A year in research · 25 selected publications · five research threads
In 2015, we asked how people organize several actions at once and identified the strategies, brain systems and individual differences that make this possible.
Rather than treating multitasking as a single capacity, the work distinguished serial and parallel goal activation, sensory integration, response selection and monitoring.
01 · STRATEGY
Causal stimulation showed that right inferior frontal cortex helps implement strategies for multi-component behaviour by altering response selection.[1] People differed in their preferred serial or overlapping style yet adapted that style similarly when the situation changed.[2] Conscientiousness explained a substantial share of efficiency differences, suggesting that strategy is linked to stable personal characteristics.[3]
Action-video-game players were faster at action cascading without showing better inhibition, separating multi-component coordination from stopping ability.[4] Mental fatigue likewise evolved from early adaptation into more specific response-selection changes over time.[5]
In plain terms: Multitasking performance reflects how goals are scheduled and selected, not one generic executive resource.
02 · DISTRIBUTED SYSTEMS
More parallel dual-task response selection relied on striatum, whereas more serial selection recruited lateral prefrontal cortex.[6] Anticipated sensorimotor transformations engaged caudate mechanisms, and circumscribed medium-spiny-neuron dysfunction impaired cascading when responses competed simultaneously.[7,8] Computational modelling of Huntington's disease pointed to combined direct- and indirect-pathway lesions, rather than dopamine change alone, as a source of learning difficulty.[9]
Deep brain stimulation of external globus pallidus improved response monitoring in Huntington's disease.[10] Resting connectivity and striatal GABA described two partly separate routes to cognitive-control differences, while striatal GABA also predicted premotor inhibition and its cortical synchronization.[11,12]
In plain terms: Parallel and serial action organization draw on complementary cortico-striatal mechanisms whose contribution depends on competition and predictability.
03 · SENSORY AND BODILY INPUT
Auditory and visual targets could evoke parallel brain responses, limiting the idea of a universal attentional bottleneck.[13] Bimodal versus unimodal input changed how task goals were formed during action cascading.[14] Proprioceptive information also interacted differently with striatal and thalamic GABA during response selection.[15]
Response selection in multidimensional space varied across stimulus dimensions only when selection demands were high.[16] Left dominance for written language appeared already in extrastriate and parietal processing.[17] Handedness was associated with androgen-receptor repeat length, adding a biological source of individual lateralization.[18]
In plain terms: The sensory modality, body state and spatial dimension of information shape how competing actions are selected.
04 · LIMITS AND ERROR
Working-memory load changed the evaluative P3 component of inhibition and impaired behaviour only after a threshold was exceeded.[19] In neurosarcoidosis, fatigue was associated with altered conflict monitoring rather than a nonspecific loss of cognition.[20] A broader synthesis treated errors as outputs of interacting perceptual, decision and motor processes that can be used to predict later adaptation.[21]
Adolescents and adults differed in how predictability shaped conflict monitoring, demonstrating that context-action links continue to develop.[22]
In plain terms: Failure becomes interpretable when workload, prediction and the specific processing stage are measured together.
05 · CLINICAL TRANSLATION
In premanifest Huntington's disease, attentional selection declined while some neural-plasticity effects were enhanced, showing that neurodegeneration can have divergent cognitive consequences.[23] A review of autism organized action-control findings around neurobiology and the use of prior experience.[24]
For Tourette syndrome, neurofeedback was proposed as a targeted option, particularly when ADHD comorbidity contributes to control difficulties.[25] Across these areas, translation depended on matching intervention to a defined circuit and operation.
In plain terms: Treatments become more credible when they target a specified mechanism rather than a broad diagnostic label.
The 2015 work described multi-component action as an architecture of strategies and interacting systems. It showed how striatum, prefrontal cortex, sensory input and personality jointly determine whether several goals can be coordinated efficiently.
Curated from PubMed records returned for Beste C[au] in 2015. Citation numbers in the story link to entries below. DOI links open the publisher landing page; PubMed links open the indexed record.
Dippel G, Beste C. Nature communications. 2015;6:6587.
DOI: 10.1038/ncomms7587 · PubMed
Mückschel M, Stock AK, Beste C. Scientific reports. 2015;5:9992.
DOI: 10.1038/srep09992 · PubMed
Stock AK, Beste C. Scientific reports. 2015;5:15731.
DOI: 10.1038/srep15731 · PubMed
Steenbergen L, Sellaro R, Stock AK, Beste C, Colzato LS. PloS one. 2015;10(12):e0144364.
DOI: 10.1371/journal.pone.0144364 · PubMed
Möckel T, Beste C, Wascher E. Scientific reports. 2015;5:10113.
DOI: 10.1038/srep10113 · PubMed
Yildiz A, Beste C. Brain structure & function. 2015;220(6):3131-42.
DOI: 10.1007/s00429-014-0847-0 · PubMed
Stock AK, Ness V, Beste C. NeuroImage. 2015;123:33-41.
DOI: 10.1016/j.neuroimage.2015.08.036 · PubMed
Beste C, Saft C. Brain structure & function. 2015;220(1):221-8.
DOI: 10.1007/s00429-013-0649-9 · PubMed
Schroll H, Beste C, Hamker FH. The European journal of neuroscience. 2015;41(9):1227-44.
DOI: 10.1111/ejn.12868 · PubMed
Beste C, Mückschel M, Elben S, J Hartmann C, et al.. Brain structure & function. 2015;220(4):2441-8.
DOI: 10.1007/s00429-014-0805-x · PubMed
Haag L, Quetscher C, Dharmadhikari S, Dydak U, Schmidt-Wilcke T, Beste C. Human brain mapping. 2015;36(11):4383-93.
DOI: 10.1002/hbm.22920 · PubMed
Quetscher C, Yildiz A, Dharmadhikari S, Glaubitz B, Schmidt-Wilcke T, Dydak U, Beste C. Brain structure & function. 2015;220(6):3555-64.
DOI: 10.1007/s00429-014-0873-y · PubMed
Finoia P, Mitchell DJ, Hauk O, Beste C, Pizzella V, Duncan J. Journal of neurophysiology. 2015;114(2):1239-47.
DOI: 10.1152/jn.01050.2014 · PubMed
Gohil K, Stock AK, Beste C. Scientific reports. 2015;5:9485.
DOI: 10.1038/srep09485 · PubMed
Dharmadhikari S, Ma R, Yeh CL, Stock AK, et al.. NeuroImage. 2015;120:36-42.
DOI: 10.1016/j.neuroimage.2015.06.066 · PubMed
Mückschel M, Beste C. Scientific reports. 2015;5:7759.
DOI: 10.1038/srep07759 · PubMed
Selpien H, Siebert C, Genc E, Beste C, Faustmann PM, Güntürkün O, Ocklenburg S. Behavioural brain research. 2015;291:325-333.
DOI: 10.1016/j.bbr.2015.05.050 · PubMed
Arning L, Ocklenburg S, Schulz S, Ness V, et al.. Scientific reports. 2015;5:8325.
DOI: 10.1038/srep08325 · PubMed
Chmielewski WX, Mückschel M, Stock AK, Beste C. NeuroImage. 2015;112:96-104.
DOI: 10.1016/j.neuroimage.2015.02.060 · PubMed
Beste C, Kneiphof J, Woitalla D. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 2015;25(4):522-30.
DOI: 10.1016/j.euroneuro.2015.01.012 · PubMed
Hoffmann S, Beste C. Frontiers in behavioral neuroscience. 2015;9:50.
DOI: 10.3389/fnbeh.2015.00050 · PubMed
Chmielewski WX, Roessner V, Beste C. Behavioural brain research. 2015;292:10-8.
DOI: 10.1016/j.bbr.2015.05.054 · PubMed
Beste C, Stock AK, Ness V, Hoffmann R, Saft C. Brain structure & function. 2015;220(3):1437-47.
DOI: 10.1007/s00429-014-0735-7 · PubMed
Chmielewski WX, Beste C. Progress in neurobiology. 2015;124:49-83.
DOI: 10.1016/j.pneurobio.2014.11.002 · PubMed
Farkas A, Bluschke A, Roessner V, Beste C. Neuroscience and biobehavioral reviews. 2015;51:87-99.
DOI: 10.1016/j.neubiorev.2015.01.012 · PubMed