The theoretical backdrop for the study is arousal-biased competition theory, developed by Mara Mather and Mary Sutherland and colleagues. According to this framework, arousal increases the competitive advantage of whatever information already dominates mental processing. If a person is focused narrowly on a specific location, arousal should further strengthen that narrow focus; if attention is broadly distributed, arousal should broaden it further. The theory draws on neuroscientific work suggesting that norepinephrine, released by the locus coeruleus during states of heightened arousal, ignites local hotspots of neuronal excitation that amplify the most active representations while suppressing weaker competitors. Earlier experiments had reported that arousal amplifies selectivity in perception and memory, and classic studies from the 1950s through the 1970s, including work by John Easterbrook on cue utilization and by Donald Cornsweet on peripheral cues under arousal, had suggested that stress and noise narrow the useful field of view.

Kolnes and Nieuwenhuis set out to test this amplification hypothesis directly for the spatial dimension of attention. Thirty-nine participants performed a visual search task specifically designed to measure the breadth of attention across the visual field. The critical manipulation involved tonic arousal, the relatively stable background level of physiological activation that fluctuates over minutes rather than seconds. In half of the experimental blocks, continuous auditory white noise was played to participants, a well-established method for raising tonic arousal without startling them or triggering phasic alerting responses. The researchers reasoned that if arousal genuinely amplifies the dominant attentional scope, then the difference in search performance between narrow-attention and broad-attention conditions should grow larger under noise than under quiet conditions.

Before each trial, the experimenters used a procedure intended to induce either a narrow or a broad breadth of attention. This manipulation of attentional scope is central to the design, because the amplification hypothesis makes a specific prediction: arousal should not change the baseline scope itself, but should exaggerate whatever scope is currently dominant. The team also drew on their own earlier findings, including a 2023 study showing that broadening attention dilates the pupil, suggesting a close relationship between attentional breadth and the autonomic arousal system. That relationship made the null result they ultimately obtained all the more theoretically pointed, since it indicates that the coupling between arousal physiology and attentional breadth does not translate into arousal-driven amplification of scope.

A crucial strength of the study lies in its manipulation checks. The researchers measured pupil size continuously, exploiting the well-documented link between pupil diameter and locus coeruleus-norepinephrine activity. Pupil measurements confirmed that the white-noise manipulation successfully raised tonic arousal, and task performance confirmed that the scope-induction procedure successfully shifted the breadth of attention between narrow and broad states. In other words, the experiment was not undermined by failed manipulations. Both arousal and attentional scope were demonstrably altered, yet the predicted interaction between them simply did not appear. The effect of attentional breadth on visual search remained statistically indistinguishable between high-arousal and low-arousal blocks.

The analysis relied on Bayesian statistical methods, which allow researchers to quantify evidence in favor of a null hypothesis rather than merely failing to reject it. The authors report strong Bayesian evidence against an amplifying effect of arousal on the dominant attentional scope. This distinction matters in the ongoing debate about replication and statistical practice in psychology, where nonsignificant p-values are often ambiguous. A Bayes factor indicating strong support for the null hypothesis means the data actively favor the absence of an amplification effect, not simply that the study lacked power. The researchers also used mixed-effects models with maximal random effects structures, following methodological recommendations for confirmatory hypothesis testing, and conducted simulation-based power analyses to ensure the design was sensitive enough to detect a plausible amplification effect if one existed.

The null result is not without precedent. Ásgeirsson and Nieuwenhuis had previously reported no arousal-biased competition in focused visuospatial attention in a 2017 study published in Cognition, and a 2019 follow-up examining attention and short-term memory produced similarly mixed support for the theory. The new findings extend this line of work by showing that even when both arousal and attentional scope are successfully manipulated and verified through physiological and behavioral measures, the amplification predicted by arousal-biased competition theory fails to materialize for spatial attention. This convergence across independent experiments and paradigms suggests that the earlier classic findings of arousal-induced narrowing, such as those from noise studies in the 1970s, may reflect mechanisms other than amplification of dominant attentional scope, such as changes in response bias, strategy, or the relative salience of stimuli.

The authors discuss the implications for arousal-biased competition theory in measured terms. The theory remains influential and has generated a large body of research on how emotion and arousal shape perception and memory, including findings that emotional arousal strengthens high-priority memory traces while weakening low-priority ones. However, the present results suggest that the amplification principle may not generalize to the spatial scaling of attention. Alternative accounts of arousal’s effects, including models emphasizing adaptive regulation of arousal and the inverted-U relationship described by the Yerkes-Dodson law, may better accommodate the full pattern of findings. Recent work on pharmacologically shifting the peak of the Yerkes-Dodson curve through catecholaminergic enhancement indicates that arousal’s effects on cognition are complex and state-dependent, defying simple amplification rules.

For everyday intuition, the study suggests that being stressed, caffeinated, or startled does not automatically zoom your mental spotlight further in or out. The spatial distribution of attention appears to be governed by its own control mechanisms, relatively insulated from the background hum of bodily arousal. This dissociation has practical implications for domains ranging from driving safety to sports performance and the design of warning systems, where it is often assumed that high arousal inevitably produces tunnel vision. The evidence here indicates that assumption is too simple. The study was not preregistered, a limitation the authors acknowledge, but subject-level data and analysis code are openly available in the Open Science Framework repository, allowing other researchers to scrutinize and extend the findings. Funded by the Estonian Research Council and the Dutch Research Council, the work exemplifies how careful manipulation checks, physiological validation, and Bayesian inference can turn an apparently negative result into a substantive theoretical contribution about how attention and arousal are, and are not, connected.

Subject of Research: Whether tonic arousal modulates the spatial scope of visual attention

Article Title: Arousal does not enhance the dominant spatial scope of attention

Article References: Kolnes, M., & Nieuwenhuis, S. (2026). Arousal does not enhance the dominant spatial scope of attention. Attention, Perception, & Psychophysics, 88(7), Article 184. https://doi.org/10.3758/s13414-026-03327-3

Image Credits: AI Generated

DOI: 10.3758/s13414-026-03327-3

Keywords: arousal, attentional scope, visual attention, arousal-biased competition, pupil size, norepinephrine, visual search, Bayesian inference, psychophysics, locus coeruleus, breadth of attention, tonic arousal

The research, led by Bernard Mulvey, Heena R. Divecha, and colleagues at the Lieber Institute for Brain Development working with collaborators at Johns Hopkins and the University of Cambridge, applied spatially resolved transcriptomics, a technique that maps gene expression across intact tissue sections while preserving information about where each gene is active, to postmortem locus coeruleus tissue from 33 neurotypical middle-aged human brain donors. Crucially, the donors were stratified by major Alzheimer’s disease risk factors, including biological sex, African or European genetic ancestry, and apolipoprotein E haplotype, specifically carriers of the APOE E4 allele, which raises disease risk, versus carriers of the APOE E2 allele, which appears protective. This design allowed the investigators to ask a subtle but important question: do the genes expressed in and around the locus coeruleus already differ, in healthy middle age, depending on which Alzheimer’s risk variants a person carries?

The answer, in several respects, is yes, and the details are illuminating. When the researchers compared gene expression patterns across APOE haplotypes, they found reduced expression of astrocytic genes, meaning genes characteristically active in star-shaped support cells called astrocytes, in the tissue immediately surrounding locus coeruleus neurons in E4 carriers. Astrocytes are far more than passive glue; they regulate synapse formation, supply neurons with cholesterol and metabolic support, control local blood flow, buffer neurotransmitters, and respond to norepinephrine signaling from the locus coeruleus itself. A diminishment of astrocytic gene expression near these noradrenergic neurons suggests that E4 carriers may have subtly weakened local support infrastructure around one of the brain’s most Alzheimer’s-vulnerable cell populations, potentially lowering the threshold at which tau pathology or other stresses become damaging.

The study also uncovered ancestry-specific differences in locus coeruleus gene expression, a finding with real public health significance given well-documented disparities in dementia incidence and outcomes across populations. Follow-up analyses using in situ sequencing at single-cell resolution demonstrated that the APOE-related differences in regional gene expression were partly attributable to astrocytes themselves, and that the haplotype effects were more pronounced in donors of European ancestry. This interaction between genetic ancestry and APOE haplotype echoes earlier work showing that the relationship between APOE E4 and Alzheimer’s pathology differs across admixed populations, and it underscores the importance of including ancestrally diverse cohorts in neuroscience research rather than extrapolating from studies of predominantly European-ancestry subjects.

Perhaps the most visually and conceptually striking component of the study concerns neuromelanin, the dark pigment that gives the locus coeruleus its name, which means “blue spot” in Latin. Neuromelanin accumulates in certain catecholaminergic neurons, including the noradrenergic neurons of the locus coeruleus and the dopaminergic neurons of the substantia nigra, as a byproduct of oxidative metabolism of neurotransmitters. It is sequestered within specialized autolysosomal organelles that bind potentially toxic metals such as iron, and its loss from these neurons is a hallmark of both Alzheimer’s and Parkinson’s disease. Neuromelanin-sensitive magnetic resonance imaging has emerged as a promising biomarker, with reduced pigment signal in the locus coeruleus predicting clinical severity and future progression in Alzheimer’s patients. What has remained unclear is the precise molecular relationship between a neuron’s pigment content and its gene expression program.

To address this, the team quantified neuromelanin content directly in the tissue and related it to spatial gene expression. They found that higher APOE gene expression correlated with reduced neuromelanin, and that genes whose expression tracked with local pigment levels were enriched for aging-related biological pathways. Taking the analysis to its finest resolution, the investigators used in situ sequencing data to examine individual locus coeruleus neurons, measuring neuromelanin in each cell and validating its associations with the expression of APOE itself, genes involved in norepinephrine metabolism, and components of the autophagy machinery, the cellular recycling system that clears damaged proteins and organelles. This constellation of pigment-linked genes paints a coherent picture: neuromelanin content reflects, at the single-cell level, the interplay of neurotransmitter handling, lipid biology, and protein quality control, all processes implicated in neurodegeneration.

The significance of these findings is best appreciated against the backdrop of what is already known about the locus coeruleus in Alzheimer’s disease. Postmortem studies stretching back decades, including the classic staging work of Heiko Braak and colleagues, established that phosphorylated tau appears in locus coeruleus neurons exceptionally early, often in individuals who died with no cognitive impairment. Autopsy studies have documented substantial neuronal loss in this nucleus in mild cognitive impairment and early Alzheimer’s disease, and neuroimaging research has repeatedly linked reduced locus coeruleus integrity to tau burden, memory decline, neuropsychiatric symptoms, and sleep disruption. Animal work has shown, conversely, that noradrenergic depletion exaggerates the inflammatory response to amyloid-beta pathology, while pharmacological enhancement of norepinephrine signaling can suppress neuroinflammation. The locus coeruleus, in other words, is not merely a passive victim of Alzheimer’s pathology; its noradrenergic output actively modulates the brain’s response to it.

The new study adds two crucial molecular threads to this narrative. First, it demonstrates that Alzheimer’s genetic risk acts on the locus coeruleus ecosystem, not just on its neurons in isolation. The astrocytic deficit observed near E4-carrier neurons is particularly intriguing in light of recent evidence that norepinephrine signals through astrocytes to modulate synaptic function, and that astrocytes undergo stereotyped transcriptomic changes across the spatiotemporal progression of Alzheimer’s disease. If E4 carriers begin adulthood with less robust astrocytic support around their noradrenergic neurons, this could help explain why these neurons succumb early, and why E4 homozygosity has recently been characterized as a distinct, nearly deterministic genetic form of Alzheimer’s disease. Second, by tying neuromelanin, a biomarker measurable in living patients with specialized MRI, to concrete gene expression programs involving autophagy and catecholamine metabolism, the study strengthens the mechanistic bridge between what clinicians can image and what is happening molecularly inside vulnerable neurons.

Technically, the study represents a tour de force of modern spatial genomics applied to a notoriously difficult brain region. The locus coeruleus is small, deeply located in the dorsal pons, and densely pigmented, making it easy to miss in standard postmortem dissection and challenging to analyze with conventional bulk methods that average away spatial relationships. The team’s spatially resolved transcriptomics data captured tissue architecture at spot-level resolution, while their in situ sequencing pushed the analysis to individual cells, using the pigment itself as an additional segmentation cue to define neuromelanin-rich cellular compartments. The authors have deposited all data in public repositories and built interactive web portals, using visualization tools such as Samui and spatialLIBD, allowing any researcher to explore the spatial domain assignments, gene expression maps, and stained tissue sections, an unusually transparent approach that should accelerate follow-up work across the field.

The implications reach toward prevention and early detection. Because the donors in this study were neurotypical and middle-aged, the observed molecular differences, diminished astrocytic gene expression in E4 carriers, ancestry-dependent expression patterns, pigment-linked autophagy and norepinephrine genes, represent the brain’s baseline state before overt pathology, a snapshot of vulnerability rather than of damage. Interventions aimed at supporting astrocytic function, enhancing autophagic clearance of tau, or modulating noradrenergic tone might therefore be most effective when targeted at these early molecular states rather than at established dementia. Meanwhile, the confirmation that APOE expression itself inversely tracks neuromelanin suggests that pigment imaging could serve not only as a marker of neuronal loss but as a window into the lipid-handling pathways that connect APOE biology to neurodegeneration. As the authors conclude, Alzheimer’s risk factors appear to modulate locus coeruleus vulnerability through molecular processes intrinsic to both the noradrenergic neurons and their astrocytic partners, a reminder that the neurons that wake us, focus us, and help us remember may hold some of the earliest clues to when and how Alzheimer’s disease takes hold.