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Smith, R.

Publications and source records attributed to Smith, R..

At least 37 records · Page 2Linked to original sources

Patient-specific functional brain architecture explains cortical patterns of tau PET in Alzheimer's disease

The spatial distribution of tau pathology, a key correlate of neurodegeneration and cognitive decline in Alzheimer's disease (AD), varies markedly across individuals. While tau is thought to spread along brain networks, the role of inter-individual variability in accounting for these patterns remains underexplored. Using resting-state fMRI and tau-PET from 805 BioFINDER participants across the AD continuum, with replication in ADNI (n=361) and A4 (n=336), we studied whether subject-specific functional connectivity (FC) profiles enhance the characterization of tau deposition patterns. A hybrid approach integrating individual and group-average FC explained individual tau-PET topographies better than either FC representation alone, particularly in symptomatic individuals and at finer spatial resolutions. Hybrid FC also better captured individual tau topographies than canonical tau-PET maps derived from cohort-level data. These effects were specific to tau and not similarly observed for {beta}-amyloid, and the explanatory advantage of FC-based models increased with spatial granularity. Furthermore, baseline hybrid FC explained follow-up tau-PET topography better than template FC, suggesting that individualized baseline connectivity contains information about future tau-PET progression. The main FC model-comparison findings replicated in ADNI and A4. Collectively, these findings show that individual functional brain architecture is associated with heterogeneity in tau-PET topography. While not establishing a causal propagation mechanism, our findings are consistent with network-spread models. This work advances the methodological characterization of tau-PET heterogeneity in AD and highlights functional connectivity as a potentially informative marker of individual tau-PET trajectories.

neuroscience↗

Weakening of subcortical and strengthening of cortical visual pathways across early adolescence

BackgroundMounting evidence suggests that amygdalar nuclei receive visual information via both a well-characterized cortical pathway through the inferior temporal cortex and a subcortical route through the superior colliculus and pulvinar. This subcortical pathway may facilitate rapid responses to salient visual stimuli and could explain phenomena such as blindsight. However, controversies remain about the organization of the subcortical pathway, its role in visual processing, and how the cortical and subcortical pathways mature across development. MethodsTo address these questions we used longitudinal diffusion magnetic resonance imaging (dMRI) data from 4361 participants in the Adolescent Brain Cognitive Development (ABCD) study, reconstructing every major segment of the cortical and subcortical amygdala pathways. We tested the existence of the subcortical pathway against null tractography models, characterized cortical and subcortical pathways development across early adolescence, and investigated their association with visual processing speed. ResultsWe provide evidence for the existence of bilateral pulvinar-amygdala pathways against a null model (all p < 0.001, corrected). While cortical tracts involving the primary and extrastriate visual cortex and the inferior-temporal cortex strengthened with chronological age and over pubertal development, we demonstrate that subcortical pulvinar-amygdala connectivity decreased over pubertal development. Greater connectivity strength of the right pulvinar-amygdala tract was associated with faster responses on a visual task for both emotional face and place stimuli, a relationship also seen for cortical tracts. ConclusionThis study provides evidence for the existence of pulvinar to amygdala tracts in the largest sample of adolescent participants studied to date. Greater connectivity in both cortical and subcortical tracts were associated with faster reaction time on a visual task, but further work will be needed to investigate the specificity of this association in terms of both task and tract. In line with the hypothesized importance of the subcortical pathway in early development, we show that the developmental trajectories of cortical and subcortical pathways diverge and highlight the influence of pubertal development, with cortical pathways generally strengthening and subcortical pathways weakening across early adolescence.

neuroscience↗

Epigenetic markers of middle-age: non-linear DNA methylation changes with aging in humans

BackgroundHuman DNA is known to exhibit an overall tendency toward demethylation with aging. However, assuming a simple linear relationship between DNA methylation and age does not align with the phenotype of human development and the aging process. This study aimed to investigate the existence of DNA methylation patterns with peaks or troughs at specific ages in addition to simple linear changes. MethodsA large-scale dataset of genome-wide DNA methylation data from 10,420 individuals was analyzed. Hierarchical multiple regression models were applied to detect patterns of the association between age and DNA methylation: linear increase, linear decrease, U-shaped curve, and inverse U-shaped curve. ResultsAmong the 864,627 CpG sites analyzed, 8.4% exhibited an increase in DNA methylation with age, 23.9% showed a decrease, and 5.5% were better explained by a quadratic model (P < 5.7815x10 ). Within the non-linear subset, inverse U-shaped CpG sites peaking in methylation during middle age were predominant. Genes exhibiting quadratic association patterns between DNA methylation and age, and those linked to diseases with common onset during middle age, were also detected. ConclusionsNon-linear age-related DNA methylation patterns, with peaks or troughs occurring at specific ages, were detected. This suggests that humans do not simply age linearly, but that programmed mechanisms or cascade-like processes may exist to promote or suppress the expression of specific genes at certain ages, contributing onset of certain diseases at specific timings.

genomics↗

Effects of wasting disease on sea star populations in southern California: Variations over a 40-year period

Sea star wasting disease has been described for asteroid populations from many parts of the world and for numerous species. The causative agents are generally unknown. However, within the Southern California Bight, a Vibrio bacterium appears to have been the cause of wasting disease in the 1980s, and probably the 1990s, during warm water episodes associated with El Ninos. Although a densovirus was implicated in the mass mortality of one species of subtidal sea star during the geographically widespread epizootics that began in 2013, the etiology appears to vary among species, locations, and time periods, and in some cases may not even be associated with a pathogen. We have been studying subtidal benthic communities in southern California since the 1970s and have documented the population effects of wasting disease epizootics associated with warm water El Nino events from 1980 through 2020. Until 2015, population declines coincident with wasting disease were followed by various degrees of recovery, whereas after 2015 there has been little or no recovery at our study sites. Prior to 2013, wasting disease in the northeast Pacific was only reported from locations in the Gulf of California, the southern California bight, and the coast of Vancouver Island, British Columbia. Since 2013, epizootics of wasting disease among sea stars have been observed along the entire west coast of North America. We speculate that the lack of recovery after 2015 may be due to a reduction in larval supply caused by the greater geographical extent of the disease.

ecology↗

microRNA-21 promotes dysregulated lipid metabolism and hepatocellular carcinoma

Backgrounds and AimsThe prevalence of hepatocellular carcinoma (HCC) is rising in parallel with increasing obesity and metabolic dysfunction-associated steatohepatitis (MASH). MicroRNAs are key post-transcriptional regulators of gene expression and are attractive targets for HCC therapy. Here we sought to identify and characterize dysregulated microRNAs in MASH-driven HCC (MASH-HCC). Approach and ResultsWe profiled microRNA expression in liver tissue from patients with MASH and/or MASH-HCC and in zebrafish HCC driven by activated {beta}-catenin (ABC), one of the most commonly mutated oncogenes in MASH-HCC. We found significant overlap between dysregulated human and zebrafish miRNAs, including miR-21, which was increasingly upregulated from normal liver to MASH to MASH-HCC. We generated transgenic zebrafish that overexpress or sponge (downregulate) miR-21. We found that miR-21 overexpression caused larval liver overgrowth and increased HCC while miR-21 sponge suppressed {beta}-catenin-driven larval liver overgrowth. By performing histologic and lipidomic analysis, we found that overexpression of miR-21, like ABC, suppressed lipid accumulation in response to a high cholesterol diet and increased accumulation of acylcarnitines. ConclusionsHere we characterize microRNA dysregulation in MASH and MASH-HCC in patients, identify miR-21 as increasingly dysregulated from MASH to MASH-HCC, and delineate the impacts of miR-21 overexpression on lipid metabolism and hepatocarcinogenesis in zebrafish {beta}-catenin-driven HCC. This study shows that miR-21, which is similarly dysregulated in human and zebrafish HCC, promotes lipid metabolic changes that may help drive hepatocarcinogenesis.

cancer biology↗

S-Nitrosylated COX-2 is a TME-regulated breast cancer biomarker of mesenchymal phenotypes

COX-2 is an inducible enzyme key to the production of inflammatory prostaglandins. COX-2 also has tumor intrinsic oncogenic activity in mouse models of breast cancer. Previously, we reported increased expression of Cys-526-nitrosylated COX-2 (SNO-COX-2), but not non-nitrosylated COX-2, with progression of early-stage human breast cancer to invasive ductal carcinoma. Here, we used a 3D culture model of early-stage human breast cancer (MCF10DCIS cells) to investigate the relationship between SNO-COX-2 expression and mesenchymal/invasive tumor cell morphology. We find that SNO-COX-2, but not non-nitrosylated COX-2, closely associated with mesenchymal phenotypes induced by fibrillar type I collagen. Interestingly, invasive phenotypes did not associate with induction of the classic epithelial-to-mesenchymal transition (EMT) markers SNAIL, CDH2 (N-cadherin), and VIM (vimentin). By contrast TGF{beta}-1 strongly induced EMT-related transcripts, but not SNO-COX-2 protein expression or mesenchymal phenotypes. These observations suggest that in MCF10DCIS cells, SNO-COX-2 associates with mesenchymal phenotypes more strongly than non-nitrosylated COX-2 protein, or expression of classic EMT transcripts. In a mouse model with breast tumor heterogeneity, mesenchymal tumor regions also have increased SNO-COX-2 expression. Testing 300 distinct tumor microenvironment conditions, we find SNO-COX-2 protein expression is driven by inflammation, wound resolution, and cancer-associated factors, especially TNC, SPP1, decorin, fibrillar type I and III collagens, INF-{gamma}, and IL-4/13, with evidence for specific extracellular matrix-ligand interactions driving both high and low SNO-COX-2 expression. In sum, in MCF10DCIS cells, expression of SNO-COX-2 is highly microenvironment-dependent and strongly associated with invasive/mesenchymal growth, indicating potential for SNO-COX-2 as a biomarker to assess risk of early-stage breast cancer progression.

cancer biology↗

Mapping Lung Cancer Ventilation Dynamics: A Pilot Mouse Study Using Functional Imaging and Lung Mechanics

In vivo models that replicate and reproduce human lung cancer and its response to therapy are necessary for the development of new therapeutic strategies and understanding drug resistance. Imaging lung tumors in live animals to monitor tumor growth and response to therapy is challenging due to the location of the lungs and their constant movement during breathing. Additionally, methods such as computed tomography (CT) only provide structural information and not functional information about how well the lungs are working. X-ray velocimetry (XV) is a novel functional lung imaging technique that generates 3D maps of regional lung expansion during breathing. In other lung diseases it has been shown to provide spatial information on where ventilation changes occur. The aim of this pilot study was to use XV and flexiVent lung mechanics assessments to determine the effect of tumor growth on lung function in mice at 2- or 3-weeks post tumor induction, and to evaluate the efficacy of these two tools. Histological analysis showed that tumour growth was not uniform between animals. At 3-weeks post tumor induction, some XV ventilation and flexiVent lung mechanics parameters were significantly different from baseline metrics. In addition, the forced expiratory volume, small-scale ventilation heterogeneity, and the average CT gray value correlated with the tumour counts from the histology. In some mice XV revealed localised regions with altered expansion rates. This pilot study demonstrated that changes in lung function can be identified following tumor induction, and that the model and techniques could be used in the future to determine response to anti-tumor drugs.

biophysics↗

Brain-epigenome wide association study (BEWAS) on the effects of two emerging psychedelics: ketamine & MDMA

Psychedelic compounds such as ketamine and MDMA have shown therapeutic promise for mood and trauma-related disorders, yet their molecular mechanisms remain unclear. This study applied a Brain-Epigenome-Wide Association Study (BEWAS) to assess DNA methylation changes in brain-enriched genes following treatment. Pre- and post-treatment blood (ketamine, N = 20) and saliva (MDMA, N = 16) samples from clinical trial participants were analyzed. Ketamine altered methylation at 1,210 CpG sites; MDMA affected 2,074 CpG sites. Functional enrichment analyses revealed changes in genes involved in neuroplasticity, immune regulation, and mental processes. Overlapping effects were observed in genes such as PTPRN2 and SHANK2, suggesting shared epigenetic mechanisms in driving increased neuroplasticity. These findings highlight psychedelics capacity to induce coordinated, lasting molecular changes relevant to neuroimmune function and psychiatric health.

genomics↗

Barriers Broken: Genetic Swamping in Restored Brook Trout Populations

Scientists use reintroductions to restore native species to their historical ranges but sometimes can overlook the effects of dispersal on the genetic structure of restored populations. In the Great Smoky Mountains National Park (GRSM), an ambitious reintroduction strategy aims to restore native Brook Trout (Salvelinus fontinalis) populations, which have lost over 75% of their historical habitat within the park. Each restoration requires removing non-native trout and selecting restoration streams with natural barriers to prevent recolonization. Multiple Brook Trout populations are mixed in restoration sites to maximize genetic diversity and to avoid depletion of any single source population. However, a miscommunication during a reintroduction in Anthony Creek, which used three source populations for restoration, inadvertently created an in-situ population genetics study. One segment of the restoration site received fish from all three source populations. However, technicians also unintentionally placed fish from just one source upstream of a natural barrier. Unbeknownst to management, fish from this separate translocation dispersed downstream, potentially altering the desired genetic diversity of the restored population. This study characterizes the genetic changes caused by this unidirectional dispersal. Population genetics theory predicts that such movement leads to genetic swamping. Here, we use genetic and population density data to confirm the directionality of dispersal, estimate the rate of genetic swamping, and assess alternative mitigation strategies. Our results indicate that it is already too late for assisted migration within the restored stream to achieve the intended genetic diversity. Instead introducing additional fish above the second natural barrier would be necessary to equalize the contribution of all three source populations. Understanding the interplay between dispersal behavior and genetic structure is crucial for planning reintroductions and refining conservation strategies for this iconic species.

evolutionary biology↗

The genetic origin of fetal growth restriction and mitochondrial complex I dysregulation

BackgroundMitochondria are organelles required for bioenergetic homeostasis, providing energy in the form of ATP to support cellular function, growth, and proliferation. Mitochondria synthesise ATP using the electron transport chain (ETC) to produce an electrochemical gradient that facilitates the conversion of ADP to ATP by ATP synthase. Mitochondrial function is governed by an intricate bidirectional relationship between the mitochondrial genome encoding 1-2% of proteins and the nuclear genome which encodes 98-99% of mitochondrial proteins. Pregnancy creates a unique environment whereby the mitochondrial genome of the placenta is maternally inherited, while the nuclear genome is comprised of both maternal and paternal contributions. Thus, mitochondrial structure and function are largely dependent on the adaptability of mitochondria to conform to the new mixed nuclear genome. In pregnancy, fetal growth restriction (FGR) is characterised by poor placental development, underlying trophoblast insufficiencies, and is associated with mitochondrial dysfunction within the placenta, although the mechanisms which underpin these changes remain unclear. This study investigated if mitochondrial dysfunction in FGR is programmed by genetic incompatibility arising from single nucleotide polymorphisms (SNPs). Methods and findingsWe performed a targeted meta-analysis of over 100 genome wide association studies within the early growth genetics (EGG) consortium, assessing 289 genes encoding mitochondrial function across the ETC and ATP synthase. This study identified 37 SNPs across 32 genes associated with low birthweight. Sanger sequencing was performed to validate the presence of 10 SNPs of interest located within the nuclear genome in a cohort of fetal growth restricted placentas. Of the 10 SNPs assessed we confirmed the presence of 6 in FGR, and identified an additional previously unidentified SNP, and detected 3 nucleotide deletions across numerous components of the electron transport chain. This analysis identified 5 mutations within genes that encode complex I. Subsequent analysis of the gene and proteins that correspond to complex I mutations was performed using PCR, proteomics, and western blotting. Notably, we identified significant downregulation of NDUFA6 at the gene and protein level in FGR, lower protein levels of NDUFS3 and NDUFS6, and confirmed the largest log2 fold change identified in NDUFS6 by western blot. Subsequent investigation of mitochondrial respiratory capacity identified decreased ATP-linked respiration in FGR using Seahorse XF Analysis. ConclusionOur results identify that there is an inheritable contribution of SNPs within the maternal and paternal nuclear genome in fetal growth restriction. These SNPs alter gene expression and protein abundance of mitochondrial complex I components, impacting structural assembly and subsequent bioenergetic function within the placenta. Collectively these findings suggest that SNPs that affect mitochondrial assembly and function are associated with low birthweight and fetal growth restriction.

developmental biology↗

Placental Iron Utilisation in Fetal Growth Restriction: Alterations in Mitochondrial Heme Synthesis and Iron-Sulfur Cluster Assembly Pathways

Fetal growth restriction (FGR) affects [~]10% of pregnancies worldwide and is often associated with placental insufficiency. Iron is essential for maternal haematopoietic adaptations and placental processes such as mitochondrial iron-sulfur (Fe-S) cluster assembly, heme synthesis, and erythropoiesis. This study aimed to characterise iron transport and downstream utilisation in FGR. Placental tissues from term uncomplicated (n=19) and FGR (n=18) pregnancies were analysed. Maternal iron status was retrospectively assessed from clinical records. Placental mRNA and protein expression of iron-dependent pathways were analysed via RT-qPCR, LC-MS, and western blotting. Placental iron content was assessed histologically, and heme levels were measured by activity assay. FGR pregnancies showed significantly elevated maternal serum ferritin and lower red cell distribution width, although remained within normal clinical values. Placental iron uptake transporters TFRC and DMT1 were significantly upregulated, while the iron exporter to the fetus, ferroportin, was reduced, indicating increased iron retention in the FGR placenta. Despite altered transporter expression, Fe3 iron levels were unchanged, suggesting iron utilisation over storage. Subsequent investigations identified reduced mitochondrial Fe-S synthesis components (FDXR, FDX2, NDUFAB1, HSPA9), and a prioritisation of mitochondrial and cytosolic heme synthesis enzymes in FGR. Protein levels of haemoglobin subunits (HBG1, HBG2, HBB, HBA1) and erythrocyte membrane markers (EPB41, EPB42, SPTA1, SPTB, ANK1) were decreased. These findings reveal a compensatory response in FGR placentae, with increased iron uptake and utilisation favouring heme synthesis over Fe-S cluster formation, possibly to support oxygen handling under poor placental vascularisation and reduced fetal oxygenation, with potential consequences for mitochondrial energy metabolism. Key PointsO_LIIron plays a critical role in placental function, while iron-dependent pathway components are well-characterised, their integrated response and adaptive reprogramming in fetal growth restriction (FGR) remain poorly understood. C_LIO_LIIn FGR, maternal iron status was unchanged, however, placental iron uptake proteins were increased and ferroportin reduced, suggesting that the placenta retains iron. C_LIO_LIFGR placentae showed altered de novo mitochondrial iron-sulfur cluster (Fe-S) formation and a bottleneck in late-stage Fe-S cluster assembly. C_LIO_LIThis shift in Fe-S synthesis prioritises mitochondrial and cytosolic heme synthesis pathways, consistent with increased heme utilisation and breakdown. C_LIO_LIGlobin subunits were lower in protein abundance and impaired placental erythrocyte structure in FGR. C_LIO_LIDysregulation of erythrocyte membrane proteins in FGR placentae suggests altered erythrocyte structure, potentially representing an adaptive response to inadequate vascularisation, attempting to optimise oxygen delivery to the fetus. C_LI

physiology↗

Electron tomography reveals mitochondrial network and cristae remodelling during cell differentiation in the human placenta

Mitochondria adapt their structure through fusion and fission, yet how their morphology and cristae architecture alter as cells differentiate remains unclear. The human placenta is an ideal model for studying mitochondrial diversity within a single tissue. As epithelial trophoblast cells of the placenta differentiate, their accompanying mitochondria morphologically and functionally transform. We used array tomography to characterise mitochondrial volume and network complexity. Cryo-electron tomography revealed two distinct subpopulations of mitochondria within progenitor cytotrophoblasts, and a singular, homogeneous population in the differentiated syncytiotrophoblast. We showcased the 3D topology of individual cristae through a standardised metric of "curvedness". Proteomic analysis of isolated mitochondria identified reduced dynamics proteins and cristae organisation complexes, accompanied by subunit variations within the electron transport chain, ATP synthase, and altered supercomplex abundance. This study highlights the advantages of combining multimodal imaging with mechanistic insights, to elucidate the process of mitochondrial morphology and cristae architecture remodelling as cells differentiate.

cell biology↗

Experimental flooding impacts soil biogeochemistry but not aboveground vegetation in a coastal forest

Rising sea levels and intensifying storms increase flooding pressure on coastal forests, triggering tree mortality, ecosystem transitions, and changes to the coastal carbon cycle. However, the mechanisms that drive coastal forest mortality remain elusive due to the complex interplay between belowground and aboveground processes during flooding disturbances and limitations of observations typically reported in coastal forest mortality studies. We used an ecosystem-scale manipulation to simulate hurricane-level flooding of a coastal forest. Monitoring real-time soil conditions and tree physiological responses, we observed consistent impacts on soil biogeochemistry aligned with belowground drivers of tree mortality, but no consistent responses in aboveground vegetation. Our findings provide unprecedented empirically based insight into the earliest stages of a hypothesized forest mortality spiral and offer critical benchmarks for predicting coastal forest resilience in the face of accelerating climate change. Significance StatementChanging sea levels and storms are causing more flooding in coastal forests. This flooding kills trees, changing how coastal ecosystems function, but we do not fully understand what factors determine whether forests survive flooding. We designed an ecosystem-scale experiment to answer this question, with controlled saltwater and freshwater floods equivalent to a hurricane in experimental forest plots. Flooding quickly changed soil conditions, but we have not yet observed consistent tree stress responses. Our study provides the most detailed measurements to date of how coastal forests respond to flooding in real time. These findings will help us better understand the early mechanisms and warning signs of forests threatened by flooding.

systems biology↗

Identification of RNF114 as ADPr-Ub reader through non-hydrolysable ubiquitinated ADP-ribose

Crosstalk between the post-translational modification processes ubiquitination and ADP-ribosylation occurs in DNA-damage and immune-responses, in addition the physical linkage of ADP-ribose and ubiquitin is found during bacterial infection. Here, we study the ubiquitination of ADP-ribose mediated by human Deltex E3 ligases and the subsequent fate of the formed hybrid post-translational modification. We prepare a non-hydrolysable ADPr-Ub probe that we employ in a chemoproteomics approach and identify RNF114 as an interacting protein. Using biophysical and biochemical experiments, we validate that RNF114 preferentially interacts with ubiquitinated ADP-ribose over non-modified ubiquitin. Subsequently, RNF114 can elongate the ubiquitinated ADP-ribose with a K11-linked ubiquitin chain. Using domain deletion analysis, we pinpoint the tandem zinc fingers and ubiquitin interacting motif (ZnF2+ZnF3+UIM) domains of RNF114 to be crucial for recognising ubiquitinated ADP-ribose. Moreover, these domains are essential for the recruitment of RNF114 to the sites of laser-induced DNA damage.

molecular biology↗

Brain network dynamics determine tau presence while regional vulnerability governs tau load in Alzheimer's disease

In Alzheimers disease (AD), tau pathology accumulates gradually throughout the brain, with clinical decline reflecting tau progression. A comprehensive understanding of, first, whether tau propagation is predominantly governed by connectome-based diffusion, regional vulnerability, or an interplay of both, and second, which types of brain connectivity or regional factors best explain tau propagation, remains crucial for advancing our understanding of AD progression. Here, we apply multi-scale, biologically informed disease progression simulations to human data, to disentangle the influence of local mechanisms on global tau progression patterns in AD. We find that whether tau reaches a brain region (presence) and how much tau accumulates there (load) are governed by different mechanisms. Tau presence patterns are highly consistent across the population, and can be largely explained through synaptic spread through white-matter networks and excitatory-inhibitory dynamics. Meanwhile tau load differs across people, and is driven by a combination of synaptic spread and intrinsic or extrinsic regional properties, including regional {beta}-amyloid load, MAPT gene expression and regional blood flow. Finally, while distinct tau patterns in the population could each be explained by established AD mechanisms, our models highlight a role of distinct brain networks (parietal networks in MTL-sparing AD tau subtype) and neurotransmitter systems (cholinergic system in posterior subtype). Together, this work suggests that network dynamics likely determine the sequence of regional tau progression, while individual-specific tissue-vulnerability factors influence regional tau load.

neuroscience↗

Hemispheric Asymmetry of Tau Pathology is Related to Asymmetric Amyloid Deposition in Alzheimer's Disease

The distribution of tau pathology in Alzheimers disease (AD) shows remarkable inter-individual heterogeneity, including hemispheric asymmetry. However, the factors driving this asymmetry remain poorly understood. We explored whether tau asymmetry is linked to i) reduced inter-hemispheric brain connectivity (potentially restricting tau spread), or ii) asymmetry in amyloid-beta (A{beta}) distribution (indicating greater hemisphere-specific vulnerability to AD pathology). 452 participants from the Swedish BioFINDER-2 cohort with evidence of both A{beta} pathology (CSF A{beta}42/40 or neocortical A{beta}-PET) and tau pathology (temporal tau-PET), were categorised as left asymmetric (n=102), symmetric (n=306), or right asymmetric (n=44) based on temporal lobe tau-PET uptake distribution. Edge-wise inter-hemispheric functional (RSfMRI; n=318) and structural connectivity (dMRI; n=352) patterns were examined but no differences in inter-hemispheric functional or structural connectivity were found between groups. However, a strong association was observed between tau and A{beta} laterality patterns based on PET uptake (n=233; {beta}=0.632, p<0.001), which was replicated in three independent cohorts (n=234; {beta}=0.535, p<0.001). In a longitudinal A{beta}-positive sample, baseline A{beta} asymmetry predicted the progression of tau laterality over time (n=289; {beta}=0.025, p=0.028). These findings suggest that tau asymmetry is not associated with a weaker inter-hemispheric connectivity but might reflect hemispheric differences in vulnerability to A{beta} pathology, underscoring the role of regional vulnerability in determining the distribution of AD pathology.

neuroscience↗

A longitudinal evaluation of localised chronic Pseudomonas aeruginosa infection in cystic fibrosis rat models

Recurrent bacterial infections with Pseudomonas aeruginosa result in chronic airway inflammation, lung damage and eventual respiratory failure, and are the major cause of morbidity and mortality in people with cystic fibrosis (CF). Animal models are essential for understanding disease progression and assessing potential treatments in the presence of infection. Previously reported P. aeruginosa lung infection rodent models for CF research have some weakness, including acute infection rather than chronic, associated mortality, use of laboratory strains of P. aeruginosa and the use of non-CF rodents. The aim of this study was to create a localised P. aeruginosa infection in wildtype and two CF rat models, by delivering bacteria embedded agar beads using a miniature bronchoscope. The resulting infection was well tolerated by all animals of all genotypes with no mortality associated with the procedure or infection. Histologically the affected regions were localised to the right lung, with bronchopneumonia present. Bacteria persisted for 9 weeks (63 days) in all genotypes, with lung function changes observed by day 63 of the infection.

pathology↗

Non-linear Age-related Change in Human Interleukin-11 and the receptor subunit alpha DNA Methylation

IntroductionInterleukin-11 (IL-11) is a cytokine involved in inflammatory processes and a previous study showed that blocking or knocking down IL11 in mice prolongs a healthy lifespan. This study investigates DNA methylation (DNAm) changes in the IL11 and IL-11 receptor subunit alpha (IL-11RA) gene across ages to reveal how aging might influence IL-11 production and sensitivity. MethodsA genome-wide DNAm database focusing on Cytosine-phosphate-Guanine (CpG) sites within the IL11 and IL11RA was analyzed. Hierarchical regression analyses examined the relationship between DNAm, age, and the squared age term for quadratic associations. ResultsThe database comprised 10,297 samples (5,156 males and 5,141 females) with a mean age of 53.9 years (SD = 14.1 years). The majority of IL11 and IL11RA CpG sites in the TSS1500 and 3UTR regions exhibited significant inverse U-shaped associations with age. DNAm levels were low during youth, increased in middle age (40s-50s), and decreased again in older age. ConclusionThe observed inverse U-shaped DNAm patterns in the IL11 and IL11RA suggest n non-linear, age-related regulation of IL-11 expression and sensitivity. These findings indicate that IL-11 may have different roles across life stages and suggest that therapeutic interventions targeting IL-11 should consider age-specific effects.

genetics↗