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Rodrigues, B.

Publications and source records attributed to Rodrigues, B..

10 recordsLinked to original sources

Prefrontal cortex resting-state connectivity is moderated by hunger expectations induced by a placebo intervention in healthy female participants.

Placebo effects, in which a patient's symptoms and subjective well-being improve in response to an inactive treatment, medication, or intervention (a placebo), are well known in clinical research. Basic research in human cognition and neuroscience has shown that these effects are linked to prognostic expectations of effectiveness and to recruitment of prefrontal cortex regions, including the medial (mPFC), ventromedial (vmPFC), and dorsolateral prefrontal cortex (dlPFC). Here, we examined how the intrinsic functional connectivity of these three brain regions at rest, in the absence of any explicit task, was affected by internal beliefs such as placebo-induced hunger expectations. We conducted a seed-based resting-state functional connectivity analysis in 60 healthy female participants who underwent a placebo intervention targeting their hunger. In line with previously published results, the intervention induced hunger expectations and biased hunger sensations. Importantly, these effects were underpinned by attenuated functional connectivity between the mPFC and the angular gyrus within the default mode network the more participants expected the placebo to decrease their hunger. Hunger-increasing expectations attenuated connectivity between the vmPFC and the dm/dlPFC within the frontoparietal network and increased connectivity between the dlPFC and the thalamus. These results suggest that placebo-induced hunger expectations shift the way the prefrontal cortex connects to other brain regions associated with valuation, cognitive control, and interoception. This evidence sheds light on how the brain may translate incoming sensory information into biased sensations under placebo conditions and improves our understanding of the neural and psychological factors that influence a person's response to a placebo.

neuroscience↗

When adiposity and listening to reasons for behavioral change make food choices healthier: Behavioral and neural mediators of weight status effects on dietary decision-making following behavioral change interventions.

Resolving the inner conflict between improving eating habits (change talk) and sticking to unhealthy ones (sustain talk) is a key target in communication-based behavioral change interventions such as motivational interviewing (MI). Recent work has shown that this inner conflict affects how tastiness and healthiness are traded off in dietary decision-making. The effect varied with body mass index (BMI). Here we aimed to identify why participants with higher BMI shifted toward healthier food choices after listening to change talk. An evidence accumulation model found that BMI affected health evidence sampling when listening to change talk, and taste evidence sampling when listening to sustain talk. A serial mediation analysis showed that the effect of BMI on change-talk-induced health evidence sampling was explained by stronger resting-state connectivity in the ventromedial prefrontal cortex within the default mode network (DMN), which in turn predicted greater motivation to change eating habits. These cross-sectional findings indicate that the intrinsic functional organization of valuation-related regions within the DMN is associated with motivation to change. They provide evidence that these neural and behavioral factors need to align with contextual cues, such as weight status (as reflected by BMI), and with reasons for behavioral change to promote healthier decision-making.

neuroscience↗

Cardiomyocyte pyruvate dehydrogenase kinase 1 knockout activates Rho-mediated remodeling and decreases fatty acyl availability in female mice

Pyruvate dehydrogenase kinase 1 (PDK1) inhibits pyruvate dehydrogenase (PDH) and therefore may regulate the balance between glucose and fatty acid oxidation in cardiomyocytes. We assessed metabolism and function in tamoxifen-inducible, cardiomyocyte-specific Pdk1 knockout (Pdk1cKO) mice, including both males and females fed a high fat diet, to resolve the role of PDK1 in the heart. Female, but not male, Pdk1cKO hearts showed the expected increase in cardiac PDH activity. Though cardiac function was largely preserved, female Pdk1cKO hearts had smaller left ventricles. Proteomics and phosphoproteomics revealed no change in classical hypertrophic markers but downregulated aerobic respiration alongside upregulated Ca2+ handling and Rho signalling, suggesting metabolic remodeling with altered cardiomyocyte contractility and cytoarchitecture in Pdk1cKO hearts. Concordantly, lipidomics revealed membrane remodeling marked by elevated saturated phosphatidylcholine in female Pdk1cKO hearts and decreased triacylglycerols, free fatty acids and fatty acid uptake proteins (CD36, FABP3). These findings reveal novel, female-predominant cardiometabolic roles for PDK1.

molecular biology↗

Molecular Insights into ANPEP in Gastric Adenocarcinoma

Alanyl aminopeptidase (ANPEP) has been implicated in various cancers, but its specific role in gastric adenocarcinoma (GC) remains incompletely understood. This study analyzed ANPEP gene expression in gastric cancer (GC), peritumoral tissue (PTT), metaplasia (M), and normal tissue (N). Total RNA was extracted, libraries were prepared and sequenced on the Illumina NextSeq 500. Data was processed using the nf-core/rnaseq pipeline. Transcript quantifications were imported with tximport and normalized using DESeq2. Differential expression (|log2FC| >2; adj. p < 0.05) and Kruskal-Wallis tests identified key genes. ANPEP was significantly upregulated in GC, PTT, and M compared to normal tissue (p < 0.01), suggesting its involvement in early mucosal transformation and malignant progression. Heatmap analysis revealed upregulation of genes related to immune function and oxidative stress, indicating an immunosuppressive and apoptosis-resistant tumor microenvironment. Correlation analyses identified strong positive associations between ANPEP and genes involved in cytoskeletal remodeling, immune modulation, and metabolic regulation, suggesting that ANPEP supports both the invasive potential of tumor cells and the establishment of an immunosuppressive niche. These findings position ANPEP as a promising biomarker for early detection and a candidate for targeted therapies.

cancer biology↗

Allosteric Modulation of Pathological Ataxin-3 Aggregation: A Path to Spinocerebellar Ataxia Type-3 Therapies

Spinocerebellar ataxia type 3 (SCA3) is a rare inherited neurodegenerative disease caused by the expansion of a polyglutamine repeat in the protease ataxin-3 (Atx3). Despite extensive knowledge of the downstream pathophysiology, no disease-modifying therapies are currently available to halt disease progression. The accumulation of protein inclusions enriched in the polyQ-expanded Atx3 in neurons suggests that inhibiting its self-assembly may yield targeted therapeutic approaches. Here it is shown that a supramolecular tweezer, CLR01, binds to a lysine residue on a positively charged surface patch of the Atx3 catalytic Josephin domain. At this site, the binding of CLR01 decreases the conformational fluctuations of the distal flexible hairpin. This results in reduced exposure of the nearby aggregation-prone region, which overlaps with the substrate ubiquitin binding site and primes Atx3 self-assembly, ultimately delaying Atx3 amyloid fibril formation and reducing the secondary nucleation rate, a process linked to fibril proliferation and toxicity. These effects translate into the reversal of synapse loss in a SCA3 cultured cortical neuron model, an improved locomotor function in a C. elegans SCA3 model, and a delay in disease onset, accompanied by reduced severity of motor symptoms in a SCA3 mouse model. This study provides critical insights into Atx3 self-assembly, revealing a novel allosteric site for designing CLR01-inspired therapies targeting pathological aggregation pathways while sparing essential functional sites. These findings emphasize that targeting allosteric sites in amyloid-forming proteins may offer unique opportunities to develop safe therapeutic strategies for various protein misfolding disorders.

biophysics↗

Listen to yourself: How motivational interviewing shifts food choices and craving-related brain responses to healthier options

Changing ones habits is challenging. Motivational interviewing (MI) has been proposed as a communication-based approach to overcome this challenge. Here, we tested how change and sustain talk suggestions, elicited by MI, influenced value-based dietary decision-making and responses of a recently developed neurobiological craving signature (NCS) in female adults. We found that following change talk, compared to sustain talk, participants food choices and activity in the ventromedial prefrontal cortex were more driven by the healthiness and less by the tastiness of food. These findings were paralleled by lower NCS responses to tasty food after change compared to sustain talk. Further, following change talk, participants body mass indices moderated the NCS decoding of healthy and tasty food choices. These results show that MI can shift value-based decision-making and reduce craving-related brain marker responses to highly palatable food items. The findings contribute to a better understanding of behavioral change interventions toward healthier eating.

neuroscience↗

Taste matters: Mapping expectancy-based appetitive placebo effects onto the brain

Expectancies, which are higher order prognostic beliefs, can have powerful effects on experiences, behavior and brain. However, it is unknown where, how, and when, in the brain, prognostic beliefs influence appetitive interoceptive experiences and related economic behavior. This study combined a placebo intervention on hunger with computational modelling and functional magnetic resonance imaging of value-based decision-making. The results show that prognostic beliefs about hunger shape hunger experiences, how much participants value food and food-value encoding in the prefrontal cortex. Computational modelling further revealed that these placebo effects were underpinned by how much and when during the decision process taste and health information are integrated into the accumulation of evidence toward a food choice. The drift weights of both sources of information further moderated ventromedial and dorsolateral prefrontal cortex interactions during choice formation. These findings provide novel insights into the neurocognitive mechanisms that translate higher order prognostic beliefs into non-aversive interoceptive sensitivity and shape decision-making.

neuroscience↗

Development of spontaneous firing of fusiform neurons from the dorsal cochlear nucleus of mice occurs after hearing onset.

The dorsal cochlear nucleus (DCN) in the auditory brainstem integrates auditory and somatosensory information. Mature fusiform neurons express two qualitative intrinsic states in equal proportions: quiet, with no spontaneous regular action potential firing, or active, with regular spontaneous action potential firing. However, how these firing states and other electrophysiological properties of fusiform neurons develop during early postnatal days to adulthood is not known. Thus, we recorded fusiform neurons from mice from P4 to P21 and analyzed their electrophysiological properties. In the pre-hearing phase (P4-P13), we found that fusiform neurons are mostly quiet, with the active state emerging after hearing onset at P14. Subthreshold properties present more variations before hearing onset, while action potential properties vary more after P14, developing bigger, shorter, and faster action potentials. Interestingly, the activity threshold is more depolarized in pre-hearing cells suggesting that persistent sodium current (INaP) increases its expression after hearing. In fact, INaP increases its expression after hearing, accordingly with the development of active neurons. Thus, we suggest that the post-hearing expression of INaP creates the active state of the fusiform neuron. At the same time, other changes refine the passive membrane properties and increase the speed of action potential firing of fusiform neurons.

neuroscience↗

The smORF-containing gene mille-pattes is required for moulting and Trypanosoma cruzi metacyclogenesis in the Chagas disease vector Rhodnius prolixus

Chagas disease is estimated to affect 8 million people worldwide and is responsible for circa 10,000 deaths in Latin America every year. Vector control has been developed as the main strategy to control disease spreading. The identification of new targets is essential, and genes containing small open reading frames (smORFs - < 100 amino acids) are present as hundreds of putative new candidate targets in insect genomes. Here, we show that the prototypic smORF containing gene mille-pattes/polished-rice/tarsalless (mlpt/pri/tal) is essential for post-embryonic development of the kissing bug Rhodnius prolixus and for the metacyclogenesis of the Trypanosoma cruzi parasite during nymphal stages. Injection of double-stranded RNA against mlpt (Rp-dsmlpt) during nymphal stages leads to a plethora of phenotypes which impairs post-embryonic development. First, nymphs of fourth or fifth stage injected with Rp-dsmlpt do not moult. Second, vector digestive physiology is largely modified, and haemozoin is significantly increased in the posterior midgut of Rp-dsmlpt nymphs. Third, Rp-mlpt knockdown inhibits the metacyclogenesis of Trypanosoma cruzi, the etiologic agent of Chagas disease. Thus, our study provides the first evidence of a smORF-containing gene regulating vector physiology, parasitic cycle and disease transmission.

molecular biology↗

Identification of a novel gammaherpesvirus in Canada lynx (Lynx canadensis)

Gammaherpesviruses (GHVs) infect many animal species and are associated with lymphoproliferative disorders in some. Previously, we identified several novel GHVs in North American felids, however a GHV had never been identified in Canada lynx (Lynx canadensis). We therefore hypothesized the existence of an unidentified GHV in lynx. Using degenerate nested and subsequently virus-specific PCR, we amplified and sequenced 3.4 kb of DNA from a novel GHV in lynx, which we named Lynx canadensis gammaherpesvirus 1 (LcaGHV1). We then estimated the prevalence of LcaGHV1 in lynx by developing a PCR-based assay and detected LcaGHV1 DNA in 36% (95% CI: 22-53%) of lynx spleen DNA samples from Maine, USA and 17% (95% CI: 8-31%) from Newfoundland, Canada. Phylogenetic analysis determined that LcaGHV1 is a distinct GHV species belonging to the genus Percavirus. The potential ecologic and pathologic consequences of this novel virus for Canada lynx populations warrant further study.

microbiology↗