A year in research · 30 selected publications · five research threads
How does the brain turn perception, knowledge and expectation into a well-timed action? In 2025, we followed that question from fundamental neural dynamics to development, expertise and clinical conditions.
A recurring lesson across our work in 2025 was that successful action cannot be read from one brain region or one neural rhythm alone. What matters is how distributed processes coordinate in time, how information moves between them, and how the resulting configuration changes with the demands of the moment.
01 · INTENTIONAL ACTION
Turning expected outcomes into actions
Intentional actions begin before a movement is made: we anticipate what an action is likely to achieve. We found that forming these action–effect links involves directed communication in a theta-frequency network connecting the insular cortex, anterior temporal lobe and inferior frontal cortex. Rather than acting as isolated modules, these regions exchange information in both directions; the temporal and insular regions appear to integrate and abstract action–effect knowledge, while frontal regions help use earlier experience as a template for what should happen next.[1]
The same research programme also clarified that different rhythms contribute different jobs. Posterior alpha and beta activity accompanies the initial integration of perceptual and motor features, while alpha activity helps keep the resulting link available over a delay.[2] Directed-connectivity analyses similarly point to alpha activity as important for sustaining perception–action associations, whereas theta activity is especially important for organizing their sequence.[3] A new tensor-decomposition approach, which preserves time, frequency, space and trial-level information together, confirmed a prominent role for midfrontal theta when an established perception–action association must be reconfigured, alongside a more selective contribution of alpha activity.[4]
Context matters. The timing of distracting information changed both activity and directed communication in a ventral-stream–parietal theta network.[5] We also perturbed the system in two complementary ways. Auricular vagus nerve stimulation altered directed cortical communication and recruited posterior temporal regions, with partly different network changes during action-effect perception and action planning.[6] Increasing catecholaminergic signalling with methylphenidate changed the strength of communication and which region served as a network hub at different stages of action–effect integration.[7] During response inhibition, the insular cortex emerged as a coordinating hub through which theta- and alpha-related information flows were linked to reconfiguration and attentional selection.[8]
In plain terms: the brain does not simply issue a motor command. It assembles, maintains and—when circumstances change—rewrites a prediction of what an action will do.
02 · ADAPTIVE CONTROL
Control is a moving target
People constantly balance persistence—staying with a goal—against flexibility—opening up to alternatives. Our 2025 findings suggest that this “metacontrol” balance is not a fixed personal setting. Changes in the aperiodic part of the EEG signal appeared after a conflict was encountered, not before it, and behavioural biases did not generalize reliably across tasks. This supports a phasic, context-sensitive account of metacontrol.[9]
This principle extends beyond classic conflict tasks. In two independent samples, updating working memory was accompanied by systematic changes in aperiodic activity.[10] When people learned from errors, alpha activity after negative feedback predicted better performance on the next trial, while aperiodic activity shaped those alpha processes.[11] And uncertainty did not automatically produce more theta activity: when uncertainty encouraged exploration and curiosity, neural dynamics looked different from the familiar “need for control” pattern.[12]
Metacontrol also changes across development. From childhood to adulthood, overall aperiodic activity decreased while the ability to adjust it strategically to task demands improved.[13] Finally, we began to specify the underlying biology. Transcranial direct-current stimulation and methylphenidate interacted in their effects on aperiodic activity and cognitive persistence,[14] while baseline GABA and glutamate-related concentrations in fronto-striatal regions predicted aspects of catecholaminergic modulation.[15]
In plain terms: cognitive control is less like selecting a permanent mode and more like continuously tuning a system to the problem immediately at hand.
03 · EVENTS AND LEARNING
How the brain finds structure in experience
Continuous experience has no natural chapter headings, yet the mind divides it into meaningful events. In a pharmacological study, methylphenidate increased the likelihood that the same incoming information was treated as meaningful; this effect depended on both situational change and prior experience.[16] Event boundaries, in turn, reached down to the microstructure of action: responses were bound more strongly within one perceived event, and retrieving a previous response was weakened when an event boundary intervened.[17]
This organization can be guided. Adolescents normally segmented events more coarsely than adults, but instructions encouraging fine-grained processing moved both their behaviour and decodable neural patterns toward the adult profile—without erasing all developmental differences.[18] During sequence learning, adaptive prior knowledge and the current learning context were represented together, particularly at abstract and motor-coding levels, allowing existing knowledge to be reused rather than simply competing with new learning.[19]
In plain terms: how we divide experience into “what is happening now” shapes what we learn, remember and do next.
04 · DEVELOPMENT AND EXPERTISE
Comparing adolescents and adults showed that maturation changes the way distributed networks solve demanding sensorimotor problems. Adults drew more strongly on directed communication between frontal regions and the ventral visual stream, whereas adolescents relied more on frontal theta signals associated with surprise and prediction error.[20] The core network for learning action effects was already present in adolescence, but younger participants showed stronger internal communication and additional recruitment of posterior sensory regions, suggesting a greater need for representational and sensory integration.[21]
Expertise provided another window on neural adaptation. Athletes with thousands of hours of training predicted occluded movement trajectories more accurately than non-athletes. Their advantage was not a simple increase in oscillatory power; instead, experts and novices appeared to use different functional anatomy for action emulation.[22] When the superior parietal lobule was perturbed with repetitive transcranial magnetic stimulation, specific neural rhythms changed but performance remained stable, suggesting that an expert system can compensate through connected regions.[23]
In plain terms: development and training do not merely make the same brain process stronger; they can change which neural route is used to reach a successful result.
05 · CLINICAL RELEVANCE
From group labels to specific processing profiles
In ADHD, tensor decomposition revealed that the most informative differences during response inhibition were not the frequently emphasized frontocentral theta response. Posterior alpha activity during attentional selection and posterior theta activity during later response control better distinguished participants with ADHD from neurotypical participants, pointing to difficulties that begin early and continue across processing stages.[24] A second study in children and adolescents linked difficulties in updating incompatible perception–action associations particularly to reduced task-sensitive modulation of alpha activity.[25]
In Tourette syndrome, behavioural performance could look similar while the temporal coordination of neural activity differed: oscillatory patterns following the creation of an event file were less tightly related to those used when it was later retrieved.[26] Under especially demanding response-inhibition conditions, stronger and more prolonged theta modulation coincided with weaker alpha modulation and an absence of the beta changes seen in neurotypical participants.[27] Automated video analysis added a complementary perspective: the clearest blinking difference was not simply “more blinking,” but a much higher frequency of individually atypical blinks, whose precise form varied from person to person.[28]
Alcohol-related work likewise underscored the importance of state and context. People with alcohol use disorder recruited different directed alpha networks during response inhibition, while the dynamic theta communication seen in controls was reduced.[29] In an animal model of alcohol dependence, direct cortical stimulation improved local neural signals but its influence propagated less widely; the effect also varied with individual drinking patterns.[30]
In plain terms: clinically relevant differences are rarely captured by one universal deficit. They emerge from when, where and how a neural system adapts—and from the state of that system when an intervention is applied.
Across methods and populations, the year moved us from asking where cognitive control “is” toward asking how it is assembled. Directed information flow, the division of labour among neural rhythms, aperiodic activity, individual neurochemistry and current brain state all proved consequential. Together, the findings support a dynamic account of action control: adaptive behaviour emerges from configurations that are built for a particular moment, maintained only as long as useful, and reorganized when the situation changes.
Curated from PubMed records returned for Beste C[au] in 2025. Citation numbers in the story link to entries below. DOI links open the publisher landing page; PubMed links open the indexed record.
Mayer J, Mückschel M, Talebi N, Hommel B, Beste C. NeuroImage. 2025;305:120965.
DOI: 10.1016/j.neuroimage.2024.120965 · PubMed
Pastötter B, Beste C, Münchau A, Frings C. Journal of cognitive neuroscience. 2025;37(11):1913-1928.
DOI: 10.1162/JOCN.a.52 · PubMed
Eggert E, Prochnow A, Talebi N, Frings C, Münchau A, Beste C. Communications biology. 2025;8(1):1147.
DOI: 10.1038/s42003-025-08601-y · PubMed
Gholamipourbarogh N, Prochnow A, Beste C. Cerebral cortex (New York, N.Y. : 1991). 2025;35(7):bhaf176.
DOI: 10.1093/cercor/bhaf176 · PubMed
Hao Y, Münster N, Pastötter B, Talebi N, et al.. Cortex; a journal devoted to the study of the nervous system and behavior. 2025;189:242-255.
DOI: 10.1016/j.cortex.2025.06.003 · PubMed
Mückschel M, Mayer J, Hommel B, Beste C. iScience. 2025;29(2):114571.
DOI: 10.1016/j.isci.2025.114571 · PubMed
Mayer J, Helin Koyun A, Mückschel M, Roessner V, Hommel B, Beste C. The international journal of neuropsychopharmacology. 2025;28(6):pyaf031.
DOI: 10.1093/ijnp/pyaf031 · PubMed
Eggert P, Mückschel M, Talebi N, Beste C, Ghin F. Cerebral cortex (New York, N.Y. : 1991). 2025;35(10):bhaf292.
DOI: 10.1093/cercor/bhaf292 · PubMed
Wang X, Zhou X, Beste C, Hommel B. Scientific reports. 2025;15(1):32699.
DOI: 10.1038/s41598-025-20479-8 · PubMed
Zhang H, Konjusha A, Yu S, Mückschel M, Hommel B, Colzato L, Beste C. Psychophysiology. 2025;62(9):e70148.
DOI: 10.1111/psyp.70148 · PubMed
Jia S, Liu D, Yue Y, Colzato L, Hommel B, Beste C. NeuroImage. 2025;317:121341.
DOI: 10.1016/j.neuroimage.2025.121341 · PubMed
Prasad S, Talebi N, Wendiggensen P, Mückschel M, Hommel B, Beste C. Human brain mapping. 2025;46(14):e70333.
DOI: 10.1002/hbm.70333 · PubMed
Pi Y, Pscherer C, Mückschel M, Colzato L, Hommel B, Beste C. Scientific reports. 2025;15(1):18349.
DOI: 10.1038/s41598-025-00736-6 · PubMed
Gao Y, Koyun AH, Roessner V, Stock AK, et al.. Brain stimulation. 2025;18(3):720-729.
DOI: 10.1016/j.brs.2025.03.024 · PubMed
Gao Y, Koyun AH, Stock AK, Werner A, et al.. Human brain mapping. 2025;46(4):e70173.
DOI: 10.1002/hbm.70173 · PubMed
Ghorbani F, Zhou X, Roessner V, Hommel B, Prochnow A, Beste C. The international journal of neuropsychopharmacology. 2025;28(2):pyaf008.
DOI: 10.1093/ijnp/pyaf008 · PubMed
Moeller B, Beste C, Münchau A, Frings C. Journal of experimental psychology. General. 2025;154(4):969-979.
DOI: 10.1037/xge0001681 · PubMed
Zhou X, Ghorbani F, Roessner V, Hommel B, Prochnow A, Beste C. Developmental cognitive neuroscience. 2025;72:101521.
DOI: 10.1016/j.dcn.2025.101521 · PubMed
Takács Á, Vékony T, Pedraza F, Haesebaert F, Tillmann B, Beste C, Németh D. Cerebral cortex (New York, N.Y. : 1991). 2025;35(2):bhaf025.
DOI: 10.1093/cercor/bhaf025 · PubMed
Böttcher A, Wilken S, Raab M, Hoffmann S, Beste C. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2025;45(28):e0427252025.
DOI: 10.1523/JNEUROSCI.0427-25.2025 · PubMed
Mayer J, Mückschel M, Hommel B, Beste C. Human brain mapping. 2025;46(13):e70339.
DOI: 10.1002/hbm.70339 · PubMed
Wilken S, Böttcher A, Beste C, Raab M, Hoffmann S. Neuropsychologia. 2025;209:109085.
DOI: 10.1016/j.neuropsychologia.2025.109085 · PubMed
Wilken S, Böttcher A, Beste C, Raab M, Hoffmann S. Cerebral cortex (New York, N.Y. : 1991). 2025;35(6):bhaf158.
DOI: 10.1093/cercor/bhaf158 · PubMed
Gholamipourbarogh N, Roessner V, Bluschke A, Beste C. Biological psychiatry. Cognitive neuroscience and neuroimaging. 2025:S2451-9022(25)00143-0.
DOI: 10.1016/j.bpsc.2025.05.001 · PubMed
Graf K, Jamous R, Bluschke A, Beste C. NeuroImage. Clinical. 2025;48:103905.
DOI: 10.1016/j.nicl.2025.103905 · PubMed
Hao Y, Wendiggensen P, Bluschke A, Rawish T, et al.. NeuroImage. Clinical. 2025;48:103844.
DOI: 10.1016/j.nicl.2025.103844 · PubMed
Prochnow A, Bluschke A, Rawish T, Friedrich J, et al.. Brain communications. 2025;7(3):fcaf172.
DOI: 10.1093/braincomms/fcaf172 · PubMed
Verrel J, Schappert R, Brügge N, Rawish T, et al.. Parkinsonism & related disorders. 2025;142:108121.
DOI: 10.1016/j.parkreldis.2025.108121 · PubMed
Ghin F, Talebi N, Stock AK, Beste C. Human brain mapping. 2025;46(14):e70338.
DOI: 10.1002/hbm.70338 · PubMed
Habelt B, Talebi N, Afanasenkau D, Schwarz C, et al.. Scientific reports. 2025;15(1):35407.
DOI: 10.1038/s41598-025-21802-z · PubMed