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Biology subjects

Jeon, S.

Publications and source records attributed to Jeon, S..

At least 19 recordsLinked to original sources

Conserved Brain-Associated CD8+ T Cell Programs and Their Regulation by the Brain Microenvironment

CD8+ T cells are increasingly recognized as components of the healthy brain, yet whether their specialized functional characteristics are conserved across species and how the brain microenvironment regulates their effector programs remain poorly understood. Here, we characterized brain-associated CD8+ T cells in the common marmoset and investigated their regulation by brain-derived signals. Flow cytometric analysis revealed a substantial population of CD8+ T cells in the healthy marmoset brain parenchyma that exhibited high IFN-{gamma} competence but minimal granzyme B (GzmB) expression, resembling the functional phenotype previously identified in mice. Single-cell transcriptomic analyses of mouse and marmoset CD8+ T cells revealed tissue-associated transcriptional heterogeneity and distinct differentiation- and effector-associated programs. To investigate how the brain microenvironment shapes these characteristics, we exposed activated mouse CD8+ T cells to brain lysate and performed targeted CRISPR interference screening of 107 cell-surface receptor genes coupled with single-cell RNA sequencing. Brain lysate selectively reduced Gzmb and Ifng expression while increasing Tnf and Xcl1, indicating differential regulation of cytotoxic and inflammatory effector programs. Receptor perturbations revealed heterogeneous transcriptional responses and identified candidate pathways potentially involved in sensing brain-derived signals. Together, these findings identify shared functional characteristics of brain-associated CD8+ T cells across rodents and nonhuman primates and establish a framework for understanding how the neural microenvironment shapes adaptive immune function.

immunology↗

Genotype-Dependent Variation in Vitamins B1, B2, B3, B6, B9, and C in Mungbean Sprouts

Water-soluble vitamins are essential micronutrients that are not stored extensively in the human body and must therefore be replenished through dietary intake. Mungbean sprouts are widely consumed in some populations; however, their contributions as dietary sources of water-soluble vitamins and the extent of genotype-dependent variations remain insufficiently characterized. In this study, six water-soluble vitamins (B1, B2, B3, B6, B9, and C) were quantitatively and qualitatively analyzed using ultra performance liquid chromatography in sprouts derived from 34 mungbean genotypes. With the exception of pyridoxine (vitamin B6), all analyzed vitamins were detected across all genotypes, and their contents showed significant genotype-dependent variation. To determine whether differences in vitamin composition are reflected in functional responses, antioxidant capacity and enzyme-based bioactivity were evaluated. Antioxidant activity varied significantly among genotypes and showed a positive correlation with nicotinamide (B3) content, while tyrosinase inhibition was positively correlated with thiamine (B1). Evaluation of vitamin contents on a fresh-weight basis demonstrated that a single 104 g serving of mungbean sprouts can provide 46%- 206% of the recommended daily allowance of thiamine depending on genotype, while supplying all analyzed water-soluble vitamins, including B1, B2, B3, B6, B9, and C. This studys findings support the potential of mungbean sprouts to serve as plant-based dietary sources of water-soluble vitamins and offer a basis for selecting genetic resources to improve the vitamin-related nutritional quality of mungbean sprouts.

plant biology↗

GeroEngine: Generative single-cell aging trajectories reveal a bidirectionally traversable identity core and direction-specific inflammatory remodeling

Single-cell RNA sequencing (scRNA-seq) maps aging tissues at high resolution but is destructive, preventing longitudinal tracking; dropout and zero-inflation artifacts, amplified by shift-invariant linear simulations, confound age-associated variability. We developed Gero-Engine, a technical-artifact-aware framework combining VAE-based trajectory simulation, LOPO cross-validation, linear baselines, reverse traversal, and reverse-directed network inference. In microglia and HSCs, the VAE reduced technical-artifact carryover while preserving trajectory heterogeneity and improving alignment to artifact-reduced reference manifolds. Consensus GeroTargets and GeroRegulators defined tissue-specific GeroNetworks organized into three pillars: lineage/replication identity collapse, a sex-dimorphic endocrine/stress core, and inflammatory remodeling. Forward and reverse simulations aligned to the common young[->]old aging axis revealed a sign-coherent, direction-specific program: identity/replication targets were bidirectionally recovered, whereas MHC/NF-{kappa}B inflammatory programs were preferentially forward-recovered. These results support identity collapse as a deep traversable core of aging and nominate upstream homeostatic restoration over downstream inflammatory suppression.

bioinformatics↗

Telomere-to-telomere, accurate, and gapless genome assembly (TTAGGA) of the Korean Jindo dog with a single-contig Y chromosome

Complete canine reference genomes are essential for studies of structural variation, sex-chromosome evolution, and breed-specific architecture, yet existing references remain incomplete on the Y chromosome and retain internal gaps across multiple chromosomes. Here, we introduce TTAGGA (Telomere-to-Telomere, Accurate, Gapless Genome Assembly), a stricter completeness standard requiring chromosomes assembled end-to-end with zero internal gaps and Merqury consensus QV [≥] 50, and present Jindo1-G-TTAGGA, the first canine assembly to meet this standard, achieved under a stringent QV [≥] 60 threshold. From 813 Gb ([~]340x coverage) of multi-platform data (PacBio HiFi [~]150x, ONT ultra-long [~]103x, parental Illumina [~]40x per parent) generated from a male Korean Jindo dog, trio binning with hifiasm produced two haplotype-resolved assemblies of 2,441.6 Mb (Hap1, maternal, chrX-carrying) and 2,340.5 Mb (Hap2, paternal, chrY-carrying). Both haplotypes are gap-free at every internal position, with canonical telomeric repeats verified at both ends of all 39 chromosomes (tidk), Merqury consensus QV of 78.0 (Hap1) and 76.8 (Hap2), trio switch-error rates below 0.13%, BUSCO completeness of 99.3% (Hap1) and 96.4% (Hap2; the lower value reflects absent X-linked orthologues in the Y-bearing haplotype), and Genome Continuity Index values of 98.2 (Hap1) and 94.7 (Hap2). Hap2 carries a single 21,255,890 bp gap-free Y chromosome with TTAGGG telomeric repeats at the q-arm terminus and an acrocentric satellite-rich p-arm, representing a 5.4-fold increase over the 3.94 Mb chrY of ROS_Cfam_1.0 and adding approximately 14 Mb of newly resolved Y-linked sequence; this corresponds to roughly 79% of the cytogenetically estimated 27 Mb full-length canine chrY. Jindo1-G-TTAGGA provides a chromosome-scale, haplotype-resolved, gap-free canine reference for studies of canine structural variation, sex-chromosome evolution, and canid phylogenomics.

genomics↗

AAV-mediated neuronal expression of FOXG1 restores oligodendrocyte maturation, myelination, and hippocampal structure in mouse models of FOXG1 Syndrome

FOXG1 syndrome is a devastating neurodevelopmental disorder caused by haploinsufficiency of the transcription factor FOXG1, leading to intellectual disability, epilepsy, and white-matter deficits. Although FOXG1 is well known for its neuronal functions, its role in glial pathology remains poorly understood. Here, we show that reducing FOXG1 selectively in neurons impairs oligodendrocyte lineage progression and myelination, establishing a critical non-cell-autonomous role for neuronal FOXG1 in glial maturation. To restore FOXG1 in neurons, we developed AAV vectors expressing human FOXG1 under neuron-specific promoters. Neonatal administration of these vectors normalized oligodendrocyte precursor cell (OPC) accumulation, enhanced myelination, and corrected hippocampal structural abnormalities in Foxg1 conditional heterozygous mice. To test therapeutic robustness under stringent conditions, we used the patient-specific W300X heterozygous model, which combines FOXG1 loss-of-function with a toxic truncated protein and represents one of the most severe FOXG1 syndrome genotypes. Remarkably, neuron-restricted AAV-FOXG1 delivery produced substantial rescue even in this high-bar model, suppressing OPC overaccumulation, restoring myelination, and progressively improving dentate gyrus morphology, with benefits persisting into adulthood. Moreover, adolescent administration remained highly effective, rescuing myelination, axonal bundle thickness, and microglial activation. These findings identify neuronal FOXG1 as a master regulator of neuron-glia interactions and establish neuron-targeted AAV-FOXG1 as a potent and clinically translatable therapeutic strategy across diverse severities of FOXG1 syndrome.

developmental biology↗

Telomere-to-Telomere Accurate and Gapless Korean Standard Reference Genome

We present KOREF1-G-TTAGGA, the first Telomere-to-Telomere Accurate and Gapless Genome Assembly, standing as the Korean standard reference genome. The paternal and maternal haplotypes spanned 2.91 and 3.03 Gb. Genome-wide, at least 99.15% of assembled sequences were reliably haplotype-resolved, and over 95% remained accurate even in the most error-prone loci, including centromeric satellite arrays and segmental duplications. Rare-k-mer copy-number concordance within satellite arrays held up 98.9% and 98.8% per haplotype. Bionano optical maps fully spanned all canonical rDNA arrays on the five acrocentric chromosomes. The assembly quality index (AQI) of 99.77 and 99.69 exceeded the reference-quality threshold of 90, and more than 99.99% of gene and cCRE sequence was free of structural error. Both haplotypes further showed high base-level accuracy, with consensus quality value (QV) of 81.19 and 79.03, corresponding to one error per 131 and 80 Mb. KOREF1-G-TTAGGA is among the highest-quality East Asian telomere-to-telomere assemblies. It moreover anchors a decade-spanning multi-ome reference dataset for defining individual molecular states. Together, these resources define the personal referenceome as a foundation for individual biology and precision medicine, with the assemblies, annotations, and all multi-omic data openly available at https://koreanreference.org.

genomics↗

10,239 whole genomes with multiomic and clinical health information as the Korean population multiomic reference dataset

We present Korea10K, the largest genomic dataset of the Korean population, comprising 10,239 high-coverage whole genomes (mean depth 30x) with matched multiomic profiles and phenotype data. Korea10K achieves complete and near-complete discovery of very rare and ultra-rare alleles, respectively, at 9,000 Korean genomes. This dataset provides the high-quality population-specific imputation panel, enabling accurate inference of low-frequency variants. Admixture analyses confirm the genetic homogeneity of the Korean population, despite its diverse Y-chromosomal, mitochondrial, and HLA repertoires. This pattern reflects a long and continuous lineage history characterized by persistent internal admixture and genomic homogenization over thousands of years on the Korean peninsula. We also identified 16.8 million genomic variants that directly modify CG sites by creating or abolishing CG dinucleotides, providing the population-scale evidence of coordinated genomic-epigenomic regulatory mechanism in Koreans.

genomics↗

Human patient-specific FOXG1 syndrome mouse model revealed FOXG1-MYCN-mediated regulation of protein homeostasis in neurodevelopmental disorder

Neurodevelopmental disorders are characterized by disruptions in brain development, resulting in cognitive, behavioral, and neurological impairments. FOXG1 syndrome (FS), caused by heterozygous mutations in the FOXG1 gene, exemplifies a severe monogenic neurodevelopmental disorder. To investigate its pathogenesis, we generated a patient-specific W300X mouse model carrying a truncation variant of FOXG1. We found that the truncated FOXG1 protein in W300X-heterozygous (W300X-Het) mice is more abundant and more nuclear-localized than the full-length FOXG1 protein, implicating a pathogenic mechanism involving the truncated protein. Interestingly, W300X-Het mice exhibited profound abnormalities in the dentate gyrus, including disrupted neurogenesis, impaired granule cell migration, and altered dendritic morphology. Transcriptomic profiling identified broad dysregulation in protein homeostasis pathways, particularly ribosomal biogenesis, translation, and proteostasis. Disruption of the FOXG1-MYCN pathway, critical for robust protein synthesis during neural stem cell division, synaptogenesis, and synaptic plasticity, emerged as a key mechanism underlying these defects. In parallel, microglial activation and inflammation were markedly increased in the dentate gyrus, contributing to a pro-inflammatory environment that exacerbates neurogenic and structural deficits. Consistent with hippocampal dysfunction in FS patients, W300X-Het mice exhibited significant spatial learning and memory impairments. Together, our study highlights disrupted protein homeostasis and neuroinflammation as key drivers of FS pathogenesis, providing a framework for developing therapeutic strategies targeting these pathways.

neuroscience↗

Identification of reactive CpGs and RNA expression in early COVID-19 through cis-eQTM analysis reflecting disease severity and recovery

Multi-omics analyses of severe COVID-19 cases are crucial in deciphering the complex interplay between genetic and epigenetic factors. Here, we present an analysis of Expression Quantitative Trait Methylation (eQTM) to investigate the complex interplay of methylation and gene expression pattern during the acute phase of severe COVID-19. We identified 16 differentially expressed genes and 30 nearby differentially methylated CpG sites. Six key genes--SRXN1, FURIN, IL18RAP, FOXO3, GCNT4, and FKBP5--were either up-regulated or down-regulated near hypomethylated CpG sites. These genes are associated with viral infiltration, immune activation, lung damage, and oxidative stress-related multi-organ failure, which are the hallmarks of severe COVID-19. Interestingly, during the recovery phase, methylation and gene expression levels returned to baseline, underscoring the rapid and reversible nature of these molecular changes. These findings provide insight into the dynamics of epigenetic and transcriptomic shifts according to the infectious stage, supporting potential prognostic and therapeutic approaches for severe COVID-19.

bioinformatics↗

Select azo compounds post-translationally modulate HTRA1 abundance and activity potentially through interactions at the trimer interface

High-temperature requirement protein A1 (HTRA1) is a secreted serine protease with diverse substrates, including extracellular matrix proteins, proteins involved in amyloid deposition, and growth factors. Accordingly, HTRA1 has been implicated in a variety of neurodegenerative diseases including a leading cause of blindness in the elderly, age-related macular degeneration (AMD). In fact, genome wide association studies have identified that the 10q26 locus which contains HTRA1 confers the strongest genetic risk factor for AMD. A recent study has suggested that AMD-associated risk alleles in HTRA1 correlate with a significant age-related defect in HTRA1 synthesis in the retinal pigmented epithelium (RPE) within the eye, possibly accounting for AMD susceptibility. Thus, we sought to identify small molecule enhancers of HTRA1 transcription and/or protein abundance using an unbiased high-throughput screening approach. To accomplish this goal, we used CRISPR/Sp.Cas9 engineering to introduce an 11 amino acid luminescent peptide tag (HiBiT) onto the C-terminus of HTRA1 in immortalized ARPE-19 cells. Editing was very efficient ([~]88%), verified by genomic DNA analysis, short interfering RNA (siRNA), and HiBiT blotting. Nineteen-hundred and twenty compounds from two libraries were screened. An azo compound with reported anti-amyloidogenic and cardioprotective activity, Chicago Sky Blue 6B (CSB), was identified as an enhancer of endogenous HTRA1 secretion (2.0 {+/-} 0.3 fold) and intracellular levels (1.7 {+/-} 0.2 fold). These results were counter-screened using HiBiT complement factor H (CFH) edited ARPE-19 cells, verified using HiBiT blotting, and were not due to HTRA1 transcriptional changes. Importantly, serine hydrolase activity-based protein profiling (SH-ABPP) demonstrated that CSB does not affect HTRA1s specific activity. However, interestingly, in follow-up studies, Congo Red, another azo compound structurally similar to CSB, also substantially increased intracellular HTRA1 levels (up to 3.6 {+/-} 0.3 fold) but was found to significantly impair HTRA1 enzymatic reactivity (0.45 {+/-} 0.07 fold). Computational modeling of potential azo dye interaction with HTRA1 suggests that CSB and Congo Red can bind to the non-catalytic face of the trimer interface but with different orientation tolerances and interaction energies. These studies identify select azo dyes as HTRA1 chemical probes which may serve as starting points for future HTRA1-centered small molecule therapeutics.

biochemistry↗

A Novel Aptamer-Based Approach for Lipoprotein Removal to Achieve Ultra-Pure Blood EV Isolation

Blood extracellular vesicles (EVs) are nanoscale lipid-bilayer particles that carry proteins, nucleic acids, and metabolites, rendering them powerful tools for non-invasive liquid biopsy and targeted drug delivery. However, clinical translation of blood-derived EVs is severely limited by the co-isolation of lipoproteins--whose size (30-100 nm) and density overlap with EVs--resulting in contaminated preparations that compromise biomarker accuracy and jeopardize therapeutic safety, efficacy, and biodistribution. To overcome this critical bottleneck, we developed ApoFilter, an aptamer-based affinity filtration platform engineered to selectively capture ApoB100- and ApoA1-containing lipoproteins (VLDL, LDL, HDL) while preserving EV integrity. In solutions containing only mixed lipoproteins, ApoFilter demonstrated a capture efficiency of 97% for ApoB100- and ApoA1-containing particles, yielding filtrates with >99% depletion of target lipoproteins. Crucially, this high selectivity was preserved in human plasma--a complex protein milieu--where ApoFilter removed over 99% of lipoproteins without any detectable loss of EV yield. Furthermore, when size-exclusion chromatography (SEC) or ExoTFF was integrated with ApoFilter, the limitations of each technique were innovatively complemented, achieving a highly advanced level of separation and purification. Notably, the ApoFilter-ExoTFF combination delivered the highest performance, attaining 99.9% protein removal and a 98.2% EV recovery rate, enabling ultrapure EV isolation from blood plasma. This synergistic purification strategy addresses both analytical and therapeutic requirements by eliminating lipoprotein interference in downstream molecular profiling and minimizing off-target effects in drug delivery. ApoFilter thus represents a versatile, scalable solution for isolating clinically relevant EVs from blood, substantially improving the reliability of liquid biopsy assays and accelerating the development of EV-based therapeutics.

bioengineering↗

Scalable, high-throughput isolation of extracellular vesicles using electrokinetic-assisted mesh filtration

As extracellular vesicles (EVs) are increasingly recognized for their superior functions for therapeutics, the need for large-scale EV isolation technology is becoming more critical for clinical and industrial applications. Most existing EV isolation methods are optimized for small-scale laboratory samples, limiting their efficiency and scalability for large-scale production. Here, an electrokinetic-assisted filtration system (ExoFilter), which introduces charge interaction into physical mesh flow filtration, is proposed as a new candidate to address the challenges of scalable EV isolation. The hybrid filtration system demonstrates outstanding high-throughput EV isolation performance (a flux of [~]750 mL/min) using only a coarse physical filter, by electrokinetically arresting EVs flowing through the filter lattice. Furthermore, the recovery efficiency of ExoFilter, analyzed based on the ELISA results, was found to be approximately 98%, demonstrating the filters exceptional efficiency in EV isolation. Additionally, ExoFilter enables the rapid isolation of EVs from small samples as little as 200 {micro}L, facilitating quick and easy blood-based EV research. Furthermore, low-molecular-weight albumin from plasma samples was effectively removed. The high-throughput and high-efficiency characteristics of ExoFilter make it well-suited for scalable EV production, offering greater convenience for various clinical applications. HighlightsO_LIElectrokinetic-assisted mesh filtration (ExoFilter) enables scalable and rapid isolation of extracellular vesicles (EVs). C_LIO_LIA high throughput of [~]750 mL/min is demonstrated while maintaining high yield and purity. C_LIO_LIExoFilter effectively removes albumin contaminants from EVs through size-exclusive electrokinetic-assisted mesh filtration. C_LIO_LIEfficient EV isolation performance is achieved for human plasma, saliva, urine, and cell culture media. C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=167 SRC="FIGDIR/small/645682v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@7ac3d5org.highwire.dtl.DTLVardef@1ced638org.highwire.dtl.DTLVardef@521c63org.highwire.dtl.DTLVardef@c5bd49_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

Advanced Extracellular Vesicle Isolation: A Hybrid Electrokinetic-Tangential Flow Filtration Approach for Improved Yield, Purity, and Scalability

As extracellular vesicles (EVs) become increasingly important in diagnostics and therapeutics, achieving both high purity and yield during isolation remains a critical challenge. Conventional techniques often suffer from the co-isolation of non-vesicular particles and soluble proteins, limiting their clinical and research utility. In response, we introduce ExoTFF, a hybrid isolation technology that sequentially integrates electrokinetic filtration (ExoFilter) with size-exclusion tangential flow filtration (TFF) to deliver unprecedented performance gains through an iterative, synergistic mechanism. In the ExoTFF system, the sample is repeatedly circulated through an electrokinetic mesh filter and TFF until the liquid is removed. This recirculating flow gradually eliminates contaminants, while the electrokinetic filter continuously captures EVs as the sample is purified. Finally, any residual impurities in the TFF unit are completely removed via a dead volume elimination process. The complementary actions of these two distinct separation mechanisms double EV recovery rates and reduce impurity levels by 80% compared to conventional TFF, culminating in an impressive 800% improvement in the purity ratio. In proof-of-concept experiments, ExoTFF processed 10 mL of plasma within 10 minutes, efficiently depleting albumin and HDL while achieving superior EV recovery. To further explore scalability, an automated ExoTFF system processed 500 mL of sample in 50 minutes, maintaining consistent yield and purity. The ability to sustain performance across different scales highlights ExoTFFs potential for both laboratory research and industrial-level EV production. Beyond biological applications, this platform also offers broad applicability for the isolation of negatively charged nanoparticles, demonstrating its potential impact across multiple nanotechnology-driven fields.

bioengineering↗

Generative frame interpolation enhances tracking of biological objects in time-lapse microscopy

Object tracking in microscopy videos is crucial for understanding biological processes. While existing methods often require fine-tuning tracking algorithms to fit the image dataset, here we explored an alternative paradigm: augmenting the image time-lapse dataset to fit the tracking algorithm. To test this approach, we evaluated whether generative video frame interpolation can augment the temporal resolution of time-lapse microscopy and facilitate object tracking in multiple biological contexts. We systematically compared the capacity of Latent Diffusion Model for Video Frame Interpolation (LDMVFI), Real-time Intermediate Flow Estimation (RIFE), Compression-Driven Frame Interpolation (CDFI), and Frame Interpolation for Large Motion (FILM) to generate synthetic microscopy images derived from interpolating real images. Our testing image time series ranged from fluorescently labeled nuclei to bacteria, yeast, cancer cells, and organoids. We showed that the off-the-shelf frame interpolation algorithms produced bio-realistic image interpolation even without dataset-specific retraining, as judged by high structural image similarity and the capacity to produce segmentations that closely resemble results from real images. Using a simple tracking algorithm based on mask overlap, we confirmed that frame interpolation significantly improved tracking across several datasets without requiring extensive parameter tuning and capturing complex trajectories that were difficult to resolve in the original image time series. Taken together, our findings highlight the potential of generative frame interpolation to improve tracking in time-lapse microscopy across diverse scenarios, suggesting that a generalist tracking algorithm for microscopy could be developed by combining deep learning segmentation models with generative frame interpolation.

cell biology↗

The patient-specific mouse model with Foxg1 frameshift mutation provides insights into the pathophysiology of FOXG1 syndrome

AbstractsSingle allelic mutations in the forebrain-specific transcription factor gene FOXG1 lead to FOXG1 syndrome (FS). To decipher the disease mechanisms of FS, which vary depending on FOXG1 mutation types, patient-specific animal models are critical. Here, we report the first patient-specific FS mouse model, Q84Pfs heterozygous (Q84Pfs-Het) mice, which emulates one of the most predominant FS variants. Remarkably, Q84Pfs-Het mice recapitulate various human FS phenotypes across cellular, brain structural, and behavioral levels, such as microcephaly, corpus callosum agenesis, movement disorders, repetitive behaviors, and anxiety. Q84Pfs-Het cortex showed dysregulations of genes controlling cell proliferation, neuronal projection and migration, synaptic assembly, and synaptic vesicle transport. Interestingly, the FS-causing Q84Pfs allele produced the N-terminal fragment of FOXG1, denoted as Q84Pfs protein, in Q84Pfs-Het mouse brains. Q84Pfs fragment forms intracellular speckles, interacts with FOXG1 full-length protein, and triggers the sequestration of FOXG1 to distinct subcellular domains. Q84Pfs protein also promotes the radial glial cell identity and suppresses neuronal migration in the cortex. Together, our study uncovered the role of the FOXG1 fragment derived from FS-causing FOXG1 variants and identified the genes involved in FS-like cellular and behavioral phenotypes, providing essential insights into the pathophysiology of FS.

neuroscience↗

Effect of the daily exposure of 1.7 GHz LTE electromagnetic field in early fetal brain development using a human brain organoid model of the cerebral cortex

Wireless communication technologys ubiquity means constant exposure to radiofrequency electromagnetic fields (RF-EMF). While concerns exist about RF-EMFs effects on fetal brain development, studying this in pregnant women poses ethical and safety challenges. Our study examined 1.7 GHz LTE RF-EMFs impact on early human fetal brain development using brain organoids derived from human induced pluripotent stem cells (hiPSCs). Previous research showed that 100-day-old human cerebral cortical brain organoids correspond to 19-24 weeks post-conception of fetal brain development. We exposed organoids to 1.7 GHz LTE RF-EMF at 8 W/kg specific absorption rate (SAR) for 5 hours daily up to 100 days. We monitored size, developmental morphology, and developmental stage markers using immunofluorescence microscopy and qPCR analysis. Comparing RF-EMF-exposed organoids with controls showed no significant differences in size, development, or expression of key markers: SOX2 and PAX6 (pluripotent cell markers), NEUN (mature neuronal marker), MAP2 (dendrite marker), and SYN1 (synapse marker). Results suggest that daily exposure to 1.7 GHz LTE RF-EMF at 8 W/kg SAR may not significantly affect early human fetal brain development.

developmental biology↗

ACE1 Does Not Influence Cerebral Aβ Degradation or Amyloid Plaque Accumulation in 5XFAD Mice

Alzheimers disease (AD) is the most common form of dementia, and multiple lines of evidence support the relevance of A{beta} deposition and amyloid plaque accumulation in the neurotoxicity and cognitive decline in AD. Rare mutations in angiotensin-converting-enzyme-1 (ACE1) have been highly associated with late onset AD patients; however, the mechanism for ACE1 mutation in AD pathogenesis is unknown. Given the relevance of ACE1 with AD and the strong association of A{beta} to AD pathogenesis, we investigated whether ACE1 degrades A{beta} and affects amyloid burden in 5XFAD mice in vivo. To investigate this, we analyzed 6-month-old 5XFAD mice with ACE1 loss of function. ACE1 loss of function was mediated either by crossing 5XFAD mice to ACE1 conditional knockout mice or administering 5XFAD mice with the ACE1 inhibitor enalapril. Our analyses revealed that ACE1 loss of function through both genetic and pharmacological methods does not affect amyloid plaque load and neuroinflammation in the hippocampus and cortex of 5XFAD mice.

neuroscience↗

Reversible Transcriptomic Age Shifts from Physiological Stress in Whole Blood

We developed a genome-wide transcriptomic clock for predicting chronological age using whole blood samples from 463 healthy individuals. Our findings reveal profound age acceleration, up to 24.47 years, under perturbed homeostasis in COVID-19 patients, which reverted to baseline upon recovery. This study demonstrates that the whole blood transcriptome can track reversible changes in biological age induced by stressors in real physiological time, suggesting a potential role for anti-aging interventions in disease management.

bioinformatics↗