When a beloved artist is revealed to have committed serious wrongdoing, how do people hold on to their past appreciation for that artist’s work? Research from the University of South Florida, published in the Journal of Experimental Social Psychology, shows that the mind resolves this conflict through a process the authors call “differential memory reconstruction.” Instead of discarding the work or defending the creator, people often rewrite their autobiographical memories: they downgrade retrospective admiration for the creator while preserving fond memories of the work itself.

Key Facts:

• Differential Memory Reconstruction: When confronted with revealed transgressions by an admired creator, people tend to retroactively reduce how positively they remember the artist while maintaining past enjoyment of the art.
• Asymmetry Between Past and Present: Present-day evaluations of both the creator and the creation decline after negative revelations. However, the psychological separation of art from artist is most pronounced when people reconstruct their past memories.
• Cross-Genre Consistency: The effect appeared across five behavioral experiments involving high-profile figures from television, soul and jazz, and rock and pop, suggesting memory reconstruction is a broad emotional defense that protects nostalgia from moral contamination.

Source: University of South Florida

Learning that a cultural figure you admired has committed reprehensible acts creates intense cognitive dissonance. Decades of laughter, memorable movie moments, or formative songs can suddenly clash with revelations of abuse, neglect, or criminal behavior. Philosophers and cultural critics have long debated whether it is possible—or desirable—to separate the art from the artist. This study shows that, in practice, people’s memories often do exactly that for them.

The study demonstrates that the mind does not simply erase or wholly condemn prior enjoyment. Instead, it performs a selective revision that preserves personal nostalgia while distancing the self from the transgressor.

The Mechanics of “Moral Surgery”

Led by Dr. Sally MyungJin Shin of the University of South Florida’s Muma College of Business, with co-authors Paul Rozin and Gal Zauberman, the research examined how news of wrongdoing changes both current attitudes and recollections of prior attitudes. Across five pre-registered experiments, participants reviewed creators and their work and then were exposed to documented transgressions involving those creators.

The experiments used real-world examples across different media, including:

• Television: Reactions to Bill Cosby after widely publicized allegations and legal actions following decades of popularity for The Cosby Show.
• Soul & Jazz: Responses to knowledge of Ray Charles’s history of severe parental neglect.
• Rock & Pop: Reassessment of John Lennon in light of reports about his past domestic and physical abuse.

After learning about a creator’s moral failings, participants’ immediate evaluations of both the artist and their work declined: they reported liking both less in the present. But when asked to recall how they felt in the past, participants typically downgraded how much they thought they had admired the creator while insisting that their past enjoyment of the work remained intact and meaningful. The authors labeled this selective retrospective decoupling “differential memory reconstruction.”

As Dr. Shin explains, people often revise their personal histories so they can claim they were skeptical of the creator all along, while preserving the emotional value of songs, shows, or films that helped shape their identity. Rather than overhauling the entire memory network, the mind performs what the researchers describe as a precise “moral surgery”: it severs the emotional link between author and artifact, but primarily in the reconstructed past.

Nostalgia as a Protected Cognitive Asset

Why protect nostalgia? Autobiographical memories tied to music, television, and film are woven into personal identity: a favorite song can evoke high school friendships or formative moments; a childhood TV show can recall family rituals and feelings of safety. If acknowledging an artist’s wrongdoing forced people to see those formative memories as tainted, it would threaten their positive self-narrative.

By revising past impressions of the creator while keeping past enjoyment of the work, people reduce moral discomfort without surrendering cherished memories. The study shows this form of reconstruction is an emotion-driven coping strategy, not simply rationalization or denial of facts.

Implications for Culture and Cognitive Science

These findings highlight memory as an active, reconstructive process shaped by current social and moral contexts. While public debate often frames responses to problematic creators as binary—either condemn the person and the art, or separate them cleanly—human cognition tends to take a more nuanced route. By preserving the personal significance of cultural works while downgrading the creators in recollection, people protect their sense of self, manage cognitive dissonance, and retain positive emotional experiences.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this cognitive dissonance Research:

• Media Contact: John Dudley
• Source: University of South Florida
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: Journal of Experimental Social Psychology (Oct 1, 2026). “Moral surgery: Negative revelations differentially alter retrospective evaluations of creators and creations.” Authors: Sally MyungJin Shin, Paul Rozin, and Gal Zauberman.
• DOI: 10.1016/j.jesp.2026.104992

Abstract

Moral surgery: Negative revelations differentially alter retrospective evaluations of creators and creations

When people learn that a creator they once admired committed a moral transgression, they face a painful gap between their earlier positive evaluations and the new negative information. While prior research emphasized changes in current attitudes, this study focuses on how people reconstruct their past attitudes. Across five preregistered experiments, we find a reliable pattern: individuals reconstruct prior evaluations by separating the art from the artist. Specifically, revelations of wrongdoing prompt a substantial downward revision of recalled evaluations of the creator, while recalled evaluations of the creation remain relatively resilient to the negative information. This differential memory reconstruction appears for both experimentally induced and pre-existing positive evaluations, across multiple creative domains, and across varying transgression severities. Additional tests confirm the effect reflects a genuine psychological process rather than methodological artifacts, and it persists across incentive-compatible, multi-wave longitudinal, and separate-measurement designs that control for alternative explanations such as low cognitive effort, temporal proximity, and demand characteristics.

The post Why Your Brain Protects Nostalgia From Scandals first appeared on Anksiyete.

A combined cross-sectional epidemiological and targeted lipidomics study of 1,917 community-dwelling older adults found that higher dietary intake of lecithin—a major source of phosphatidylcholine—was associated with a lower prevalence of mild cognitive impairment (MCI) and better overall cognitive performance measured by the Montreal Cognitive Assessment (MoCA). Targeted blood lipid profiling showed that participants with MCI had lower total phosphatidylcholine levels and a shift in phosphatidylcholine composition away from polyunsaturated fatty acids toward saturated fatty acids. The protective association between dietary lecithin and cognition was strongest among individuals with lower formal education, indicating a potentially accessible nutritional approach to reduce cognitive health disparities.

Key Facts:

• Meaningful cognitive protection: In a cohort of 1,917 older adults, greater dietary lecithin intake correlated with reduced odds of mild cognitive impairment and higher global MoCA scores, after adjusting for age, sex, education, and chronic disease history.
• Distinct lipidomic signature: Targeted lipidomics revealed that people with MCI had lower circulating phosphatidylcholine (PC) concentrations, fewer PC species containing polyunsaturated fatty acids (PUFAs), and a higher proportion of PC species containing saturated fatty acids (SFAs).
• Education modifies effect: The cognitive benefit associated with dietary lecithin was most pronounced among older adults with junior high school education or less, suggesting dietary lecithin could offer particular advantages for populations with lower cognitive reserve.

Source: Neuroscience News / Research Team Release

Context: As global life expectancy rises, age-related cognitive decline and mild cognitive impairment (MCI) have become pressing public health concerns. With limited pharmacological options to reverse neurodegenerative damage, scalable nutritional strategies that support neuronal membrane integrity and synaptic function are receiving growing attention.

Lecithin is a complex of lipids rich in phosphatidylcholine (PC), an essential component of cell membranes. Phosphatidylcholine contributes to membrane fluidity, synaptic plasticity, and the biosynthesis of acetylcholine, a neurotransmitter critical for memory and learning. Although animal and small clinical studies have long suggested neuroprotective roles for choline-containing phospholipids, comprehensive population-based and lipidomic evidence has been limited—until now.

This multicenter study of nearly two thousand older adults provides both epidemiological and biochemical evidence linking dietary lecithin intake, membrane lipid composition, and cognitive status.

Dietary Lecithin and Cognitive Assessment

Researchers assessed habitual dietary intake using structured food frequency questionnaires calibrated to estimate daily lecithin consumption. Cognitive function was evaluated with the Montreal Cognitive Assessment (MoCA), a widely used, sensitive measure of mild cognitive impairment that captures executive function, memory, attention, and visuospatial skills.

After adjusting for possible confounders—including age, sex, education, and histories of cardiometabolic disease—the analysis showed that participants with higher dietary lecithin intake had significantly better global MoCA scores and lower odds of MCI. The association remained statistically significant when controlling for other dietary and clinical variables, supporting a robust link between lecithin-rich diets and preserved cognitive function in older adults.

Lipidomic Fingerprint of Cognitive Impairment

To explore biochemical correlates, the investigators performed targeted lipidomic profiling of blood samples. The analysis revealed a characteristic lipidomic pattern in those with MCI:

• Lower total PC: Overall circulating levels of phosphatidylcholine were reduced in participants with MCI compared with cognitively intact peers.
• Fewer PUFA-containing PC species: The proportion of PC molecules bound to polyunsaturated fatty acids—lipids that favor membrane fluidity and anti-inflammatory signaling—was diminished in the MCI group.
• Higher SFA-containing PC species: The relative abundance of PC species containing saturated fatty acids was increased in MCI participants, a profile associated with greater membrane rigidity and higher oxidative susceptibility.

These findings suggest that both the amount and quality of phosphatidylcholine in circulation—reflecting membrane composition—are linked to cognitive health in older adults.

Education as an Effect Modifier: Reducing Disparities

The study found that educational attainment modified the association between dietary lecithin and cognition. Individuals with junior high school education or less derived the largest cognitive benefit from higher lecithin intake. This aligns with cognitive reserve theory, which proposes that higher formal education can buffer clinical symptoms of brain pathology; accordingly, those with lower education may gain greater benefit from nutritional strategies that support membrane health.

Lecithin-rich foods include eggs, soybeans, sunflower seeds, and certain organ meats. Promoting increased dietary lecithin intake through accessible food choices or community nutrition programs could be a practical, low-cost approach to help narrow cognitive health disparities among socioeconomically vulnerable older adults.

The authors note the study’s cross-sectional design limits causal inference: the results demonstrate strong associations but cannot confirm that lecithin intake directly prevents cognitive decline. Prospective cohort studies and randomized controlled trials are needed to determine whether increasing dietary lecithin preserves membrane lipid composition and slows cognitive deterioration over time.

Funding information
This research was funded by the National Natural Science Foundation of China (82273620).

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by staff.

About this cognition and diet research:

• Media Contact: Tingting Yang
• Source: Chinese Medical Journal
• Image Credit: Image credited to Neuroscience News
• Original research (open access): Chinese Medical Journal (Oct 1, 2026). “Association of dietary lecithin intake with mild cognitive impairment and cognitive performance in elderly population.” Authors: Xiaoying Li, Chengyan Qi, Yuebao Fu, Wenjing Wang, Huini Ding, Yijia Liu, and Yuandi Xi. Huttunen.
• DOI: 10.1097/CM9.0000000000004246

Abstract

Association of dietary lecithin intake with mild cognitive impairment and cognitive performance in elderly population

Background:

Interest is growing in the potential cognitive benefits of dietary lecithin, but population-level evidence remains limited. This study explored the relationship between lecithin intake and cognitive function, and examined associations with the prevalence of mild cognitive impairment in adults aged 60 years and older.

Methods:

This cross-sectional study enrolled participants aged over 60 from Beijing, Jincheng City (Shanxi Province), and Linyi City (Shandong Province) between 2020 and 2023. Cognitive function was assessed with neuropsychological tests, including the MoCA, and dietary intake was measured using a food frequency questionnaire to estimate lecithin consumption. Body composition was measured by bioelectrical impedance analysis, and blood lipids by automated biochemical assays. Statistical analyses included Spearman correlation, multiple linear regression, logistic regression, and receiver operating characteristic (ROC) curve analysis. Targeted lipidomic profiling was performed on blood samples.

Results:

Of 1,917 participants, 1,023 (53.4%) met criteria for MCI; 542 of those with MCI (53.0%) were women. Multiple linear regression found that higher dietary lecithin, total cholesterol (TC), and high-density lipoprotein cholesterol (HDL-C) were each associated with higher MoCA scores (regression coefficients 0.49, 0.44, and 0.38, respectively, after dichotomizing by median). Logistic regression indicated that participants with higher dietary lecithin intake had lower odds of MCI (odds ratio 0.80, 95% confidence interval 0.64–0.99) compared with those with lower intake. A predictive model combining dietary lecithin, energy intake, demographic and clinical characteristics yielded an area under the curve (AUC) of 0.735 (95% CI: 0.713–0.757). Targeted lipidomics showed that the MCI group had lower total phosphatidylcholine, a smaller proportion of PUFA-containing PC species, and a higher proportion of SFA-containing PC species.

Conclusion:

Higher dietary lecithin intake was associated with better cognitive performance and a lower prevalence of mild cognitive impairment among adults aged 60 and older. These findings highlight lecithin and membrane phosphatidylcholine composition as promising targets for future nutritional interventions aimed at preserving cognitive health in aging populations.

The post Dietary Lecithin May Lower Risk of Cognitive Impairment first appeared on Anksiyete.

A new mathematical and computational framework published in The Innovation addresses a central problem in empirical science: how to infer genuine cause and effect in complex, non-linear systems from observational data alone, without performing physical interventions. Developed by researchers at Fudan University, the Chinese Academy of Sciences, and the University of Tokyo, the Interventional Dynamical Causality (IntDC) framework introduces an information-theoretic metric, Interventional Embedding Entropy (IEE). By using delay-coordinate state-space reconstruction, IntDC infers intervention-level causal directionality while eliminating spurious associations produced by hidden common drivers. The method successfully reconstructed functional neural connectomes in Caenorhabditis elegans, identified COVID-19 transmission pathways, and recovered gene regulatory interactions underlying circadian rhythms.

Key Facts:

• Intervention-Level Standard: Rather than measuring predictive dependence as in Granger causality, transfer entropy, or convergent cross mapping, IntDC asks whether an external perturbation to variable X would change variable Y — a stricter, intervention-focused definition of causal influence.
• Confounder-Free Delay Embedding: Building on Takens’ delay-embedding theorem, the approach demonstrates that the reconstructed state-space of Y contains the topological imprint of perturbations to X. Interventional Embedding Entropy (IEE) uses this property to reject false links caused by shared drivers (Z).
• Validated Across Biological Domains: The algorithm accurately reconstructed whole-brain functional connectivity from C. elegans calcium imaging, mapped regional COVID-19 transmission vectors in Japan, and isolated core regulatory genes in circadian transcriptional networks.

Source: Fudan University / Chinese Academy of Sciences / University of Tokyo

Establishing true cause and effect is the primary aim of empirical science. Neuroscientists want to pinpoint neural microcircuits that trigger behavior; geneticists need to identify the transcription factors that control cell fate; and climate scientists must distinguish which forcings drive global change. The classical way to confirm causality is to intervene: change one variable while holding others fixed and observe the outcome. But direct intervention is often infeasible, costly, or ethically unacceptable in many real-world systems, from chaotic climate dynamics to living neural circuits.

Consequently, researchers typically rely on passive observational time-series and use predictive tools such as Granger causality, transfer entropy, or convergent cross mapping. Those methods detect constructive dynamical causality — whether past values of X help forecast Y — but they are vulnerable to false positives when an unobserved common driver drives both variables simultaneously.

Interventional Dynamical Causality (IntDC) and Embedding Entropy

The IntDC framework formalizes the difference between observational dependence and true interventional causality in dynamical systems. Following intervention-centered causal criteria (similar in spirit to do-calculus), X should be labeled a cause of Y only if intervening on X produces a change in Y. To infer this from observational records without performing interventions, the authors exploit delay-coordinate embedding results from nonlinear dynamics.

Takens’ theorem implies that the multi-dimensional manifold of a coupled dynamical system can be reconstructed from the lagged measurements of a single variable. The researchers reasoned that if X truly intervenes on Y, then the reconstructed state-space of Y will carry the topological imprint of X’s perturbations. They developed Interventional Embedding Entropy (IEE), an information-theoretic measure that quantifies directional information flow between these reconstructed state spaces. IEE estimates causal strength from passive time-series without needing the system’s governing equations or real experimental perturbations.

Robustness Against Confounders and Computational Benchmarks

The team evaluated IntDC and IEE on standard synthetic benchmarks — including coupled logistic maps, Hénon attractors, and chaotic recurrent neural networks — to test the method’s behavior under confounding scenarios. In canonical three-node setups where a shared driver Z synchronizes variables X and Y without direct interaction, conventional tools often infer spurious X → Y links. IEE consistently rejected these false connections and demonstrated stability across variations in time-series length, measurement noise, embedding dimension, and coupling strength.

Applications: From Nematode Brain Maps to Epidemic Routes

The utility of IntDC was demonstrated on several real-world biological and epidemiological problems:

1. Whole-Brain Connectomics: Using calcium imaging time series from the nematode C. elegans, IEE reconstructed directed functional connections among sensory, inter-, and motor neurons, producing interpretable signaling pathways.
2. Epidemic Transmission Modeling: Applied to Japan’s COVID-19 regional case records, the method identified geographic transmission vectors and localized sources that seeded secondary outbreaks.
3. Circadian Gene Regulatory Networks: Analyzing oscillatory transcriptomics, IEE recovered regulatory loops and ranked the influence of core circadian pacemaker genes.

By converting passive time-series into ranked, quantitative causal strengths, the IntDC/IEE framework offers a principled path from observation to testable causal hypotheses. This advances automated causal discovery across neuroscience, systems biology, and computational medicine and creates a bridge between observational inference and experimental validation.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this neuroscience Research:

• Media Contact: Yong Han
• Source: Innovation Press
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: The Innovation (Oct 1, 2026). “Deciphering interventional dynamical causality from non-intervention complex systems.” Authors: Jifan Shi, Yang Li, Juan Zhao, Siyang Leng, Rui Bao, Kazuyuki Aihara, Luonan Chen, and Wei Lin.
• DOI: 10.1016/j.xinn.2026.101358

Abstract

Deciphering interventional dynamical causality from non-intervention complex systems

Detecting and quantifying causal influence is central across science and engineering, yet inferring intervention-level causality in non-intervention systems remains highly challenging. Delay-embedding methods offer a promising route. Here we introduce Interventional Dynamical Causality (IntDC) to complement traditional constructive dynamical causality (ConDC), which includes Granger causality, transfer entropy, and convergent cross mapping. ConDC measures predictive relationships without explicitly addressing interventions.

We propose Interventional Embedding Entropy (IEE), a computational criterion that quantifies causal strength in an interventional sense within delay-embedding space. IEE represents intervened causal information flow reconstructed from observational time series, and it enables inference of IntDC without requiring knowledge of the underlying dynamical models or real experimental perturbations. IEE can rank causal effects, construct directed networks, and robustly eliminate confounding influences compared with traditional indices. Numerical experiments on logistic dynamics, coupled Hénon maps, and chaotic neural networks show accurate edge detection and resilience to confounders. Applications to C. elegans neural data, COVID-19 transmission in Japan, and circadian gene regulatory circuits further demonstrate IEE’s practical effectiveness for causal analysis from observational data alone. Together, the IntDC framework and IEE algorithm provide a rigorous approach for understanding causal influence in diverse, non-intervention complex systems.

The post Noninvasive Neural Circuit Mapping Without Touching a Neuron first appeared on Anksiyete.

A genomic and transcriptomic study led by the Germans Trias i Pujol Research Institute (IGTP) finds that blood platelets provide a sensitive peripheral window into the molecular evolution of Parkinson’s disease. Published in the journal Movement Disorders, the team followed longitudinal gene expression in a patient with a rare de novo SNCA gene triplication as the illness progressed to dementia over three years.

Isolated platelets revealed substantially stronger transcriptomic changes than whole blood, implicating mitochondrial dysfunction, altered protein translation, and inflammation. Key molecular shifts—including dysregulation of SNCA, YWHAB (14-3-3 family), and MMRN1—were validated in an independent cohort of patients with sporadic early-onset Parkinson’s disease.

Key Facts:

• Platelets outperform whole blood for progression signals: Purified platelets captured disease-associated transcriptomic shifts more clearly than standard whole-blood assays, revealing disruptions in mitochondrial respiration, ribosomal function, and inflammatory pathways.
• Rare SNCA triplication followed longitudinally: Researchers tracked a non-inherited (de novo) 2.41-megabase triplication spanning 21 genes, including SNCA, comparing molecular profiles at age 41 (early motor phase) and age 44 (onset of dementia).
• Findings validated in sporadic Parkinson’s: Several transcript-level changes—such as decreased expression of a specific SNCA isoform and of YWHAB, and increased MMRN1—were confirmed in a separate group of 15 sporadic early-onset Parkinson’s patients versus 18 controls.

Source: Germans Trias i Pujol Research Institute (IGTP)

Monitoring Parkinson’s disease progression in clinical practice remains challenging: clinical scales rely on subjective motor and cognitive assessments and there is a lack of minimally invasive biomarkers that track neurodegenerative velocity or flag early transitions to dementia. Whole-blood transcriptomics has been explored widely, but circulating immune cells and serum components often introduce biological noise that can mask signals originating from the nervous system.

Platelets (thrombocytes) share several functional and molecular properties with neurons: they contain regulated secretory granules, metabolize monoamines such as dopamine and serotonin, express high baseline levels of alpha-synuclein, and maintain active mitochondrial networks—making them a plausible peripheral model for neuronal processes.

Researchers from the Genomics and Transcriptomics of Synucleinopathies (GTS) group at IGTP in Badalona, Spain, therefore evaluated whether platelet RNA profiles could reflect progression-related molecular changes in Parkinson’s disease.

Published in Movement Disorders, the study examined molecular expression across disease stages and identified shared transcriptomic features between an extreme monogenic case and more typical sporadic Parkinson’s patients.

Insights from a De Novo SNCA Triplication

The study, co-led by Katrin Beyer, PhD, and Pau Pastor, MD, PhD, with Susanna Jiménez-Román as first author, focused on a single exceptional case: an individual with early-onset Parkinson’s who progressed rapidly to dementia within three years. Genetic analysis identified a de novo 2.41-megabase triplication on chromosome 4q22.1 that includes SNCA, the gene encoding alpha-synuclein, and 20 other genes.

Because the patient was assessed at two distinct clinical milestones—age 41 (early motor symptoms) and age 44 (after dementia onset)—the team isolated both whole blood and purified platelet fractions at each time point. RNA sequencing and comparative analysis revealed that whole blood showed minimal transcriptomic change between time points, while platelets exhibited a widespread and coherent pattern of dysregulation.

Differentially expressed genes in platelets mapped to core biological processes relevant to Parkinson’s disease:

• Mitochondrial homeostasis: Alterations in electron transport chain components and cellular bioenergetics consistent with impaired mitochondrial function.
• Ribosomal and translational machinery: Broad changes affecting ribosomal proteins and translation factors, indicating disrupted protein synthesis.
• Inflammatory signaling: Activation of pathways linked to systemic and vascular immune responses.

“This unique longitudinal case allowed us to observe how molecular signals shift as Parkinson’s disease progresses. Platelets display clearer changes than whole blood, underscoring their potential as an accessible source of progression biomarkers,” said Susanna Jiménez-Román.

Shared Platelet Signatures in Sporadic Parkinson’s

To test whether the platelet signatures were specific to the rare triplication or reflected broader disease biology, the researchers examined a targeted set of candidate genes in an independent cohort of 15 patients with early-onset sporadic Parkinson’s disease and 18 matched healthy controls.

Platelet profiles in the sporadic group reproduced several findings from the longitudinal case report:

• Reduced SNCA and YWHAB expression: A specific SNCA transcript variant was downregulated alongside YWHAB, which encodes a 14-3-3 protein important for alpha-synuclein binding and cell survival signaling.
• Increased MMRN1: Multimerin-1 (MMRN1), an adhesive protein found in endothelium and platelets, was elevated in patients.
• Upregulation of ribosomal genes: Two genes involved in ribosome assembly showed higher expression, consistent with altered protein synthesis regulation.

After correction for multiple comparisons, these differences remained statistically significant in purified platelets, whereas whole-blood analysis from the same individuals failed to show significant divergence from controls.

Clinical Implications and Future Directions

The overlap between molecular changes in an aggressive monogenic case and those seen in sporadic patients suggests that rare, high-penetrance mutations can illuminate pathogenic pathways shared across the Parkinson’s population. Such shared signatures support the idea that platelets can serve as a minimally invasive source of biomarkers for disease progression and potential cognitive decline.

The authors emphasize that the longitudinal component is limited to a single patient, so the results establish proof-of-concept rather than a validated clinical test. The GTS group plans to expand longitudinal sampling across diverse sporadic cohorts to determine whether platelet RNA signatures can predict cognitive decline or serve as pharmacodynamic markers in forthcoming disease-modifying trials.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by staff.

About this Neuroscience Research:

• Media Contact: Tamara Gutiérrez
• Source: IGTP (Germans Trias i Pujol Research Institute)
• Image Credit: Image credited to Neuroscience News
• Original Research (Open Access): Movement Disorders (Oct 1, 2026). Title: “Severe Parkinson’s Disease Linked to SNCA Locus Triplication Is Associated with Expression Changes in Platelets: A Case Report.” Authors: Susanna Jiménez-Román MSc, David Adamuz MSc, Jorge Mena PhD, Abril Tuset BSc, Mar Mallo PhD, Alex Menendez MD, Daniela Samaniego MD, Lourdes Ispierto MD, PhD, Dolores Vilas MD, PhD, Pau Pastor MD, PhD, Katrin Beyer PhD.
• DOI: 10.1002/mds.70529

Abstract

Severe Parkinson’s Disease Linked to SNCA Locus Triplication Is Associated with Expression Changes in Platelets: A Case Report

Parkinson’s disease is defined by alpha-synuclein aggregation, dopaminergic neuron loss, and chronic neuroinflammation. Growing evidence also points to systemic immune dysregulation. Platelets have emerged as a relevant peripheral model because they share many functional and molecular features with neurons, making platelet transcriptomics a promising avenue for discovering progression biomarkers in Parkinson’s disease.

The post Overlooked Blood Cell Could Reveal Parkinson’s Brain Changes first appeared on Anksiyete.

A major new study published in Science by researchers at Children’s National Hospital and Seattle Children’s challenges the long-held belief that premature birth simply delays brain growth that later “catches up.” By combining multi-year neuroimaging of 176 living infants with high-resolution spatial transcriptomics from 83 postmortem human cerebellar specimens, the investigators found that preterm birth fundamentally changes the molecular programs guiding Purkinje and granule cell development. On average, each additional week an infant spent developing outside the womb before full term was associated with a loss of about 230 cubic millimeters of cerebellar volume, a deficit that correlated with measurable delays in motor, cognitive, and language milestones between 9 and 36 months of age.

Key Facts:

• Volumetric loss tied to gestational age: Every week of development outside the uterus before term corresponded to an average reduction of roughly 230 cubic millimeters in cerebellar volume.
• Not just slower growth: The evidence indicates that premature birth does not simply slow down a normal developmental program. Instead, forced extrauterine maturation redirects molecular pathways that shape Purkinje and granule cell wiring.
• Predictive of functional outcomes: Reduced cerebellar volume observed in preterm infants strongly predicted later deficits in motor coordination, expressive language, and executive cognitive skills assessed between 9 and 36 months.

Source: Children’s National Hospital / Seattle Children’s

Between 24 and 40 weeks of human gestation, the cerebellum undergoes a dramatic period of growth and circuit refinement. During the third trimester its volume increases roughly fivefold as millions of granule neurons migrate and form complex dendritic trees around large Purkinje cells. These events establish the sensorimotor, language, and cognitive circuits essential for later development. In a full-term pregnancy this sensitive period unfolds within the biochemical stability of the amniotic environment.

When birth occurs prematurely, that same critical period of neurogenesis and synaptic organization must proceed outside the womb, exposed to the sensory stimuli, physiological stressors, and clinical interventions characteristic of the neonatal intensive care unit (NICU).

For years, clinicians observed that many children born preterm experience long-term challenges with balance, fine motor skills, language acquisition, and higher-order learning—even when standard imaging shows no focal hemorrhage or overt structural injury. The prevailing clinical assumption was that prematurity mainly slows development and that children eventually “catch up.” This new study provides a different, causally informed explanation: preterm birth displaces the intrinsic timing and molecular programs that normally coordinate cerebellar assembly.

Connecting spatial transcriptomics with longitudinal clinical data

Led by co-first authors Georgios Sanidas, MD, and Gabriele Simonti, the research team integrated longitudinal patient follow-up with cutting-edge spatial molecular profiling. They tracked 176 preterm infants over several years, performing repeated neuroimaging and standardized developmental assessments at 9, 18, 24, and 36 months. In parallel, they analyzed spatial transcriptomic and histopathological data from 83 postmortem infant cerebella, spanning preterm and full-term specimens sourced from national tissue repositories.

Spatial transcriptomics allowed the investigators to map gene expression precisely within the intact tissue architecture, revealing how molecular programs are organized across cerebellar layers. This approach highlighted lineage-specific alterations: granule cells showed incomplete maturation, while Purkinje cells exhibited impaired structural refinement when development occurred extrauterinely. Rather than a simple delay, these changes reflect a shift into alternative maturation states driven by premature exposure to the extrauterine environment.

“We could see the developmental differences in preterm children clinically, but the cellular mechanisms were elusive,” said Panagiotis Kratimenos, MD, PhD. “By combining living-patient imaging with human tissue transcriptomics, we can now trace how molecular programs set at the time of birth map onto long-term developmental outcomes.”

Measuring the cerebellar volume deficit and its consequences

The neuroimaging data reflected the transcriptomic findings. Each week that a baby spent developing outside the uterus prior to term was associated with an estimated 230 cubic millimeters less total cerebellar volume. These volumetric deficits were significantly associated with poorer performance in gross and fine motor tasks, expressive and receptive language, and executive cognitive measures during toddlerhood (9–36 months).

Importantly, while gestational age at birth established the primary developmental trajectory, the study found that postnatal exposures in the NICU—such as physiological stress, systemic illness, and specific care practices—further influenced cerebellar growth. This suggests that both timing of birth and the neonatal clinical environment shape cerebellar maturation.

“Studying human tissue alongside longitudinal clinical data allowed us to link molecular programs to functional outcomes years later,” explained Dr. Sanidas. Co-first author Gabriele Simonti added that decoding these human-specific mechanisms makes it possible to develop interventions targeted to the actual biological state of the premature brain.

Implications for precision neonatal care

The demonstration that the premature cerebellum follows a distinct molecular schedule has immediate implications for neonatal care. Assessment and treatment strategies should prioritize developmental maturity rather than relying solely on chronological age. Identified molecular markers can improve risk stratification, serve as biomarkers of cerebellar maturity, and guide the timing of neuroprotective therapies.

“With this human cellular map, we can design and time neuroprotective strategies to match the biological state of a baby’s brain cells,” said Dr. Kratimenos. Supported by the Raynor Cerebellum Project Foundation, the research team is now testing neuroprotective compounds and optimized clinical protocols aimed at protecting Purkinje and granule cell networks during vulnerable windows in the NICU, with the goal of preserving cerebellar volume and improving lifelong outcomes for preterm infants.

Funding: This study was supported by the Raynor Cerebellum Project Foundation.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• The journal paper was reviewed in full.
• Additional context was added by staff.

About this neurodevelopmental research:

• Media Contact: Anita Kelly
• Source: Children’s National Hospital
• Image Credit: Image credited to Neuroscience News
• Original Research (Open Access): Science (Oct 1, 2026). Title: “Intrinsic gestational timing governs human cerebellar development after preterm birth.” Authors include Georgios Sanidas, Gabriele Simonti, Vittorio Gallo, Panagiotis Kratimenos, and colleagues.
• DOI: 10.1126/science.aeb9095

Abstract

Intrinsic gestational timing governs human cerebellar development after preterm birth

Intrinsic developmental programs guide brain maturation, but which of these programs prematurity perturbs and through which molecular pathways remained unclear. The human cerebellum provides a clear example of extrauterine disruption, since its rapid growth and circuit formation peak during the third trimester—a period frequently interrupted by preterm delivery. Integrating in vivo neuroimaging and longitudinal neurodevelopmental outcomes with postmortem spatial transcriptomics and histopathology, the study demonstrates that prematurity diverts cerebellar developmental trajectories.

Cerebellar growth and later functional outcomes scaled with gestational age, even after accounting for perinatal exposures. Spatially resolved analyses revealed incomplete granule cell maturation and impaired Purkinje cell structural refinement—evidence of lineage-specific asynchrony. In effect, prematurity creates biologically displaced maturation: infants with the same postmenstrual age may occupy distinct cellular and molecular developmental states.

The post Premature Birth Disrupts Cerebellar Wiring and Brain Development first appeared on Anksiyete.

Researchers at the University of Eastern Finland (UEF) have identified the sodium-dependent multivitamin transporter (SMVT) as a viable pathway to deliver creatine derivatives across the blood-brain barrier (BBB).

Published in ACS Chemical Neuroscience, the study demonstrates an alternative method for restoring cerebral energy metabolism in Creatine Transporter Deficiency Syndrome (CTDS), a serious genetic disorder in which the native creatine transporter is nonfunctional. By exploiting the brain’s own nutrient-uptake systems rather than disrupting vascular defenses, this strategy offers a promising platform to transport a range of therapeutics into the central nervous system (CNS).

Key Facts:

• Alternative Gateway Identified: The sodium-dependent multivitamin transporter (SMVT), which normally mediates uptake of water-soluble vitamins, can recognize and transport chemically modified creatine derivatives across the blood-brain barrier.
• Overcoming Genetic Transport Blocks: This approach addresses Creatine Transporter Deficiency Syndrome (CTDS), an X-linked metabolic disorder caused by mutations in the SLC6A8 gene that render the primary creatine transporter inactive and leave the brain chronically low in creatine.
• Broad CNS Drug Delivery Platform: Leveraging SMVT’s native carrier mechanisms provides a modular chemical framework to improve the brain availability of neurotherapeutics that otherwise cannot cross brain capillary endothelial cells.

Source: University of Eastern Finland

The blood-brain barrier is the central nervous system’s most selective gatekeeper. Built from tightly joined capillary endothelial cells and supported by astrocytic end-feet, it protects neural tissue from toxins and systemic fluctuations but also excludes most drugs—roughly 98% of small molecules and nearly all biologics—from entering the brain.

Instead of attempting to breach this delicate barrier, which raises the risk of inflammation and systemic side effects, neuroscientists have been developing targeted “Trojan horse” approaches: chemically modifying therapeutic compounds so they can be carried across the BBB by endogenous nutrient transporters.

In the reported study, investigators in UEF’s School of Pharmacy tested whether SMVT could act as such a carrier, successfully demonstrating that engineered creatine prodrugs are taken up by SMVT and transported across cerebral microvessels.

Rescuing Brain Bioenergetics in CTDS

Creatine is central to rapid cellular energy transfer, buffering ATP production through the creatine kinase circuit. Because the brain’s own creatine synthesis is limited, neural tissue depends on circulating creatine imported by dedicated membrane transporters.

In Creatine Transporter Deficiency Syndrome (CTDS), caused by loss-of-function mutations in the SLC6A8 gene that encodes the CRT1 transporter, the primary route for cerebral creatine uptake is blocked. Affected individuals exhibit profound brain creatine deficiency and severe neurodevelopmental symptoms, including intellectual disability, speech impairment, early-onset epilepsy, and autistic-like traits. Oral creatine supplements are ineffective for CTDS because creatine cannot cross the BBB without a functioning CRT1.

To bypass this obstacle, the UEF team evaluated whether SMVT—a solute carrier that normally transports vitamins such as biotin and pantothenic acid—could recognize synthetic creatine conjugates and mediate their uptake into the brain.

Through a combination of in silico analyses, in vitro transport assays, and molecular studies conducted during doctoral projects by Adéla Králová and Ville Kuorikoski, the group designed creatine prodrugs that mimic SMVT substrates. They confirmed SMVT-mediated recognition and transport of these derivatives in cultured cells, demonstrating that the brain’s multivitamin transporter can act as a secondary uptake route when native creatine transport is impaired.

Turning the Barrier Into a Carrier

The implications of this work extend well beyond treating CTDS. SMVT is stably expressed along human brain capillary endothelium, which means conjugating neuroactive molecules to SMVT-recognized chemical motifs could consistently improve brain penetration for many therapeutic classes, from neuroprotective agents to anticonvulsants.

Associate Professor Kristiina Huttunen, who led the team, summarizes the significance: SMVT is not only a nutrient channel but also a practical gateway for drug delivery into the brain. Rather than attempting to overcome or disrupt the BBB, using its own transport systems provides a safer and potentially more effective route to deliver therapies to neural tissue.

Supported by a Proof of Concept award from the Jane and Aatos Erkko Foundation, the researchers are advancing their most promising synthesized derivatives into preclinical pharmacokinetic studies to confirm sustained brain uptake and functional restoration of ATP levels in vivo.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by staff.

About this Neuroscience Research:

• Media Contact: Kristiina Huttunen
• Source: University of Eastern Finland
• Image Credit: Image credited to Neuroscience News
• Original Research (Open Access): ACS Chemical Neuroscience (Oct 1, 2026). Title: “Sodium-Dependent Multivitamin Transporter Facilitates Brain and Neuronal Uptake of a Creatine Analogue.” Authors: Adéla Králová, Ville Kuorikoski, Landry Anamea, Janne Tampio, Arun Kumar Tonduru, Hengjing Cui, Henri Leinonen, Jaana Rysä, Antti Poso, Tetsuya Terasaki, Aaro Jalkanen, Thales Kronenberger, and Kristiina M. Huttunen.
• DOI: 10.1021/acschemneuro.6c00484

Abstract

Sodium-Dependent Multivitamin Transporter Facilitates Brain and Neuronal Uptake of a Creatine Analogue

Creatine transporter 1 (CRT1, SLC6A8) is essential for transporting creatine across the blood–brain barrier into neurons and glia. Loss-of-function mutations in CRT1 cause creatine transporter deficiency syndrome (CTDS), a severe X-linked neurological condition lacking effective therapies.

To identify alternative routes for creatine delivery, this study deployed a carrier-mediated strategy targeting the sodium-dependent multivitamin transporter (SMVT) as a potential neuronal uptake pathway. SMVT was characterized using in silico modeling and in vitro assays to reveal substrate-binding residues and functional activity in human glioblastoma (U-87MG) and mouse neuronal cells.

Four novel creatine derivatives designed to engage SMVT were synthesized and tested in vitro. The lead compound, COMP 1, displayed SMVT-mediated uptake at concentrations below 100 μM and was taken up by both human glioblastoma cells and mouse neurons. In vivo studies showed COMP 1 accumulation in mouse brain tissue, and biochemical assays indicated interactions with the creatine kinase system relevant to ATP/ADP dynamics. Molecular dynamics simulations supported the proposed transporter–substrate interactions.

Together, these results identify SMVT as a promising route for brain uptake of creatine analogues and justify further evaluation of SMVT-targeted derivatives in animal models of CTDS and other conditions where enhanced brain delivery is needed.

The post New Transporter Crosses Blood-Brain Barrier to Deliver Creatine first appeared on Anksiyete.

A 25-year epidemiological study of more than 500,000 adults in the United Kingdom, published in Neurology, links residential proximity to industrial sites reporting water pollution with a higher risk of developing progressive supranuclear palsy (PSP). Conducted by researchers at Harvard Medical School, the study found that living within about three miles of facilities that discharge pesticides, inorganic pollutants, organic compounds, or heavy metals was associated with up to a 66% greater likelihood of developing this rare and rapidly progressive neurodegenerative movement disorder. The elevated risk declined steadily as residential distance from polluting facilities increased.

Key Facts:

• 66% Increased Risk Near Pesticide Discharges: Residents living within roughly three miles of facilities releasing agricultural pesticides such as atrazine, simazine, and diuron had a 66% higher chance of developing PSP compared with those living farther away.
• Distance-Related Pattern: The study observed a dose-response relationship: risk diminished with increasing distance from polluting sites, and longer cumulative residence near such facilities correlated with higher risk.
• Multiple Pollutant Classes Implicated: Statistically significant increases in PSP incidence were also observed near sites emitting inorganic pollutants (about 60%), organic compounds such as benzene and toluene (about 52%), and heavy metals including lead, cadmium, and mercury (about 38%).

Source: American Academy of Neurology / Harvard Medical School

Progressive supranuclear palsy (PSP) is a rare, severe neurodegenerative disorder in the family of atypical parkinsonian syndromes. Although PSP shares motor symptoms with Parkinson’s disease—such as rigidity, slowness, and balance problems—it typically progresses faster and is marked by early falls, vertical gaze palsy, cognitive decline in executive function, and poor response to dopaminergic therapies.

Pathologically, PSP is characterized by abnormal accumulations of four-repeat (4R) tau protein in basal ganglia and brainstem circuits. While the biological mechanisms that trigger tau pathology remain uncertain, environmental exposures have long been suspected as possible contributors.

The new population-based longitudinal study, published October 28, 2026, in Neurology (the journal of the American Academy of Neurology), provides epidemiological evidence linking ambient industrial water contamination to the development of PSP.

Led by Charlie Weige Zhao, MD, of Harvard Medical School and Massachusetts General Hospital, the research team followed a prospective cohort of over 500,000 UK adults for 25 years to evaluate associations between residential proximity to regulated industrial dischargers and subsequent PSP diagnosis.

Mapping Industrial Proximity Across 25 Years

During the 25-year follow-up, 221 participants developed clinically confirmed PSP. For each case, investigators matched ten control participants by age and sex. Using baseline residential addresses recorded in 2007, they geocoded how close participants lived to industrial sites that officially reported water pollutant emissions, including wastewater treatment facilities, intensive aquaculture operations, chemical plants, and thermal power stations.

The team categorized emissions into six classes: heavy metals, chlorinated solvents, persistent organic pollutants, agricultural pesticides, other organic pollutants, and other inorganic compounds. Individuals who had lived at their recorded address for less than one year were excluded to reduce exposure misclassification.

Spatial analysis showed that roughly one-third of those who developed PSP lived within three miles of an industrial polluting facility, compared with about one-quarter of matched controls.

Pollutant Breakdown: Pesticides and Heavy Metals

After adjusting for age, sex, and socioeconomic and educational factors, residential proximity to certain effluent categories demonstrated distinct associations with PSP risk:

• Agricultural Pesticides: Living within three miles of sites discharging pesticides—including atrazine, simazine, and diuron—was associated with a 66% higher risk of PSP.
• Inorganic Pollutants: Residence near facilities releasing inorganic compounds, such as fluorides, phosphorus, and nitrogen derivatives, was linked to a roughly 60% increased risk.
• Organic Compounds: Proximity to dischargers of volatile and semi-volatile organics, including benzene, ethylbenzene, and toluene, correlated with about a 52% higher risk.
• Heavy Metals: Living near sites that released heavy metals—such as cadmium, lead, and mercury—was associated with an approximate 38% increase in risk.

The investigators did not find statistically significant associations between PSP and residential proximity to facilities reporting chlorinated solvents or persistent organic pollutants in this analysis.

“These results suggest that environmental water pollutants may play a role in the development of progressive supranuclear palsy,” said Dr. Zhao. “Further research is needed to confirm these findings and to clarify specific mechanisms, but this study is a step forward in identifying environmental factors that may raise PSP risk.”

Distance-Decay Effects and Toxicological Considerations

A notable distance-decay effect emerged: the association between industrial proximity and PSP weakened as distance from polluting sites increased, with most associations tapering off beyond roughly six miles. The total duration of residence within these industrial radii also influenced risk, suggesting cumulative exposure matters.

Dr. Zhao underscored that PSP remains an extremely rare condition—affecting on the order of 5 to 6 people per 100,000—so absolute lifetime risk for any individual remains low, even for those living near industrial facilities.

The authors acknowledge limitations: the study establishes statistical associations but cannot prove biological causation. Detailed occupational exposure histories were not available, limiting the ability to account for workplace-related chemical exposures. Moreover, many industrial sites release complex mixtures of chemicals, making it difficult to isolate the contribution of individual compounds to disease risk.

Nonetheless, these findings support further toxicological research into how industrial contaminants may cross the blood-brain barrier and trigger tauopathies, and they reinforce the public health importance of clean water infrastructure and strong environmental regulation.

Funding: The study was supported by the Dolce Family Fund for PSP research at Massachusetts General Hospital.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• The full journal paper will be reviewed upon publication.
• Additional contextual information was provided by editorial staff.

About this PSP and neurology Research:

• Media Contact: Natalie Conrad
• Source: AAN
• Image Credit: Image credited to Neuroscience News
• Original Research: Findings reported in Neurology

The post Study Links Industrial Water Pollution to Higher PSP Risk first appeared on Anksiyete.

A cognitive psychology study explored how people use explicit reliability information when deciding which sources to trust. The experiments, funded by the Economic and Social Research Council (ESRC), show that while participants tended to favor sources labeled as more credible, they could not fully ignore inputs explicitly marked as no better than chance. Information tagged with a 50% chance of being correct—a value that mathematically carries no diagnostic weight—nonetheless influenced decisions. Metacognitive ratings revealed that participants were partly aware that unreliable inputs affected their choices, but that awareness did not prevent those inputs from biasing outcomes.

Key Facts:

• Persistent bias from zero-value data: Inputs explicitly labeled as 50% likely to be correct—i.e., equivalent to random chance and therefore uninformative—still swayed participants toward the content of those inputs.
• Imperfect reliability weighting: Participants generally gave greater weight to sources marked as reliable, yet their integration of those reliability metrics deviated from the optimal probabilistic calculations researchers would expect.
• Metacognitive awareness: When asked to evaluate the influence of each source, participants reported that unreliable sources had affected their judgments, indicating a gap between awareness and the ability to exclude unwanted information.

Source: Neuroscience News / ESRC Research Project

In modern digital environments, people make hundreds of judgments daily based on a mix of social feeds, algorithmic news, user reviews, and direct messages—each carrying widely varying reliability. To help users, platforms increasingly add quantitative signals such as credibility scores, verified badges, and star ratings to indicate source trustworthiness.

This raises a central cognitive question: when a source’s reliability is presented as an explicit probability, do people use that number appropriately to form objective judgments?

A set of behavioral and metacognitive experiments addressing how explicit reliability information is combined shows a clear limitation: people struggle to exclude dubious inputs, even when those inputs are explicitly labeled as uninformative. In practice, data marked as equivalent to a coin flip still biased participants’ decisions.

The cognitive friction of multi-source integration

In the main experimental task, participants had to combine predictions from several independent sources to choose between two alternatives. Each source came with an explicit numerical reliability score that indicated the stated probability its claim was correct.

Behavioral outcomes made two patterns clear:

• Proportional weighting: Participants were able to distinguish sources and generally weighted higher-scoring sources more heavily, showing an intuitive sensitivity to reliability labels.
• Calibration failures: Despite that sensitivity, people did not treat the stated probabilities as exact mathematical inputs. Their aggregation of evidence departed systematically from optimal Bayesian updating.
• The 50% problem: Most strikingly, information tagged as 50% accurate—mathematically neutral and diagnostically meaningless—was not treated as neutral. Instead, it shifted choices in the direction of its content.

Rather than converting entirely to neutral background noise, such uninformative inputs seem to be processed at a semantic level, leaving a residual effect on the decision process that explicit probability markers fail to eliminate.

Recognizing the bias: metacognitive gaps

To determine whether participants noticed this contamination, researchers conducted follow-up tests of metacognitive awareness. After making decisions, participants rated how much each source had influenced their final choice.

Results showed a nuanced split: people were consciously aware, to some extent, that low-credibility inputs had affected their judgments. Yet this awareness did not translate into cognitive control sufficient to isolate or neutralize those inputs during decision making.

In short, participants both recognized and struggled to prevent the unwanted influence of unreliable evidence—an important dissociation between monitoring and control in everyday information processing.

System design and the limits of fact-checking

These findings have practical implications for platform designers, content moderators, and public communicators. Labeling claims with “low credibility” or presenting numerical reliability indicators may not be enough to stop unreliable content from shaping beliefs and choices, because once content is read it can leave an imprint that numerical tags alone do not remove.

Designers should therefore consider how credibility signals are presented and combined with other interface strategies, media literacy training, and moderation practices that reduce the initial impact of uninformative content. Understanding how people misinterpret, partially internalize, and fail to fully disregard explicit reliability metrics is crucial for developing better tools to limit misinformation.

Funding: This work was supported by ESRC grant ES/V00378X/1 awarded to Lucie Charles and Patrick Haggard.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by staff.

About this psychology Research:

• Media Contact: YAMASHINA Naoko
• Source: University of Tsukuba
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: PLOS Computational Biology (Oct 1, 2026). “How does explicit reliability guide choices? Effect of trustworthiness on choice and metacognition.” Authors: Keiji Ota, Anthony Ciston, Patrick Haggard, Thibault Gajdos-Preuss, and Lucie Charles.
• DOI: 10.1371/journal.pcbi.1014818

Abstract

How does explicit reliability guide choices? Effect of trustworthiness on choice and metacognition

Integrating information from multiple sources with varying reliability is a central challenge in contemporary information environments. Despite the widespread use of explicit probabilistic indicators of source accuracy, we know little about how such markers are used in decision-making.

This research introduced a task in which participants viewed predictions from sources with explicit, stated reliability values to choose between two options. After each decision, participants reported how much each source had influenced their choice. Computational modeling estimated the effective reliability participants assigned to each source.

Findings indicate that people do not accept stated reliability values at face value. Participants systematically distorted the provided probabilities when combining evidence, and even sources explicitly labeled as unreliable biased choices as if they held moderate credibility. Furthermore, the presence of sources known to predict incorrect answers degraded performance by introducing leakiness into the evidence accumulation process.

Despite these distortions, participants retained some metacognitive insight: they could identify and report the influence of unreliable sources on their decisions. Overall, the results show a divergence between how people consciously perceive the role of reliability markers and how those markers are actually integrated into choice—a gap with direct implications for platform design, fact-checking, and media literacy initiatives.

The post Noisy Labels Still Bias AI and ML Decisions first appeared on Anksiyete.

A molecular neurobiology study from King’s College London’s Institute of Psychiatry, Psychology & Neuroscience (IoPPN) uncovers a cellular explanation for why females consistently prefer warmer environments than males. The research, published in The Journal of Physiology, shows that two thermosensitive ion channels in peripheral sensory nerves—TRPM2 (warm-sensitive) and TRPM8 (cold-sensitive)—are tuned to activate at higher temperatures in females. This shift in channel activation thresholds explains a conserved difference in thermal preference across species and reveals that circulating testosterone helps set baseline thermosensitivity.

Key Facts:

• Higher activation thresholds in females: In mice, the warmth sensor TRPM2 and the cool sensor TRPM8 become active at warmer temperatures in females than in males, making temperatures that feel comfortably warm to females feel relatively hotter to males.
• Testosterone modulates preference: Lowering testosterone in males shifts their temperature preference toward the warmer range typical of females, while administering testosterone to females increases heat aversion. Estrogen and progesterone produced no measurable effect on these sensory channels.
• Sensory mechanism, not core temperature: Core body temperature and paw skin temperature were the same in males and females, indicating the sex difference arises from peripheral sensory detection rather than metabolic or insulating differences.

Source: King’s College London

The familiar thermostat debate—where women often prefer ambient temperatures near 25°C (77°F) and men prefer cooler rooms near 22°C (71.6°F)—is not purely cultural. Across many mammal species and in birds, females consistently select warmer environments than males. Until now, the molecular sensors that drive these sex-specific thermal preferences were not clearly identified.

Researchers at the Wolfson Sensory, Pain and Regeneration Centre, IoPPN, conducted a series of behavioral, pharmacological and genetic experiments to identify the underlying cellular mechanism. Their work points to two transient receptor potential (TRP) ion channels in sensory nerve endings that differ in activation range between sexes.

Thermosensation in a Two-Plate Choice Test

To measure thermal preference under controlled conditions, mice explored two adjacent metal plates with independently regulated surface temperatures. One plate stayed at a neutral baseline of 33°C while the other plate was adjusted across a range of temperatures.

Female mice showed a clear preference for warmer surfaces, spending more time on plates at 36°C and even 38°C. Male mice, by contrast, avoided the hotter plates and spent more time on cooler surfaces near 32°C.

The team examined two TRP ion channels that mediate non-painful temperature sensation:

• TRPM2: the principal neural sensor for gentle warmth.
• TRPM8: the main sensor for cool and innocuous cold.

Using selective genetic knockouts and pharmacological blockers, the researchers demonstrated causality: deleting TRPM2 made males choose warmer plates, while blocking or deleting TRPM8 caused females to prefer cooler plates. Parallel results from both genetic deletion and drug inhibition confirmed that behavioral differences are driven by these peripheral ion channels.

“We found that the activation ranges of TRPM2 and TRPM8 are shifted toward warmer temperatures in females, and this shift changes how males and females sense and react to environmental temperature,” said Peter McNaughton, Professor of Pharmacology at the Wolfson Centre. While the study was performed in mice, humans express the same types of ion channels and show similar sex differences in temperature preference, suggesting the mechanism may be conserved.

Role of Sex Hormones

To determine whether hormones or core temperature explain the sex difference, investigators measured body and paw temperatures with rectal thermometry and infrared imaging. Both measures were equivalent between sexes, ruling out metabolic or insulation-based explanations.

Endocrine manipulations did, however, alter preference. Removing testosterone from males pushed their choices toward the warmer range typical of females, while giving testosterone to females increased their avoidance of heat. Manipulating estrogen or progesterone did not change thermal selection. Testosterone account for a significant portion of the sex difference but did not fully explain the baseline gap, indicating additional factors may contribute.

Open Questions and Clinical Implications

Because the genetic deletions removed TRPM2 and TRPM8 systemically, it remains unclear whether the sex-specific tuning originates solely in peripheral sensory terminals in the skin or also involves spinal or hypothalamic circuits. When sensory neurons were isolated and cultured, the sex-specific activation differences disappeared, suggesting that local tissue environment or intact physiological signaling is required to maintain channel tuning.

Future work will target localized genetic knockdown in peripheral nerve endings to test whether site-specific tuning changes behavior. Because TRPM2 and TRPM8 are conserved in humans and implicated in conditions such as neuropathic pain, fibromyalgia, and thermal hyperalgesia, understanding their sex-specific operation could shed light on why certain chronic pain syndromes are more common in women.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by staff.

About this neuroscience Research:

• Media Contact: Francesca Greenstreet
• Source: King’s College London
• Image Credit: Image credited to Neuroscience News
• Original Research: Journal of Physiology (Oct 1, 2026). “TRPM8 and TRPM2 ion channels determine sex differences in thermal preference in mice.” Authors: Bruno Vilar, Peter A. McNaughton.
• DOI: 10.1113/JP288076

Abstract

TRPM8 and TRPM2 ion channels determine sex differences in thermal preference in mice

Several ion channels in the TRP family respond to temperature increases or decreases, but which channels set non-noxious thermal sensation from about 20°C to 40°C has been unclear. This study shows that below 33°C male cool preference depends on TRPM8, while warm preference is mainly influenced by TRPM2. Female thermal preference is shifted roughly 4°C warmer than males, matching shifts in the activation ranges of both TRPM8 and TRPM2. Removing testosterone shifts male preference toward the female pattern, and giving testosterone to females shifts their preference toward the male pattern. Manipulating female hormones produced no effect. The findings indicate that TRPM8 and TRPM2 are primary detectors in the non-noxious thermal range and that testosterone partly determines sex differences in thermal preference.

The post Why Women Prefer Warmer Indoor Temperatures first appeared on Anksiyete.

A large psychological survey of 15,049 adults in the UK, published in PLOS One, found that nearly 70% of respondents remember hugs for their comforting and supportive emotional qualities. Researchers at the University of Bristol identified several psychological traits that predict whether an embrace will leave a lasting positive memory: higher cognitive and emotional empathy, greater bodily awareness, and anxious attachment increased the likelihood of remembering hugs as meaningful, while avoidant independence and a dislike of touch reduced that emotional recall.

Key Facts:

• Lasting Emotional Salience: About 69.5% of the 15,049 participants reported recalling hugs for their positive emotional impact, describing them as moments of comfort, validation, or safety.
• Psychological Predictors: Stronger emotional and cognitive empathy, heightened body perception, and frequent greeting hugs predicted a greater likelihood of remembering hugs for their emotional value.
• Attachment and Independence: People scoring high on relationship independence (an avoidant attachment style) were less likely to retain emotionally positive memories of hugs; those with higher separation anxiety (anxious attachment) placed greater emotional value on embraces.

Source: University of Bristol / PLOS

Hugging is one of the most universal forms of nonverbal human communication. As a gentle form of social touch, embraces activate C-tactile nerve fibers, can reduce physiological stress responses, lower heart rate, and promote oxytocin release.

Despite these typical benefits, people experience interpersonal touch very differently: for some a hug is deeply comforting, while for others it may feel awkward or unwelcome. Until now, empirical evidence has been limited on which individual psychological characteristics determine whether an embrace will form a vivid, emotionally positive memory.

In research published on October 28, 2026, in PLOS One, Anna Lena Dueren and colleagues at the University of Bristol examined the traits and perceptual factors that shape autobiographical memories of social touch.

Assessing Touch Across 15,000 Individuals

To capture emotional responses to physical contact on a large scale, the team recruited 15,049 healthy adults across the UK via public broadcasting and national media. Participants completed a detailed psychometric battery assessing hugging frequency, somatic body awareness, attachment behaviors, trait empathy, and written recollections of memorable embraces.

Overall results supported the comforting role of interpersonal touch: almost seven in ten participants recalled hugs primarily for their emotional benefits—solace, validation, and safety. However, the data also revealed systematic differences tied to stable psychological characteristics.

• Empathy: Higher cognitive empathy (understanding another’s perspective) and affective empathy (sharing another’s feelings) predicted a greater likelihood of remembering hugs as emotionally meaningful.
• Body Perception: Elevated scores on standardized body-perception measures—reflecting stronger conscious integration of bodily sensations and cutaneous touch—were associated with more positive hug memories.
• Habitual Practice: Social habits mattered: those who commonly greet friends and family with embraces were more likely to retain positive memories, while people uncertain about hugging or who showed touch aversion reported fewer emotionally comforting recollections.

Attachment Styles: Seeking Connection vs. Self-Reliance

Attachment orientation emerged as a robust predictor of how hugs are remembered. Individuals high in relational independence—typical of avoidant attachment, marked by emotional self-reliance and interpersonal distance—were less likely to report hugs as emotionally rewarding.

Conversely, participants scoring higher in separation anxiety—reflecting worries about emotional distance and a desire for reassurance—consistently described hugs as salient, supportive, and emotionally grounding experiences.

The authors suggest that these differences help explain why the same physical act can be perceived very differently by different people. They recommend further work to explore how personality, earlier life experiences, and the context surrounding a hug influence its emotional meaning and whether interventions can increase the comforting value of social touch for those who find it challenging.

Methodological Context and the Science of Touch

The researchers caution that the sample was comprised of about 75% women and reflects attitudes within a Western cultural context; touch norms and interpersonal distance vary across societies. The cross-sectional design highlights correlations but does not establish causal links between personality traits and the neural consolidation of touch memories.

Nonetheless, the study connects social psychology with tactile neurobiology, showing that memories of hugs depend not only on the physical qualities of an embrace but also on individual differences in empathy, attachment, and bodily self-awareness.

Funding: MJB was supported by the ESRC [ES/R007527/1] and Leverhulme Trust [RF-2025-350]. The Touch Test was commissioned by the Wellcome Collection. AF’s work was supported by a European Research Council Consolidator Award [ERC-2018-COG-818070] and by the European Union’s Horizon 2020 programme (Consolidator grant agreement No 818070 for project METABODY). No additional external funding was received for this study.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• The journal paper was reviewed in full.
• Additional context was added by our staff.

About this social neuroscience Research:

• Media Contact: Hanna Abdallah
• Source: PLOS
• Image Credit: Image credited to Neuroscience News
• Original Research (Open Access): PLOS One (Oct 1, 2026). “Why we hug: Individual differences predict emotional touch memories.” Authors: Anna Lena Dueren, Paul M. Jenkinson, Aikaterini Vafeiadou, Athanasios Koukoutsakis, Claudia Hammond, Natalie C. Bowling, Aikaterini Fotopoulou, and Michael J. Banissy.
• DOI: 10.1371/journal.pone.0359868

Abstract

Why we hug: Individual differences predict emotional touch memories

Hugging is a widespread form of social touch, but little is known about how individual differences influence the way these experiences are remembered. In a large-scale survey (N = 15,049), the researchers examined whether traits such as empathy, body perception, and attachment orientation predict the likelihood of recalling a hug for its positive emotional impact and the reasons for that memory.

Participants were recruited through promotion on public broadcasting programs and other media outlets. Overall, 69.5% of participants reported recalling a hug for its positive emotional impact. Regression analyses showed that higher empathy, increased body perception, and attachment-related anxiety were associated with a greater likelihood of such recall, while attachment-related avoidance was associated with a lower likelihood. Men were more likely than women to report physically arousing hugs as the most memorable.

These results indicate that hugs are predominantly remembered because they convey comfort, support, and understanding, and that individual differences in personality and bodily awareness shape autobiographical memories of hugging.

The post Why Some People Seek Hugs While Others Avoid Touch first appeared on Anksiyete.