A year in research · 30 selected publications · five research threads
In 2024, we examined how the brain assembles actions, changes control modes and adapts its internal state to the demands of a particular moment.
Across experiments, populations and methods, a common message emerged: effective control is not a fixed capacity located in one brain area. It depends on representations that can be bound and released, on communication between regions, and on neural states that change with context, experience and neurochemistry.
01 · ACTION REPRESENTATIONS
A shared vocabulary is essential for studying how perceptual features and actions become integrated; our consensus work therefore clarified the central concepts of perception-action integration and event coding.[1] Experiments then showed that an abandoned action plan is rapidly dismantled: discarding a plan releases its bound features rather than leaving a complete plan waiting in the background.[2] Prefrontal activity tracked how strongly stimulus and response features had to be translated and bound, while changing spatial relations weakened the later retrieval of an established action episode.[3,4]
Action control also carries a memory of the immediate past. Theta-, alpha- and beta-related processes in frontotemporal systems reflected how recently encountered information shaped the next action.[5] When people imagined the effects of an action, alpha and beta activity in cingulate and sensory regions supported predictions about the future state of the body or an external object.[6]
In plain terms: Actions are temporary structured representations: the brain creates them, uses them and actively unbinds them when they are no longer useful.
02 · NETWORK DYNAMICS
Predictive coding during perception-action integration relied on directed, nonlinear communication in theta and alpha networks rather than on activity in a single region.[7] Conflict processing likewise combined top-down control with the retrieval and integration of previous action features, supporting hybrid accounts in which control and memory jointly guide behaviour.[8]
A machine-learning analysis of directed connectivity separated local increases in neural activity from reduced communication across temporo-occipital and fronto-occipital networks during the reconfiguration of perception-action associations.[9] Representational analyses identified the insular cortex as an integrative element during stopping under conflict, while tensor decomposition distinguished shared and task-specific neural configurations for action restraint and action cancellation.[10,11]
In plain terms: The same behavioural adjustment can involve stronger local processing but weaker communication between regions; activity and connectivity therefore answer different questions.
03 · METACONTROL
Task switching reduced the aperiodic component of the EEG signal, consistent with a flexible shift in metacontrol rather than an automatic increase in persistence whenever control is challenged.[12] Across experimental blocks, persistence was accompanied by stronger directed communication even when changes in alpha and beta power did not simply mirror behaviour.[13] Resting aperiodic activity also predicted whether individuals expressed a more stable or more adaptive control style.[14]
Conflict temporarily increased the aperiodic exponent, suggesting that the system reduces neural noise to prepare tighter control on the following trial rather than merely correcting the current response.[15] Event segmentation provided a complementary example: instructions changed sensitivity to incoming information and the use of event boundaries, with the insula contributing to the monitoring of potentially meaningful change.[16]
In plain terms: Control is not simply strong or weak. It is a dynamic choice between stabilizing what matters and opening the system to change.
04 · NEUROBIOLOGY AND STIMULATION
Methylphenidate increased the aperiodic exponent, linking catecholaminergic enhancement to lower cortical noise and a shift in metacontrol state.[17] Yet neurochemical and electrical interventions were not additive without limit: methylphenidate and anodal stimulation shared theta-related effects in supplementary motor regions and interacted when combined.[18] Baseline GABA+ in the anterior cingulate cortex was particularly informative when cognitive effort was high, helping to predict responsiveness to catecholaminergic enhancement.[19]
Individual capacity mattered as well. The cognitive effect of pharmacologically altering catecholamines depended on how well a person could voluntarily regulate theta activity.[20] In working memory, stimulation selectively affected gate opening and its alpha- and norepinephrine-related dynamics, while directed network analyses revealed opposing, threshold-dependent mechanisms for opening and closing the gate.[21,22]
In plain terms: An intervention acts on an already organized brain; baseline chemistry, current state and self-regulatory capacity help determine the result.
05 · CLINICAL AND TRANSLATIONAL RESEARCH
In adolescents with ADHD, additional conflict disproportionately impaired inhibition and was linked to delayed alpha modulation, while event segmentation relied less on social information and more on inferior-frontal attentional control.[23,24] In functional movement disorders, stronger post-movement beta synchronization predicted excessive perception-action binding, locating the difficulty in the integration stage rather than only in retrieval.[25]
Tourette syndrome again showed that an apparent symptom can reflect an altered learning architecture: enhanced statistical learning was associated with more efficient resting theta networks and with a heightened sensitivity to complex regularities.[26,27] By contrast, binding and retrieval of event files proved comparatively robust across the adult age groups studied.[28] Work with MDMA and methamphetamine users linked altered decision processes to stronger P3 modulation, while the ReCoDe programme connected such laboratory mechanisms to longitudinal monitoring and individualized interventions for addiction.[29,30]
In plain terms: Clinical relevance lies in identifying which operation changes, at which processing stage, and under which conditions - not in assigning one global deficit to a diagnostic group.
The 2024 studies converged on a dynamic view of control. Perception-action representations are assembled and released; rhythmic and aperiodic activity describe complementary aspects of the system; and interventions depend on the state they encounter. This shifts the central question from where control is located to how an adaptive configuration is created for a particular demand.
Curated from PubMed records returned for Beste C[au] in 2024. Citation numbers in the story link to entries below. DOI links open the publisher landing page; PubMed links open the indexed record.
Frings C, Beste C, Benini E, Möller M, et al.. Communications psychology. 2024;2(1):7.
DOI: 10.1038/s44271-023-00050-9 · PubMed
Mocke V, Beste C, Pastötter B, Kunde W. Journal of experimental psychology. Human perception and performance. 2024;50(9):903-917.
DOI: 10.1037/xhp0001219 · PubMed
Geissler CF, Schöpper LM, Engesser AF, Beste C, Münchau A, Frings C. Journal of cognitive neuroscience. 2024;36(1):95-106.
DOI: 10.1162/jocn_a_02071 · PubMed
Selimi S, Frings C, Münchau A, Beste C, Moeller B. Psychological research. 2024;88(5):1727-1736.
DOI: 10.1007/s00426-024-01973-6 · PubMed
Rawish T, Wendiggensen P, Friedrich J, Frings C, Münchau A, Beste C. NeuroImage. 2024;288:120526.
DOI: 10.1016/j.neuroimage.2024.120526 · PubMed
Wilken S, Böttcher A, Adelhöfer N, Raab M, Beste C, Hoffmann S. Behavioural brain research. 2024;469:115063.
DOI: 10.1016/j.bbr.2024.115063 · PubMed
Jamous R, Ghorbani F, Mükschel M, Münchau A, Frings C, Beste C. NeuroImage. 2024;301:120891.
DOI: 10.1016/j.neuroimage.2024.120891 · PubMed
Pastötter B, Haciahmet CC, Beste C, Münchau A, Frings C. Cerebral cortex (New York, N.Y. : 1991). 2024;34(8):bhae326.
DOI: 10.1093/cercor/bhae326 · PubMed
Talebi N, Prochnow A, Frings C, Münchau A, Mückschel M, Beste C. iScience. 2024;27(10):110995.
DOI: 10.1016/j.isci.2024.110995 · PubMed
Ghin F, Eggert E, Gholamipourbarogh N, Talebi N, Beste C. Human brain mapping. 2024;45(6):e26643.
DOI: 10.1002/hbm.26643 · PubMed
Gholamipourbarogh N, Eggert E, Münchau A, Frings C, Beste C. NeuroImage. 2024;295:120667.
DOI: 10.1016/j.neuroimage.2024.120667 · PubMed
Yan J, Yu S, Mückschel M, Colzato L, Hommel B, Beste C. Scientific reports. 2024;14(1):24088.
DOI: 10.1038/s41598-024-74867-7 · PubMed
Wang X, Talebi N, Zhou X, Hommel B, Beste C. NeuroImage. 2024;302:120915.
DOI: 10.1016/j.neuroimage.2024.120915 · PubMed
Pi Y, Yan J, Pscherer C, Gao S, et al.. Psychophysiology. 2024;61(8):e14576.
DOI: 10.1111/psyp.14576 · PubMed
Jia S, Liu D, Song W, Beste C, Colzato L, Hommel B. Cerebral cortex (New York, N.Y. : 1991). 2024;34(5):bhae185.
DOI: 10.1093/cercor/bhae185 · PubMed
Zhou X, Ghorbani F, Roessner V, Hommel B, Prochnow A, Beste C. Human brain mapping. 2024;45(11):e26727.
DOI: 10.1002/hbm.26727 · PubMed
Gao Y, Roessner V, Stock AK, Mückschel M, Colzato L, Hommel B, Beste C. The international journal of neuropsychopharmacology. 2024;27(8):pyae033.
DOI: 10.1093/ijnp/pyae033 · PubMed
Koyun AH, Wendiggensen P, Roessner V, Beste C, Stock AK. The international journal of neuropsychopharmacology. 2024;27(6):pyae023.
DOI: 10.1093/ijnp/pyae023 · PubMed
Koyun AH, Talebi N, Werner A, Wendiggensen P, et al.. NeuroImage. 2024;293:120619.
DOI: 10.1016/j.neuroimage.2024.120619 · PubMed
Prochnow A, Mückschel M, Eggert E, Senftleben J, et al.. The international journal of neuropsychopharmacology. 2024;27(1):pyae003.
DOI: 10.1093/ijnp/pyae003 · PubMed
Yu S, Konjusha A, Ziemssen T, Beste C. NeuroImage. 2024;289:120541.
DOI: 10.1016/j.neuroimage.2024.120541 · PubMed
Elmers J, Yu S, Talebi N, Prochnow A, Beste C. iScience. 2024;27(4):109521.
DOI: 10.1016/j.isci.2024.109521 · PubMed
Graf K, Jamous R, Mückschel M, Bluschke A, Beste C. NeuroImage. Clinical. 2024;44:103677.
DOI: 10.1016/j.nicl.2024.103677 · PubMed
Prochnow A, Zhou X, Ghorbani F, Roessner V, Hommel B, Beste C. General psychiatry. 2024;37(3):e101486.
DOI: 10.1136/gpsych-2023-101486 · PubMed
Pastötter B, Weissbach A, Takacs A, Moyé J, et al.. Brain communications. 2024;6(5):fcae301.
DOI: 10.1093/braincomms/fcae301 · PubMed
Takacs A, Toth-Faber E, Schubert L, Tarnok Z, et al.. Human brain mapping. 2024;45(8):e26719.
DOI: 10.1002/hbm.26719 · PubMed
Takacs A, Toth-Faber E, Schubert L, Tárnok Z, et al.. Brain communications. 2024;6(2):fcae092.
DOI: 10.1093/braincomms/fcae092 · PubMed
Münster ND, Schmalbrock P, Bäumer T, Hommel B, Beste C, Münchau A, Frings C. Acta psychologica. 2024;244:104190.
DOI: 10.1016/j.actpsy.2024.104190 · PubMed
Opitz A, Zimmermann J, Cole DM, Coray RC, et al.. NeuroImage. Clinical. 2024;41:103579.
DOI: 10.1016/j.nicl.2024.103579 · PubMed
Spanagel R, Bach P, Banaschewski T, Beck A, et al.. Addiction biology. 2024;29(7):e13419.
DOI: 10.1111/adb.13419 · PubMed