bims-ripira 2026-05-17 papers

bims-ripira

Biomed News

on RRM2B MDMD in Adults

Issue of 2026–05–17
thirteen papers selected by
Martín Lopo

Mitochondria and Qi: Merging Eastern and Western Medicine.
170 Years of Mitochondrial Research and the Emergence of Mitochondrial Medicine.
Modulation of mitochondrial DNA copy number: therapeutic potential of phytochemicals and plant extracts-a comprehensive review.
Quantitative proteomic profiling of neural cells-specific metabolic reprogramming in response to mitochondrial dysfunction using iMPAQT2.
Therapeutic Impact of Mitochondrial Transplants for Cardiovascular Diseases.
The role of choline in neurodevelopment.
Understanding Dysfunctional Autophagy and Mitophagy in Inflammatory Cardiovascular Disease.
The metabolic effects of post-sepsis feeding of meals with only essential amino acids.
Prospective Associations of Serum Vitamin B12, Homocysteine, and Ferritin Levels with Probable Sarcopenia.
Neutrophil-to-lymphocyte and neutrophil-to-platelet ratios for predicting 28-day mortality in sepsis: A retrospective cohort study.
Ergothioneine as a potential geroprotector: Targeting molecular hallmarks of ageing and age-related diseases.
Research progress on the biological function and molecular mechanism of GDF-15 in solid malignant tumors.
Beyond expectations: nocebo suggestion affects cognitive performance in older adults.

Pharmacol Res. 2026 May 11. pii: S1043-6618(26)00158-1. [Epub ahead of print] 108243

Mitochondria and Qi: Merging Eastern and Western Medicine.

Wanqing Xie, Deborah G Murdock, Douglas C Wallace.

  Since the discovery of mitochondrial DNA (mtDNA) diseases almost 40 years ago, large numbers of diseases have been linked to mutations in both mtDNA and nuclear DNA (nDNA) genes that perturb the mitochondrial energy-generating system, oxidative phosphorylation (OXPHOS). Mitochondrial dysfunction is being implicated not only in rare primary mitochondrial diseases but also a wide range of common diseases, yet the availability of effective mitochondrial therapies remains limited. One potential source of mitochondrial therapeutic approaches is Traditional Chinese Medicine (TCM). TCM emphasizes the health-preservation philosophy and practical experience centered around the concept of "Qi", or vital force, and has generated Qi-oriented therapies over the past several thousand years. We propose that various properties and functions attributed to Qi may be explained by modulation of mitochondrial bioenergetics, the interplay between OXPHOS and fatty acid oxidation versus glycolysis and the pentose phosphate pathway (PPP), and the mitochondrial regulation of the immune system through mitochondrial reactive oxygen species (mROS). Hence, TCM therapeutics may provide approaches for treating the increasing spectrum of mitochondria associated diseases.

Keywords:  Mitochondria; Qi; TCM; energy; mtDNA; therapy

DOI:  https://doi.org/10.1016/j.phrs.2026.108243
J Clin Pharmacol. 2026 May;66(5): e70209

170 Years of Mitochondrial Research and the Emergence of Mitochondrial Medicine.

Volkmar Weissig.

  One hundred and sixty-eight years lie between the first description of mitochondria as "pale roundish granules" and their eventual recognition as the "chief executive organelle" of the cell. Booming mitochondrial research during the last three decades has revealed that being the "powerhouse of the cell" is just one of many fundamental roles mitochondria play for cellular life. Mitochondria are at the crossroads of complex metabolic pathways; they regulate cellular signaling and innate immunity, and they determine whether a cell should divide, differentiate, or die. Human disorders caused by malfunctioning mitochondria have been described starting at the beginning of the 1960s, nowadays, it seems widely accepted that there are hardly any human diseases anymore that are not associated with dysfunctioning mitochondria. Even the process of aging seems to be controlled by this powerful organelle. This review is written for Pharmacologists, Physicians, and Healthcare Providers who are not familiar with mitochondrial biology and with the tremendous insights gained during the last three decades into the vital roles this cell organelle plays for life and death. It is aimed at raising awareness of still underappreciated mitochondrial diseases, which represent the largest group of inborn errors of metabolism.

Keywords:  aging; apoptosis; cellular signaling; drug development; energy metabolism; immunity; mitochondria; mitochondrial diseases

DOI:  https://doi.org/10.1002/jcph.70209
Arch Pharm Res. 2026 May 10.

Modulation of mitochondrial DNA copy number: therapeutic potential of phytochemicals and plant extracts-a comprehensive review.

Maria Rosaria Perri, Annamaria Cerantonio, Maria Grazia Cipriani, Ida Manna, Anna Aureli, Beatrice Marziani, Francesco Andreozzi, Gaia Chiara Mannino, Elettra Mancuso, Carolina Averta, Giancarlo Statti, Luigi Citrigno, Davide Mainieri.

  Mitochondrial DNA copy number (mtDNA-CN) is a critical marker of mitochondrial health and plays a key role in cellular bioenergetics. Alterations in mtDNA-CN have been associated with aging, metabolic disorders and neurodegenerative diseases. Recent studies have revealed that various plant-derived extracts, as well as the secondary metabolites they produce, known as phytochemicals, can modulate mtDNA-CN through mechanisms including the regulation of mitochondrial biogenesis, oxidative stress, and mtDNA repair. This review examines plant-derived extracts and phytochemical compounds from a wide range of plant species- including Ginkgo biloba, Crocus sativus, Curcumin and many others- able to modulate mtDNA dynamics, scavenging oxygen free radicals and improving antioxidant defense systems.

Keywords:  Mitochondria; Mitochondrial DNA copy number; Mitochondrial function; Phytochemicals; Plant extracts

DOI:  https://doi.org/10.1007/s12272-026-01620-1
Mitochondrion. 2026 May 14. pii: S1567-7249(26)00058-9. [Epub ahead of print] 102168

Quantitative proteomic profiling of neural cells-specific metabolic reprogramming in response to mitochondrial dysfunction using iMPAQT2.

Akito Tani, Mikako Yagi, Natsuki Horiuchi, Kento Nagata, Tomohiro Tanaka, Hiroki Kittaka, Ko Igami, Takeshi Uchiumi.

  Age-related mitochondrial dysfunction is increasingly recognized as a key contributor to neurodegenerative disease pathogenesis. In the central nervous system, neurons, oligodendrocytes, and astrocytes which derived from neural stem cells, fulfill distinct metabolic and functional roles. However, the specific vulnerabilities of these cell types to mitochondrial impairment remain unclear. In this study, we employed the iMPAQT2 proteomics platform to systematically compare the metabolic profiles of neurons, oligodendrocytes, and astrocytes, and to elucidate the molecular consequences of mitochondrial dysfunction induced by chloramphenicol and oligomycin. Our findings indicate that neurons and oligodendrocytes primarily rely on oxidative phosphorylation (OXPHOS) for ATP production, whereas astrocytes predominantly utilize glycolysis. It is noteworthy that oligodendrocytes exhibited enriched pathways for cholesterol synthesis, fatty acid degradation, and heme catabolism-processes that are critical for myelin maintenance. Treatment with the mitochondrial function inhibitors chloramphenicol or oligomycin reduced the expression of OXPHOS enzymes in all cell types. This reduction was particularly pronounced in oligodendrocytes for glycolysis, cholesterol synthesis, heme degradation, and fatty acid degradation. These results suggest that oligodendrocytes are particularly vulnerable to mitochondrial dysfunction, which may play a pivotal role in the pathogenesis of age-related neurodegenerative disorders.

Keywords:  Metabolic enzyme; Mitochondrial dysfunction; Neural cells; Proteomics; iMPAQT2

DOI:  https://doi.org/10.1016/j.mito.2026.102168
Int J Mol Sci. 2026 Apr 30. pii: 4018. [Epub ahead of print]27(9):

Therapeutic Impact of Mitochondrial Transplants for Cardiovascular Diseases.

Konstantina Antoniadou, Ioannis Shiammoutis, Christina Piperi.

  Mitochondria are vital organelles for human cells with fundamental roles in major metabolic processes such as calcium homeostasis, ATP production, apoptosis and signal transduction. Defective morphology and activity of these organelles have been tightly associated with the pathological onset of severe human disorders, including cardiovascular diseases. Targeting mitochondrial dysfunction has been an area of extensive research encompassing several approaches ranging from pharmacological agents to mitochondrial replacement techniques. Among them, mitochondrial transplantation has been a rapidly evolving approach, especially in the field of cardiovascular dysfunction for the restoration of injured or damaged myocardial cells. Various methods including tunneling nanotubes, nanoblade and "mitopunch" ensure the effective mitochondrial transfer from the donor to the recipient cell, with the internalization of the organelles, via endocytosis, enabling functional restoration. Results of preclinical and clinical trials involving mitochondrial transfer support the application of this technique in improving the function of the myocardium after damage caused by ischemia reperfusion injury. Herein, we discuss the beneficial role of mitochondrial transplantation in cardiovascular diseases and the current technical challenges of mitochondrial isolation, preservation, and targeted delivery, as well as their role in advancing precision medicine, offering a patient tailored therapeutic approach.

Keywords:  CVD; ischemia/reperfusion injury; mitochondrial replacement therapy; mitochondrial transplantation; mtDNA

DOI:  https://doi.org/10.3390/ijms27094018
Pediatr Res. 2026 May 13.

The role of choline in neurodevelopment.

Nicholas C Rickman, Gloria Liu, Axel R Franz, Wolfgang Bernhard, Cynthia F Bearer.

Choline was first declared to be an essential nutrient in 1998. Current research on choline intake has been sufficient for the Food and Nutrition Board of the National Academies of Science, Engineering & Medicine to establish a loose guideline, but more investigation into healthy choline intakes is necessary to clarify guidelines. Choline is intimately involved in human metabolism, as an essential precursor for cell membrane components such as phosphatidylcholine and sphingomyelin, lipoprotein and fatty acid trafficking, and the neurotransmitter acetylcholine. It plays an essential role in histone, RNA, and DNA methylation, creatine synthesis, and more. Choline-related pathologies have already been implicated in multiple severe developmental diseases, such as schizophrenia, Down syndrome, and neural tube defects, and age-related diseases such as Alzheimer's. Choline supplementation has been shown to alleviate the symptoms of neurodevelopmental diseases, such as Fetal Alcohol Spectrum Disorder and neonatal hyperbilirubinemia. The choline intake by most adults is estimated to be less than the current recommendations. Choline supplementation, particularly for vulnerable populations such as pregnant women, preterm infants, and cystic fibrosis patients, requires further investigation to establish adequate recommendations and to fully elucidate the consequences of malnutrition. Outcomes of choline deficiency and supplementation, such as neurodevelopment, should be measured. IMPACT: What this article adds to the existing literature An up-to-date summary of the metabolism of choline A review of the role of choline in normal and abnormal neurodevelopment A concise description of sources of choline.

DOI: https://doi.org/10.1038/s41390-026-05021-4
Cardiol Rev. 2026 May 11.

Understanding Dysfunctional Autophagy and Mitophagy in Inflammatory Cardiovascular Disease.

Michael Kaiser, Toni-Ann Lewis, Michael Malekan, Manish A Parikh, Gioia Turitto, William H Frishman, Stephen J Peterson.

  Mitochondria are critical cellular powerhouses that produce adenosine triphosphate to maintain the structure and integrity of the cell. Mitochondria generate 90% of the energy of a cell. Chronic inflammation causes damage to mitochondria. When enough mitochondria are dysfunctional, the involved organ will suffer. Mitochondria become dysfunctional in the setting of chronic inflammation. Under noninflammatory conditions, the body generates new mitochondria (mitochondrial biogenesis) and removes old and damaged mitochondria via mitophagy. When mitochondria are damaged, they "spontaneously" leak out reactive oxygen species, mitochondrial DNA, and damage-associated molecular patterns, generating erroneous innate immune responses. Autophagy is a recycling and housekeeping process that removes dysfunctional components, organelles, and proteins, promoting the recovery and maintenance of cell health. Mitophagy is a specific variant of this process that removes dysfunctional mitochondria from the cell. Mitophagy declines with age, allowing dysfunctional mitochondria to accumulate, and chronic inflammation leads to cardiovascular disease (CVD). In CVD, impairment of both autophagy and mitophagy leads to more chronic inflammation, characterized by hyperactivation of the nucleotide-binding oligomerization domain (NOD)-, leucine-rich repeat (LRR)- and pyrin domain-containing protein 3 (NLRP3) inflammasome, a key component of the immune system. Once activated, it triggers inflammation, leading to excessive cytokine activity, proinflammatory macrophage polarization, pyroptosis, and increased immune cell infiltration into cardiac and vascular tissues. Pyroptosis is a form of inflammatory cell death triggered by programmed cues; however, in autoimmunity and cancer, when overactivated, this process can become detrimental. Adequate regulation of these events reduces oxidative stress, inflammatory cascades, fibrosis, and maladaptive remodeling, thereby improving overall cardiovascular health. Targeted therapeutic enhancement of autophagy and mitophagy represents a promising strategy to modulate immune-driven pathology and improve outcomes in cardiovascular conditions. We will review the mechanisms of how this inflammation causes CVD.

Keywords:  NLRP3 inflammasome; atherosclerosis; autophagy; cardiovascular disease; cytokine release; endothelial dysfunction; heart failure; immune cell infiltration; inflammasome crosstalk; inflammation; innate immunity; ischemia-reperfusion injury; macrophage polarization; mitochondrial DAMPs; mitophagy; oxidative stress; pyroptosis; redox signaling; sterile inflammation; therapeutic modulation

DOI:  https://doi.org/10.1097/CRD.0000000000001302
Clin Sci (Lond). 2026 May 14. pii: CS20250414. [Epub ahead of print]

The metabolic effects of post-sepsis feeding of meals with only essential amino acids.

Nicolaas E P Deutz, Gabriella Am Ten Have, Sarah A Rice, Marina B W Horner, Ilaria Minussi, Mariëlle Pkj Engelen.

  Nutritional support is a vital component of the rehabilitation process following sepsis. Essential amino acids (EAA) are recognized as a critical component for stimulating anabolism. However, it remains unclear whether EAA supplementation alone is more effective than providing a complete profile of all amino acids (TAA). We studied amino acid metabolism in 51 catheterized pigs (±27kg) using the pulse tracer approach over a 7-day recovery period following sepsis. Animals were randomly and blindly assigned to receive post-sepsis nutrition containing either an EAA or a TAA mixture based on the composition of pig muscle. Statistical analyses were performed using a generalized linear mixed model. Plasma concentrations of EAA increased substantially in the EAA group post-sepsis (interaction effect, p<0.001), while those of non-essential amino acids increased in both groups (time effect, p<0.001). Whole body intracellular production of most AA was reduced on day 3 and remained low on day 7 post-sepsis, with only small differences observed between the two groups. On day 7 post-sepsis, pigs receiving only EAA showed significantly (all p<0.001) lower intracellular production of hydroxyproline (-36%), ornithine (-11%), and tryptophan (-20%) and higher production of arginine (66%), citrulline (18%), glutamine (18%), taurine (22%) and some EAA. The EAA group showed a significantly higher net protein breakdown post-sepsis. In this sepsis-recovery pig model, dietary supplementation of both EAA and TAA failed to normalize the intracellular production of amino acids. More importantly, providing only EAA resulted in a significantly greater net protein breakdown compared to the TAA group.

Keywords:  amino acids; metabolism; nutrition; sepsis

DOI:  https://doi.org/10.1042/CS20250414
Nutrients. 2026 Apr 25. pii: 1362. [Epub ahead of print]18(9):

Prospective Associations of Serum Vitamin B12, Homocysteine, and Ferritin Levels with Probable Sarcopenia.

Inkyung Baik.

  Background/Objectives: Previous cross-sectional studies investigated the associations of low handgrip strength (HS), a primary indicator of probable sarcopenia (PS), with biomarkers related to anemia. However, existing evidence is inconsistent, and data establishing causality remain limited. The present prospective study aimed to evaluate whether serum vitamin B12, folate, homocysteine (Hcy), and ferritin levels are associated with PS risk. Methods: This study analyzed data from 1930 adults aged 45-76 years who had normal muscle quantity at baseline. Serum biomarkers were assessed at baseline and PS defined by low HS was determined at 6-year follow-up. The modified Poisson regression method was employed to calculate multivariable risk ratios (RRs) and 95% confidence intervals (CIs). Results: Among all participants, PS risk was inversely related to serum vitamin B12 levels (p = 0.06), while it was lowest in the high-normal ranges of serum Hcy (12.1-15 μmol/L) and ferritin (101-200 ng/mL) levels. The RRs (95% CIs) for PS risk were 0.73 (0.60, 0.89) and 0.75 (0.64, 0.87) for high-normal Hcy and ferritin categories, respectively, compared with the lowest category. On examining the associations of elevated Hcy and ferritin levels with PS risk, age was identified as a significant modifier for elevated Hcy levels (>15 μmol/L) (p for interaction < 0.05); a reduced risk was observed in younger participants, whereas an increased risk was noted in older participants. Conclusions: These findings suggest that high-normal ferritin levels may be optimal for alleviating PS risk, irrespective of age, and that elevated Hcy levels could be detrimental for older adults in preventing PS risk.

Keywords:  ferritins; folic acid; homocysteine; muscle strength; prospective studies; sarcopenia; vitamin B12

DOI:  https://doi.org/10.3390/nu18091362
PLoS One. 2026 ;21(5): e0348268

Neutrophil-to-lymphocyte and neutrophil-to-platelet ratios for predicting 28-day mortality in sepsis: A retrospective cohort study.

Jianchun Wei, Xinjie Huang, Zhilian Wang, Hailing Zhang.

OBJECTIVE: This study aimed to evaluate the prognostic value of the neutrophil-to-lymphocyte ratio (NLR) and neutrophil-to-platelet ratio (NPR), alone and in combination with procalcitonin (PCT), for predicting 28‑day mortality in patients with sepsis.
METHODS: In this single‑center retrospective cohort study, 395 adult sepsis patients admitted to the emergency department between 2020 and 2025 were included. NLR and NPR were calculated from the first complete blood count obtained within 24 hours of initial emergency department presentation. Univariable Cox regression was used for preliminary screening. The C-index was used to compare the discriminative ability of traditional inflammatory markers (PCT, CRP, and WBC) to select a reference biomarker. Multivariable Cox regression and restricted cubic spline (RCS) analysis were performed to evaluate the linear and non-linear associations of NLR and NPR with mortality. To assess whether adding NLR or NPR provided incremental prognostic value to PCT, multivariable Cox models with interaction terms (PCT × NLR and PCT × NPR) were constructed. LASSO regression was applied for variable selection, and VIF was used to assess multicollinearity.
RESULTS: The overall 28‑day mortality was 38.2%. Neither NLR nor NPR outperformed PCT in predicting 28-day mortality, and none of the three biomarkers showed significant independent associations with mortality after adjusting for confounders (PCT: adjusted HR per IQR = 1.02, 95% CI: 0.94-1.11, p = 0.605; NLR: HR = 1.01, 95% CI: 1.00-1.02, p = 0.235; NPR: HR = 1.00, 95% CI: 1.00-1.01, p = 0.378). Restricted cubic spline (RCS) curves confirmed no non-linear associations or threshold effects for NLR and NPR. Multivariable Cox regression with interaction terms showed that adding NLR or NPR to PCT did not provide additional prognostic value beyond PCT alone (PCT × NLR: HR = 1.00, 95% CI: 0.97-1.03, p = 0.854; PCT × NPR: HR = 0.97, 95% CI: 0.92-1.01, p = 0.121).
CONCLUSION: Neither NLR nor NPR alone, nor their combination with PCT, improved 28-day mortality prediction in this elderly sepsis cohort, suggesting that a single early measurement may be insufficient for sepsis prognostication. Future studies should explore serial measurements and integrate multiple pathophysiological dimensions. The low cost and wide availability of NLR and NPR still support their potential role within a multi-parameter panel, particularly in resource-limited settings.

DOI: https://doi.org/10.1371/journal.pone.0348268
Ageing Res Rev. 2026 May 08. pii: S1568-1637(26)00150-9. [Epub ahead of print]119 103158

Ergothioneine as a potential geroprotector: Targeting molecular hallmarks of ageing and age-related diseases.

Pengfei Zhao, Ying Qi.

  Hypothesized to be a diet-derived 'longevity vitamin', Ergothioneine (ET) is increasingly recognized for its potential to modulate cellular homeostasis and support healthy ageing in preclinical models. This systematic review, encompassing evidence from 2005 to 2025, investigates ET's unique pharmacokinetics mediated by the OCTN1 (SLC22A4) transporter, which ensures its selective accumulation in tissues susceptible to age-related oxidative decline. Beyond its role as a secondary antioxidant buffer, we critically evaluate ET's ability to target molecular hallmarks of ageing, specifically focusing on telomere maintenance, mitochondrial integrity, and the NRF2-mediated cytoprotective response. Utilizing network pharmacology, this review deciphers the multi-target regulatory landscape of ET in mitigating neurodegeneration, cardiovascular remodeling, and metabolic dysfunction. Furthermore, we address clinical gaps by discussing ET's potential utility as a candidate biomarker of biological aging and emphasizing the necessity of precision nutrition strategies incorporating SLC22A4/SLC22A15 genetic stratification. By synthesizing mechanistic insights and longitudinal human data, we highlight ET as an emerging candidate with geroprotective potential that warrants rigorous clinical evaluation for extending healthspan.

Keywords:  Anti-inflammatory; Antioxidant; Ergothioneine; Medicine food homology; Therapeutic potential; Toxicology

DOI:  https://doi.org/10.1016/j.arr.2026.103158
World J Surg Oncol. 2026 May 09.

Research progress on the biological function and molecular mechanism of GDF-15 in solid malignant tumors.

Dilinaer Aishanjiang, Yiliminuer Abulajiang, Reziya Saidula, Kaderya Abudusalam, Kadierjiang Musha.

  Growth differentiation factor 15 (GDF-15), a stress-responsive member of the transforming growth factor-β (TGF-β) superfamily, is consistently upregulated in multiple solid tumors and closely linked to poor clinical outcomes. This review offers a systematic overview of the pleiotropic functions and principal signaling pathways of GDF-15 in solid malignancies. Within the tumor microenvironment (TME), GDF-15 fuels tumor progression by promoting proliferation, sustaining stemness, remodeling metabolism, and conferring therapy resistance via the TGF-β, Leukemia Inhibitory Factor (LIF)-Signal Transducer and Activator of Transcription 3 (STAT3), and AKT pathways. Notably, GDF-15 orchestrates an immunosuppressive TME by limiting T cell infiltration and expanding regulatory T cells, thereby facilitating immune evasion and resistance to immune checkpoint inhibitors (ICIs). Systemically, GDF-15 contributes to cancer cachexia through activation of the brainstem glial-cell-line-derived neurotrophic factor family receptor α-like (GFRAL)-rearranged during transfection (RET) receptor axis. Accumulating preclinical evidence positions GDF-15 as a promising therapeutic target, particularly for mitigating cachexia and potentiating immunotherapy. However, the context-dependent and dualistic nature of GDF-15 signaling, varying with tumor type, microenvironment, and disease stage, poses substantial hurdles for clinical translation. Future efforts should focus on deciphering the molecular determinants underlying GDF-15's functional duality, paving the way for precise, context-tailored intervention strategies.

Keywords:  Cancer cachexia; GDF-15; Immune escape; Mitokine; Signaling pathway; TME; Therapeutic target

DOI:  https://doi.org/10.1186/s12957-026-04341-3
Psychol Res. 2026 May 15. pii: 92. [Epub ahead of print]90(3):

Beyond expectations: nocebo suggestion affects cognitive performance in older adults.

Alessandra Barbon, Bernardo Villa-Sánchez, Mirta Fiorio, Sara Assecondi, Veronica Mazza.

  Placebo and nocebo effects are well-documented in pain perception and motor performance, yet their impact on cognitive performance remains unclear. Understanding these effects is relevant for designing interventions that leverage positive expectations to enhance cognitive outcomes while mitigating negative expectations, especially for older adults facing age-related cognitive decline. Furthermore, it is unclear whether these effects can be induced remotely, in the absence of direct participant-experimenter interactions. This study examined whether verbal suggestions about an intervention potential to enhance or impair cognitive performance could induce placebo and nocebo effects-both objective and subjective-in healthy older adults (aged 65-80) in an online setting. Participants completed an oddball task in auditory and visual modalities before (PRE) and after (POST) exposure to an inert acoustic intervention (i.e., the placebo/nocebo intervention). Prior to the intervention, individuals were randomly assigned to one of three groups, receiving neutral (Control), positive (Placebo), or negative (Nocebo) information about the intervention. The Nocebo group showed impaired performance at POST, consistent with the verbal suggestion, despite no negative shift in expectancy or perceived efficacy. In contrast, the Placebo group expected improvements and perceived benefits, but their performance did not differ from controls. This indicates a dissociation in objective and subjective components between placebo/nocebo effects in a perceptual and attentional task. Altogether, even without in-person interaction, nocebo effects are observable in cognitive performance in older adults. In contrast, placebo effects are limited to subjective beliefs, emphasizing the importance of additional factors such as motivation, and individual differences, in online contexts.

Keywords:  Cognitive performance; Expectation; Healthy aging; Nocebo effect; Online experiment; Placebo effect; Verbal suggestion

DOI:  https://doi.org/10.1007/s00426-026-02296-4