles in NUS. To investigate NUS in Chlamydomonas reinhardtii, a model photosynthetic eukaryote, we compared N-to-biomass conversion rate of mixotrophic batch cultures fed with three common N sources, ammonium, nitrate, and urea. Saturating growth was achieved at 4 mM ammonium, 4 mM nitrate, and 2 mM urea, indicating comparable molar N utilization efficiency. Residual N measurements revealed that approximately 1.2 unit of optical density (O.D. at 680 nm) biomass was produced per mM N under sub-saturating conditions, while biomass accumulation per N decreased at above-saturating conditions. To estimate N storage capacity, we tracked N uptake kinetics in high-density culture following an N pulse, showing rapid assimilation of 3~6 mM N per O.D. biomass. N source-specific transcriptome revealed N source-specific regulation of assimilation pathways and transporter genes in support of effective NUS in C. reinhardtii. These findings support a model in which C. reinhardtii can rapidly acquire and store N during exponential growth, enabling sustained growth and metabolism during periods of N scarcity. Observed variation in N storage capacity across growth stages and N conditions predicts the regulatory mechanisms governing N partitioning and storage. This study highlights flexible NUS in microalgae, offering insights for improving N assimilation capacity and resilience in agricultural and aquacultural crops.

plant biology↗

T-PGI: an engineered STITCHR system for scarless, programmable genome integration

Scarless, programmable insertion of defined DNA remains a central goal for therapeutic genome editing. We introduce T-PGI (Transposon-mediated programmable genomic integration), an engineered implementation of STITCHR that preserves target-primed reverse transcription (TPRT) while substantially improving efficiency, specificity, and modularity. T-PGI uses R2Tocc, a low-background ortholog that we further engineered through defined deletions, rational point mutations, and modular domain insertions to enhance performance. The system employs paired nCas9 nicks flanking homology arms and bicistronic co-expression with dual NLSs, together with optimized RNA donor designs. Using combinatorial guide-template screening, T-PGI achieves robust integration across diverse cargos, including precise cassette insertion following multi-kilobase deletions. Short- and long-read sequencing confirm high-fidelity insertion with minimal local indels or structural variants. Collectively, these advances establish T-PGI as a practical and adaptable platform for accurate, scarless genome integration and provide concise design principles spanning enzyme architecture, donor configuration, and guide pairing for next-generation therapeutic editing.

bioengineering↗

Dynamic Brain Network Changes Associated with Successful Smoking Cessation

BackgroundTobacco smoking continues to be a leading cause of preventable morbidity and mortality globally, with the success rate of unaided cessation remaining consistently low. Understanding the neurobiological mechanisms of smoking cessation is crucial for improving quit rates. However, there has been a lack of studies examining brain network changes associated with smoking cessation over time. In this study, we aimed to investigate longitudinal changes in the functional connectivity (FC) of large-scale brain networks underlying smoking cessation outcomes using resting-state functional magnetic resonance imaging (fMRI). MethodsA total of 98 treatment-seeking smokers participated in a 6-week cessation program and underwent resting-state fMRI scans before and after the intervention. Independent component analysis identified the salience network (SN), executive control network (ECN), and default mode network (DMN) components, and region of interest (ROI)-to-ROI FC was compared between successful and unsuccessful quitters using a group x time mixed-effects model. Correlations with smoking-related measures were explored. ResultsSignificant group-by-time interaction effects were found in FC, particularly involving connections between SN and ECN, as well as between the SN and DMN. Specifically, successful quitters exhibited greater baseline FC in the SN-ECN and SN-DMN circuits, which tended to normalize during the cessation process. Exploratory correlational analyses revealed trends suggesting that stronger pre-quit connectivity between the SN and ECN was associated with greater withdrawal severity and longer smoking history in successful quitters. ConclusionsTaken together, the normalization of initially elevated pre-quit FC in SN-ECN and SN-DMN circuits may reflect an adaptive neural process that supports successful withdrawal management and attentional reallocation during cessation. The identification of these neural substrates not only enhances our mechanistic understanding of smoking cessation over time but also underscores the need for targeted interventions that focus on these neural circuits to enhance quit outcomes.

neuroscience↗

G1899, an American ginseng extract, alleviates neuroinflammation and cognitive impairment in models of Alzheimer's disease

BackgroundAlzheimers disease (AD) is characterized by amyloid {beta} (A{beta}) accumulation, tau pathology, and chronic neuroinflammation, yet current therapeutic strategies provide only limited efficacy. Natural compounds with pleiotropic actions have emerged as potential adjunctive interventions. This study evaluated G1899, a standardized American ginseng (Panax quinquefolius) extract, for its effects on neuroinflammation, A{beta} clearance, and cognitive function. MethodsNeuronal cultures were exposed to glutamate or A{beta} oligomers (A{beta}o) and pre-treated with G1899 to assess cell viability and excitotoxicity. Primary murine microglia were analyzed for validating expression levels of TMEM119, CD68, NLRP3 inflammasome, IL-1{beta}, Caspase-1, and STAT3 phosphorylation. Behavioral testing was performed in scopolamine-injected mice with short term G1899 treatment and in 5xFAD transgenic mice following long-term G1899 administration at multiple doses. Amyloid burden, microglial recruitment, and plaque morphology were quantified by immunohistochemistry and high-resolution imaging. Human induced microglia (iMG) were examined for neuroinflammatory responses following A{beta}o exposure with or without G1899 treatment. ResultsG1899 significantly improved neuronal viability and reduced glutamate- and A{beta}o-induced toxicity. In microglia, G1899 upregulated TMEM119 and CD68, while suppressing NLRP3 inflammasome formation, proinflammatory cytokine expression, and STAT3 phosphorylation. G1899 rescued scopolamine-induced memory deficits and, in 5xFAD mice, reduced hippocampal and cortical A{beta} burden, alleviated neuroinflammatory markers, and improved both spatial/fear learning and memory, with the most consistent efficacy observed at 300 mg/kg. Imaging revealed enhanced microglial recruitment to plaques and facilitated fragmentation of A{beta} deposits. In iMG, G1899 elevated homeostatic and phagocytic markers while attenuating A{beta}o-induced NLRP3/STAT3-mediated neuroinflammatory signaling pathway. ConclusionsG1899 confers multimodal neuroprotection by preserving neuronal survival, modulating microglial activity, and facilitating A{beta} clearance. These findings highlight its potential as a safe and clinically translatable botanical intervention for AD.

neuroscience↗

A naturalistic reinforcement learning task uncovers historical neural representations

Exploration is essential for reinforcement learning (RL) in human development, facilitating cognitive and behavioral adaptation. However, conventional RL paradigms in neuroimaging studies often rely on highly constrained search spaces and artificial, non-naturalistic scenarios, limiting their capacity to reflect the complexity of real-world human exploration and decision- making. To address this gap, we developed a novel, naturalistic RL paradigm called Photographer, which involves a photograph-taking task set in a virtual street-view environment. Participants navigated city scenes and attempted to infer the paradigms covert goal solely from feedback, defined as the conceptual similarity between their photograph and a hidden target sentence. Representational similarity analysis revealed that feedback history, an encoding of recent trial attempts, was robustly represented in the middle orbital gyrus and inferior frontal gyrus. These neural representations were consistently observed across two independent participant groups. Moreover, although the two regions coactivated during exploration, each was associated with a distinct functional network.

neuroscience↗

Parietal top-down projections balance flexibility and stability in adaptive learning

Rapid behavioral adaptation requires the brain to solve a fundamental computational dilemma: how to flexibly update learned rules while maintaining stable motor performance. This flexibility-stability trade-off is central to cognitive function and artificial intelligence, yet its neural circuit basis is poorly understood. Here, we identify the circuit architecture that coordinates this balance. Using a within-session auditory reversal learning task combined with circuit-specific manipulations in mice, we demonstrate that the posterior parietal cortex (PPC) orchestrates adaptive learning through two parallel, anatomically distinct pathways to the auditory cortex (AC) and inferior colliculus (IC). These two circuits perform a double dissociation of function: the PPC-to-AC circuit facilitates flexible rule updating by encoding dynamic stimulus-outcome contingencies, while the PPC-to-IC circuit preserves stable action execution across changing rules. A feedforward network model further demonstrates that segregated stable and flexible top-down projections are necessary and sufficient for rapid reversal learning. This parallel architecture segregates adaptive and stable computations into distinct circuits, providing a mechanistic framework for cognitive flexibility and offering potential insight into conditions where this balance is disrupted, such as obsessive-compulsive disorder and schizophrenia.

neuroscience↗