Search bioRxiv⌕ Search

bioRxiv · 10.1101/2021.04.12.439570

An enhanced Bouma model fits a hundred people's visual crowding

Abstract

AbstractCrowding is the failure to recognize an object due to surrounding clutter. Our visual crowding survey measured 13 crowding distances (or "critical spacings") twice in each of 50 observers. The survey included three eccentricities (0, 5, and 10 deg), four cardinal meridians, two orientations (radial and tangential), and two fonts (Sloan and Pelli). The survey also tested foveal acuity, twice. Remarkably, fitting a two-parameter model, the well- known Bouma law -- crowding distance grows linearly with eccentricity -- explains 82% of the variance for all 13 x 50 measured log crowding distances, cross-validated. An enhanced Bouma law, with factors for meridian, crowding orientation, target kind, and observer, explains 94% of the variance, again cross-validated. These additional factors reveal several asymmetries, consistent with previous reports, which can be expressed as crowding- distance ratios: 0.62 horizontal:vertical, 0.79 lower:upper, 0.78 right:left, 0.55 tangential:radial, and 0.78 Sloan font:Pelli font. Across our observers, peripheral crowding is independent of foveal crowding and acuity. Evaluation of the Bouma factor b (the slope of the Bouma law) as a biomarker of visual health would be easier if there were a way to compare results across crowding studies that use different methods. We define a standardized Bouma factor b that corrects for differences from Boumas 25 choice alternatives, 75% threshold criterion, and linearly symmetric flanker placement. For radial crowding on the right meridian, the standardized Bouma factor b is 0.24 for this study, 0.35 for Bouma (1970), and 0.30 for the geometric mean across five representative modern studies, including this one, showing good agreement across labs, including Boumas. We found that guaranteeing fixation by gaze-contingent display halved the standard deviation across observers of the estimated log b. The reduction in standard deviation is explained by a "peeking" model in which the observer looked near an anticipated target location in 50% of unmonitored-fixation trials. Individual differences are robust, as evidenced by the much larger 0.08 SD of log b across observers than the 0.03 SD of test-retest within observers. Crowdings ease of measurement enhances its promise as a biomarker for dyslexia and visual health.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Kurzawski, J. W., Burchell, A., Thapa, D., Majaj, N. J., Winawer, J. A., Pelli, D. G.. 2021-04-14. An enhanced Bouma model fits a hundred people's visual crowding. https://doi.org/10.1101/2021.04.12.439570

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The Unreasonable Effectiveness of Cell Types in Describing Neuronal Physiological Features

Single-cell RNA sequencing (scRNA-seq) captures detailed gene expression profiles at scale, while patch-clamp recordings measure intrinsic neuronal electrophysiological properties. Modeling the relations between these two modalities remains a challenge. Here, we compare how well electrophysiological features can be predicted by traditional transcriptomic cell type classification, representations derived from a foundational model (scGPT) pretrained on large-scale scRNA-seq datasets, ion channel-coding genes, and highly variable genes. Using paired transcriptomic and electrophysiological patch-sequencing data from 495 human neurons from neurosurgical tissue, we find that cluster-level cell type representations consistently outperform highly variable gene selection, ion channel gene selection, and context-enriched scGPT embeddings. Notably, performance varies across model architectures and initializations, and the best results are obtained by combining the outputs of separate cell type and scGPT-based models. Together, these findings suggest that traditional discrete cellular classification is highly effective in predicting physiological features. For maximum performance it can be complemented by pretrained transformer models.

neuroscience↗

A nonlinear inhibition pathway underlying cortical responses to tuned holographic optogenetic perturbations

Optogenetics enables causal manipulation of cortical activity. Perturbation responses can be counterintuitive due to network interactions, making theory essential for predicting them. Existing approaches often rely on linear approximations, which fail for many biologically relevant perturbations. Here we develop a nonlinear theory of responses to holographic perturbations in cell-type-specific recurrent networks with structured connectivity. We fit a nonlinear model to mouse V1 data, which shows cotuned-ensemble suppression: perturbing spatially clustered neurons with similar preferred orientations yields markedly stronger short-range suppression than perturbing untuned ensembles. We show that cotuned-ensemble suppression arises from a feature-tuned, nonlinear inhibition pathway implicating somatostatin-positive (SST) interneurons. The theory predicts that cotuned ensembles suppress parvalbumin-positive (PV) neurons but facilitate SST neurons, and links the degree of cotuned-ensemble suppression or facilitation to the variance of the SST response. This framework identifies mechanisms by which nonlinear inhibition sculpts cortical dynamics and establishes a predictive basis for targeted optogenetic interventions.

neuroscience↗

Proteomic signatures of APOE ε4 across human tissues and cell types in Alzheimers disease

The apolipoprotein E {varepsilon}4 (APOE {varepsilon}4) allele is the strongest genetic risk factor for late-onset Alzheimers disease (AD). However, the underlying molecular mechanisms remain unclear. This study included 1691 participants from the Religious Orders Study and Rush Memory and Aging Project (ROSMAP), 1226 participants from the Accelerating Medicines Partnership - Alzheimers Disease (AMP-AD) Diverse Cohorts Study, and 735 participants from the Alzheimers Disease Neuroimaging Initiative (ADNI). To characterise APOE {varepsilon}4 molecular effects, we analysed proteomic data from plasma, cerebrospinal fluid (CSF), and induced pluripotent stem cell (iPSC)-derived astrocytes and neurons, as well as transcriptomic and proteomic data from multiple brain regions. The association of APOE {varepsilon}4 with AD neuropathology was also examined. APOE {varepsilon}4 carriers shared a plasma proteomic signature enriched for immune processes, irrespective of AD diagnosis. A machine learning classifier trained on this signature discriminated APOE {varepsilon}4 carriers from non-carriers in an independent cohort using CSF proteomics. APOE {varepsilon}4 carriage was associated with higher Braak stages and Consortium to Establish a Registry for Alzheimers Disease (CERAD) score. However, only limited APOE {varepsilon}4-associated transcriptomic and proteomic changes were observed in bulk brain tissue, with poor cross-layer concordance. Proteomic analyses of iPSC-derived astrocytes and neurons further revealed cell-type-specific APOE {varepsilon}4-associated changes. APOE {varepsilon}4 is associated with a consistent proteomic signature across plasma and CSF. Its molecular effects in the brain differ across cell types, brain regions and molecular layers. These findings support the need for cell-type-resolved multi-omic studies to elucidate how APOE {varepsilon}4 confers AD risk.

neuroscience↗