Biology subjects

Jiang, Z.

Publications and source records attributed to Jiang, Z..

At least 19 recordsLinked to original sources

bioRxiv2026

Age Associated Shifts Toward Anaerobic Taxa and Amino Acid Degradation Potential in the Canine Oral Microbiome

Introduction: Periodontal disease is common in dogs and is associated with changes in oral microbial community composition. How the canine oral microbiome restructures across age at both ecological and metabolic levels remains incompletely characterized. Methods: We analyzed shotgun metagenomic buccal-swab profiles from 1,125 dogs using MetaPhlAn. Functional profiles from HUMAnN were analyzed at pathway and functional-group levels. We annotated species-level taxa with oxygen preference and evaluated oxygen-tolerant and anaerobic taxa abundances across age. We also characterized community structure, metabolic potential, Shannon diversity, and age and weight prediction using nested cross-validated Elastic Net models. Results: Age was associated with substantial restructuring in the oral microbiome. Mean oxygen-tolerant taxa abundance decreased from 67.5% in puppies to 29.1% in mature dogs, whereas anaerobic abundance increased from 14.3% to 53.8%. The oxygen-tolerant: anaerobe log-ratio declined with age (Spearman {rho} = -0.616). Metabolic profiles also varied with age, with higher amino-acid-degradation potential and lower glycolysis and central-carbohydrate potential, and aerobic-respiration-I abundance in older dogs. Shannon diversity increased with age ({rho} = 0.537, p < 0.001). Elastic Net models trained on microbiome species abundance predicted age (Pearson r = 0.609; R-squared = 0.371) and weight (r = 0.498; R-squared = 0.248) with moderate accuracy. Discussion: Canine age was associated with coordinated changes in oral-community oxygen preference and metabolic pathways. These findings extend prior taxon-specific observations by examining a broader ecological shift and metabolic potential in the canine oral microbiome. This provides a reference for future longitudinal or clinical studies of oral maturation and periodontal disease.

microbiology↗

bioRxiv2026

Biosynthesis of Securinega alkaloids via a cyanogenic glucoside-like pathway

The elucidation of biosynthetic pathways towards bioactive compounds in plants is essential for building biotechnological platforms for their scalable synthesis. Securinine and allosecurinine form part of the complement of Securinega alkaloids in Flueggea suffruticosa, a fundamental herb of Chinese medicine. Despite their potent biological activities and a growing interest in derivatives as pharmaceutical leads, key steps in their biosynthesis remain obscure. Here we report the discovery and reconstitution of the pathway to the core Securinega alkaloid precursor menisdaurilide. Using transcriptomics, Nicotiana benthamiana transient expression, in vitro assays, and pathway reconstitution in Saccharomyces cerevisiae, we reveal that three cytochrome P450s and a reductase are required for the biosynthesis of menisdaurilide from L-tyrosine via the cyano-metabolite menisdaurigenin, revealing a surprising convergence with the biosynthesis of cyanogenic glucosides such as dhurrin. The de novo biosynthesis of allosecurinine in N. benthamiana highlights the potential for preparative-scale heterologous production of Securinega alkaloids.

biochemistry↗

bioRxiv2026

Receptor-like kinase RLK15 binds a fungal RNase effector to enhance autophosphorylation and activate host defense

Fungal pathogens secrete diverse effectors to suppress host immunity, yet the plant receptors that perceive these virulence factors often remain elusive. Here, we identify Ss1624, a secreted RNase from the sugarcane smut pathogen Sporisorium scitamineum, and show that it is recognized by the plasma-membrane-localized CrRLK1L-family receptor kinase RLK15. This recognition triggers canonical immune outputs, including reactive oxygen species burst, callose deposition, defense gene activation, and induces hypersensitive cell death. Mechanistically, Ss1624 physically interacts with the receptor-like kinase RLK15, which is required for Ss1624-triggered cell death. Functional assays indicate that this interaction enhances RLK15 autophosphorylation in a kinase activity-dependent manner, suggesting that Ss1624 can act as an elicitor. Transcript profiling further reveals coordinated expression patterns of Ss1624 and RLK15 during infection, and perturbation of Ss1624 expression alters RLK15 transcript levels and pathogenic outcomes. Extending these findings to rice, the ortholog OsRLK15 contributes positively to resistance to bacterial and fungal diseases without yield penalty in rice. Our results support a model in which a secreted RNase effector is directly sensed by a receptor kinase to initiate broad-spectrum immune responses, providing insights into host-pathogen interactions and identifying RLK15 as a candidate for crop improvement.

microbiology↗

bioRxiv2026

Cross-species analysis identifies APOBEC3-associated spliceosomal snRNA hypermutability

Spliceosomal small nuclear RNA (snRNA) genes show unusually high germline mutation rates, with R-loop formation previously implicated in this mutability. Our cross-species rare-variant and de novo mutation analyses show that hypermutability is concentrated in RNA polymerase II-transcribed spliceosomal snRNA genes, with strong enrichment in primates but a much weaker excess in rodents and chicken, consistent with lineage differences in APOBEC3 repertoires. Human Pol II-transcribed spliceosomal snRNA genes show mutational strand asymmetry, APOBEC3-associated mutational signatures and strong APOBEC3B binding signals. R-loops are also frequent at these loci, including in mouse genes with much weaker hypermutability, indicating that R-loop formation alone is insufficient to explain the phenotype. Together, cross-species comparisons support lineage-specific APOBEC3 activity, rather than R-loop formation alone, as a major contributor to spliceosomal snRNA gene hypermutability.

genomics↗

bioRxiv2026

Land use and climate warming interact to reshape global avian biodiversity through ecological filtering and homogenisation

Land-use and climate change are dominant drivers of terrestrial biodiversity change, yet are usually analysed separately although they co-occur and may interact. We integrated global bird assemblage records from PREDICTS with temperature anomalies and species' ecological characteristics to test how land use modifies biodiversity responses to climate warming across three dimensions: local abundance and richness, compositional dissimilarity among assemblages, and species occurrence across ecological groups. Land use modified warming associations for both abundance and richness. Relative to primary vegetation, warming associations were more positive in low-intensity agriculture for both responses, but more negative for richness in high-intensity agriculture and urban land. Predicted richness remained below the reference, defined as primary vegetation at temperature anomaly 0, across all modified land uses, with the largest declines in high-intensity agriculture (-17.9%) and urban land (-21.8%). Within land-use classes, greater warming exposure was generally associated with higher compositional similarity, consistent with warming associated biotic homogenisation. Occurrence models revealed ecological filtering: broad-niched generalists were favoured in warmer modified habitats, whereas range-restricted habitat specialists were filtered out under intensive land use and warming. Conservation assessments should therefore integrate land-use-warming interactions with changes in assemblage composition and ecological strategies, particularly in agricultural and urban landscapes where warming further disadvantaged range-restricted specialists.

ecology↗

bioRxiv2026

Interferon-induced OASL restricts ADAR1 p150 RNA binding and A-to-I RNA editing

The interferon (IFN)-inducible RNA editor ADAR1 p150 catalyzes adenosine-to-inosine (A-to-I) editing of host and viral double-stranded RNAs, limiting aberrant innate immune sensing and regulating gene expression. How ADAR1 p150 activity is regulated during host-virus interactions remains poorly understood. Here, we identify the IFN-stimulated gene OASL as an inhibitor of ADAR1 p150. OASL engages p150 through two distinct interactions: its N-terminal OAS domain associates with the RNA-binding domains in an RNA-dependent manner, whereas its C-terminal ubiquitin-like domains bind the Z domain independently of RNA. Despite their distinct canonical functions, the OAS and ubiquitin-like domains converge to limit ADAR1 p150 RNA binding and suppress A-to-I editing across the transcriptome. OASL also reverses p150-mediated suppression of antiviral and innate immune gene expression and counteracts p150-mediated enhancement of measles virus and vesicular stomatitis virus replication. Thus, OASL restrains ADAR1 p150, linking interferon signaling to the control of RNA editing and antiviral immunity.

molecular biology↗

bioRxiv2026

Inflammation-induced of Clec18a inhibits immune responses via Trpm7-dependent Cbl activation

Innate immune responses must be tightly controlled to maintain immuno-homeostasis. However, the regulatory mechanisms underlying the activation and early stages of the innate immune response remain poorly defined. Here, we found the soluble C-type lectin Clec18a is up-regulated in multiple inflammatory diseases, including sepsis and influenza, and secreted within minutes upon activation in multiple immune cells, including macrophages, dendritic cells (DCs), and T cells. Clec18a-myeloid-knockout mice exhibited reduced survival and exacerbated inflammation than the wild-type. However, exogenous recombinant Clec18a administration alleviated inflammation both in vitro and in vivo. Mechanistically, we identified macrophage-inducible C-type lectin (Mincle) as the receptor of Clec18a. Clec18a-Mincle binding triggers Trpm7-dependent calcium influx, which activates the ubiquitin E3 ligase Cbl and leads to Mincle-Cbl-MyD88-Trpm7 complex formation and degradation. Cbl deficiency, calcium inhibition and Trpm7 knockdown abrogated Clec18a-mediated immune suppression. Thus, our study revealed Clec18a as a critical checkpoint on the initiation of innate immune response through an intrinsic crosstalk between CLR and TLR signaling.

immunology↗

bioRxiv2026

Loss of DNA Demethylase Enhances Arsenic Resistance Via Reducing of PIN2 Antisense Long Noncoding RNA

DNA methylation dynamics regulate diverse plant stress responses, but the mechanisms governing arsenic (As) tolerance through epigenetic pathways remain largely unknown. Here we report that Arabidopsis mutants lacking the DNA demethylase, REPRESSOR OF SILENCING (ROS1), show substantially enhanced As resistance. Integrating transcriptome and methylome data, we found that PIN-FORMED 2 (PIN2), encoding an auxin efflux carrier that also transports As out of cells, represents a key ROS1 target. In ros1, we observed increased methylation in the last exon of PIN2, a region functioning as the promoter for an antisense long non-coding RNA (lncRNA). Hypermethylation of the promoter suppresses the antisense lncRNA, which follows reduction of sense PIN2 transcription. As a result, PIN2 expression increases in ros1 mutants during As exposure, enhancing As tolerance. Analysis of ros1 pin2 double mutants confirmed that PIN2 acts downstream of ROS1 in As tolerance. Our study demonstrates an epigenetic pathway in which ROS1 regulates As tolerance by controlling PIN2 expression through antisense lncRNA-mediated transcriptional interference, offering new epigenetic strategies using plants in heavy metal contaminated environments.

plant biology↗

bioRxiv2026

Modular core network constructed from Escherichia coli transcriptome datasets using a hypergraph-based pan-network approach

We have developed a method to integrate transcriptomic coexpression networks across diverse experimental conditions within a single species. Our framework expands previous pannetwork approaches into a hypergraph based pannetwork. It first identifies coexpressed gene clusters within each individual dataset and extracts frequently co-expressed gene sets across multiple datasets using a frequent itemset mining algorithm. This process yields a hypergraph where each hyperedge is assigned a frequency (universality, U). We then extracted a subnetwork comprising high U hyperedges as the core network and formed modules within it. We applied our method to 106 Escherichia coli transcriptome datasets from the GEO database. The modularity of the core network peaked at a universality cutoff of 15, which was subsequently used to define it. Approximately 70% of the resulting core modules correspond to operons, and conversely, approximately 70% of all operons are covered by these core modules. We visualized the core network via an inter-modular network and analyzed core module dataset relationships using a modularity profile matrix. Based on these analyses, we successfully visualized the dynamic reorganization of the coexpression network in response to environmental changes in bacteria.

bioinformatics↗

bioRxiv2026

Changes in Neural Dynamics of Brain Activity and Connectivity Independently Predict Post-Stroke Aphasia Recovery

Post-stroke language recovery involves reorganization of left-hemisphere language and bilateral domain-general multiple-demand networks. Neuroimaging predictors of recovery are widely used, yet, they are often grouped into broad predictor families, limiting clinical translation and the identification of specific therapeutic targets. Here, we assess brain region-specific neural predictors of recovery using task-related activity and connectivity within a multivariate, cross-validated predictive framework. Forty-seven patients with aphasia were examined longitudinally in the acute, subacute, and chronic phases after ischemic stroke using a sentence comprehension paradigm during functional neuroimaging, with regions of interest spanning language and multiple-demand networks. Confound-controlled multivariate regularized regression with feature ablation tested whether predictor families explained language recovery beyond lesion, age, and aphasia severity, and identified the most relevant region-specific predictors. Early recovery was independently predicted by acute and subacute activity and connectivity, whereas later improvement was predicted by activity alone. Subacute connectivity from multiple-demand to language regions predicted early recovery, while acute multiple-demand network activity predicted long-term outcomes. Later subacute-to-chronic recovery was instead predicted by subacute and chronic activity in bilateral inferior frontal regions. These findings identify phase-specific functional biomarkers of aphasia recovery beyond traditional clinical measures, highlighting multiple-demand and inferior frontal regions as candidate targets for phase-adapted neurostimulation approaches.

neuroscience↗

bioRxiv2026

Phytosulfokine signaling modulates salt stress responses and cell wall remodeling in Arabidopsis

Salinity severely impairs plant growth and development. Increasing evidence suggests that the cell wall (CW) plays a central role in salt stress acclimation, not only as a structural barrier but also as a dynamic sensor that activates downstream stress signaling pathways. To identify extracellular factors involved in cell wall remodeling and integrity signaling during salt stress, we performed a comparative proteomic analysis of the Arabidopsis seedling apoplast. Among the proteins that accumulated under salt stress, we focused on three members of the Subtilisin-Like Protease family (SBT1.1, SBT1.6, and SBT5.3), which have previously been implicated in the processing of signaling peptides and CW-associated proteins. Functional analyses revealed that sbt1.1 and sbt5.3 mutants exhibit enhanced lignin deposition under salt stress, suggesting altered CW remodeling during stress application. Given the established role of SBT1.1 in processing PHYTOSULFOKINE (PSK) peptides, we investigated the involvement of PSK signaling in salt stress responses. Mutants lacking the two PSK RECEPTORS (pskr1 pskr2) displayed reduced growth and increased lignification under salt treatment. Exogenous application of PSK attenuated salt-induced responses, including MITOGEN ACTIVATED PROTEIN KINASE 6 (MPK6) phosphorylation, salt stress marker gene expression, and lignin accumulation, ultimately promoting root elongation under salt stress. Furthermore, PSK treatment mitigated salt-induced changes in CW composition. In cell wall integrity (CWI) mutants, PSK treatment failed to restore wild-type root growth under salt stress and induced a pronounced root bending phenotype in fer-4, indicating that CWI signaling influences PSK-mediated root growth responses. Together, these results support a role for PSK signaling in modulating CW-associated responses to salinity stress in Arabidopsis.

plant biology↗

bioRxiv2026

From pose to behavior: SABER integrates identity-resolved multi-animal pose tracking with language-model-based behavioral factor discovery

Quantifying social behavior requires accurate assignment of posture and actions to individual animals, which is often hindered by close contact, occlusion, and identity switches. Meanwhile, current behavioral recognition pipelines still lack stable predictive accuracy. Here we developed SABER, a locally deployable framework that couples multianimal pose estimation with identity preserving tracking, interpretable behavioral factor mining, and multiscale temporal behavior prediction from a single overhead video stream. Across spontaneous two mice social interaction, mating, aggression, and four mice recordings, SABER improved pose estimation accuracy and tracking continuity relative to comparator pipelines. Its behavioral factor-mining procedure identified interpretable kinematic, postural, and social descriptors, and temporal integration improved classification of behavioral categories. SABER offers an intuitive, open-source interface to facilitate use. Applied to social defeat stress mice, SABER detected reduced approach behavior and a multivariate behavioral profile that distinguished depression susceptible from control animals. SABER outputs could also be synchronized with miniscope calcium recordings, enabling joint analysis of behavioral states and neuronal population activity. SABER therefore provides an accessible, identity resolved route from single view social interaction video to behavioral phenotyping and brain behavior analysis.

animal behavior and cognition↗

bioRxiv2026

Neuroinflammation and metabolic dysfunction in POLG-related mitochondrial epilepsy

Super-refractory status epilepticus is a common neurological manifestation of mitochondrial disease caused by bi-allelic pathogenic variants in POLG. Epilepsy in POLG-related disease typically presents with an explosive onset of status epilepticus, often from an occipital focus, and is associated with extensive neurodegeneration. The neuropathological mechanisms underlying POLG-related mitochondrial epilepsy remain poorly understood, however, neuroinflammation and glial dysfunction are hypothesised to play a significant role. In this study, we performed a neuropathological and proteomic investigation of post-mortem brain tissues from 12 patients with POLG-related mitochondrial epilepsy (age range: 3 - 28 years) and matched control cases. Given that the primary visual cortex is prominently involved in this epileptic disorder, occipital cortical tissues (Brodmann area 17) were compared to frontal cortical tissues (Brodmann area 9). Liquid chromatography-mass spectrometry (LC-MS/MS) analysis identified a distinct immunometabolic signature in the occipital cortex, and to a lesser extent in the frontal cortex, in POLG-related epilepsy. This was characterised by decreased abundance of mitochondrial proteins coupled to an increased expression of innate immune and inflammatory proteins, consistent with neuroinflammation. To validate these observations, we confirmed an increased density of cells immunoreactive for acute phase proteins (C-reactive protein, osteopontin and serpin A3), immune co-receptors (CD14 and HLA-DR), the inflammatory glycoprotein YKL40, the cytokine TNF-alpha, and mitochondrial translocator protein (TSPO). We also demonstrate a decreased expression of mitochondrial oxidative phosphorylation (OXPHOS) subunits within POLG patient microglia, indicative of mitochondrial dysfunction. Finally, we show enrichment of mitochondrial OXPHOS and interneuron proteins in the control primary visual cortex compared with the frontal cortex, which may underlie the selective regional vulnerability observed in POLG-related mitochondrial disease. Overall, these findings provide strong neuropathological evidence implicating neuroinflammation and glial dysfunction in POLG-related epilepsy.

neuroscience↗

bioRxiv2026

Bexobrutideg: A Selective, Catalytic Degrader of Bruton's Tyrosine Kinase Overcomes Inhibitor Resistance and Suppresses Autoantibody-Mediated Disease

Brutons tyrosine kinase (BTK) transduces B-cell receptor (BCR), Toll-like receptor (TLR), and Fc receptor (FcR) signaling, and overactivation of these pathways drives B-cell malignancies and antibody-mediated autoimmune disease. Small molecule inhibitors block the enzymatic functions of BTK, but this inhibition is undermined by resistance mutations, several of which abolish BTKs kinase activity yet promote oncogenic signaling through BTK scaffolding functions. We report the discovery and characterization of bexobrutideg (NX-5948), a heterobifunctional degrader that recruits cereblon (CRBN) to selectively degrade BTK while sparing molecular glue neosubstrates. We demonstrate that bexobrutideg acts catalytically, degrading thousands of copies of BTK per molecule per hour, and this event-driven pharmacology renders it resilient to mutations that confer resistance to both covalent- and noncovalent-inhibitors. Bexobrutideg is orally bioavailable, driving deep and durable BTK degradation across species. Bexobrutideg demonstrates strong efficacy in wild-type and ibrutinib-resistant lymphoma models and robustly suppresses pathway activation in models of autoimmune disease.

cancer biology↗

bioRxiv2026

Engineered probiotic Escherichia coli-mediated intestinal nicotine clearance alleviates nonalcoholic steatohepatitis in mice

Nicotine accumulates in the gut and drives non-alcoholic steatohepatitis (NASH) via the gut-liver axis, yet no effective clinical intervention is currently available. To address this challenge, the probiotic Escherichia coli Nissle 1917 (EcN) was engineered for in situ nicotine clearance in the gut. Mutational screening of nicotine oxidoreductase 2 (PpNicA2) identified a highly active variant, PpNicA2A107R. Its incorporation into EcN together with an electron transfer protein (CycN) and a newly identified transporter (T3/T7) yielded 80% nicotine-degrading activity. Chromosomal integration of this module generated a stable strain, EcN-N12, which in NASH mouse models depleted intestinal nicotine, rescued hepatic lipid metabolism, alleviated tissue damage, and intercepted the nicotine-mediated gut-liver axis pathological progression. This work thus offers an effective and clinically translatable approach for nicotine-associated diseases.

synthetic biology↗

bioRxiv2026

Internalized Components of Membrane Attack Complexes Disrupt Proteostasis and Acquire Alarmin-Like Properties

Immune effects of membrane attack complexes (MAC) have been widely attributed to their abilities to cause cell death. Here, we show that the MAC component, C9, forms non-cytolytic aggregates with pro-inflammatory effects. Intracellular aggregates of C9 are detected within inflamed tissues of patients in association with endothelial cell (EC) activation but not increased cell death. We identify NUMBL as a Rab35 effector that directly binds surface-bound C9 to promote C9 internalization and entry into the endolysosomal pathway. Within acidified endolysosomes, C9 forms insoluble aggregates that are targeted for degradative aggrephagy in a process that activates NF-{kappa}B. For C9 aggrephagy to occur, ZFYVE21, a Rab5 effector, complexes with RNF34 to bridge C9 aggregates to LC3B+ aggresome membranes. We detect C9 aggregates in vivo, and we show that a ZFYVE21-RNF34 signaling axis is required for C9 aggrephagy and NF-{kappa}B -dependent EC activation in three separate mouse models. Mice with conditional loss of ZFYVE21 in ECs show reduced aggregraphy, resulting in attenuated systemic inflammation and reduced tissue injury following skin transplantation. Our data show that the C9 component of MACs forms intracellular aggregates with alarmin-like properties.

biochemistry↗

bioRxiv2026

A Hypothalamic Inhibitory Circuit Encoding the Scalability of Stress Responses

An appropriate stress response is essential for properly responding to, coping with, and subsequently recovering from disturbing environmental stimuli. However, how the brain dynamically encodes the scalability of stress responses remains poorly understood. Here, we found that, GABAergic neurons in the arcuate nucleus (Arc, denoted as ArcGABA neurons) send direct inputs to corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus (PVH, denoted as PVHCRH neurons), the primary regulators of the hypothalamic-pituitary-adrenal (HPA) axis. Although PVHCRH neurons exhibited time-locked activation in response to various environmental stressors, both GABA release onto PVHCRH neurons and the activity of PVHCRH-projecting ArcGABA neurons were selectively reduced during exposure to prolonged, high-intensity stressors, but not following exposure to transient, low-intensity stressors. Notably, GABA release onto PVHCRH neurons was positively correlated with PVHCRH-projecting ArcGABA neuron activity, yet anticorrelated with PVHCRH neuronal activity in response to the same prolonged, high-intensity stressors. Selective silencing of PVHCRH-projecting ArcGABA neurons was sufficient to elevate HPA axis activity and stress levels, phenocopying the effect of direct of PVHCRH neuron activation. Conversely, selective activation of PVHCRH-projecting ArcGABA neurons reduced both HPA axis activity and stress levels, this effect was completely abolished by concurrent excitation of PVHCRH neurons. Molecular identity screening further revealed that these PVHCRH-projecting ArcGABA neurons are not subsets expressing agouti-related peptide (AgRP) and tyrosine hydroxylase (TH) markers. Collectively, these findings indicate that the non-AgRP/TH ArcGABA PVHCRH neurocircuit serves as a critical neural substrate that directly encodes the scalability of stress responses to environmental stressors by modulating inhibitory GABA release in a stimulus intensity-dependent manner.

neuroscience↗

bioRxiv2026

Targeted Photodegradation of Misfolded Proteins via Self-photosensitizing with Molecularly Produced Light

Misfolded proteins are tightly associated with various neurodegenerative diseases, and removing these misfolded proteins is one of the actively pursued approaches for seeking therapeutics for these diseases. In this study, we demonstrated that molecularly produced light (molecular light) from ADLumin-5, a self-photosensitizing chemiluminescence compound, could induce photo-oxidation and photodegradation of misfolded proteins, including beta-amyloid, tau, alpha-synucleins, and TDP-43 proteins in vitro. We validated the oxidation and degradation via LC-MS, MADLI-MS, and western blotting. Using beta-amyloid as a showcase, we demonstrated that, upon photo-oxidation and photodegradation, the toxicities of this misfolded protein were significantly reduced. To investigate the therapeutic effects of ADLumin-5 in vivo, we used the 5xFAD mouse model for longitudinal treatment for 4 months. In vivo molecular imaging results indicated that ADLumin-5 could reduce the accumulation of beta-amyloid proteins. Our study presents a novel approach to seek therapeutics for neurodegenerative disease via molecular light-induced degradation of misfolded proteins. In addition, because ADLumin-5 is dual-functional--enabling both photodegradation and in vivo imaging of misfolded protein changes--it can be considered a photo-theranostic agent for neurodegenerative diseases, representing a novel approach to drug discovery for neurodegenerative diseases.

neuroscience↗