bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2022.11.28.518250

Despite impaired binocular function, binocular disparity integration across the visual field is spared in normal aging and glaucoma

Maiello, G.·Kwon, M.
View original source ↗Export metadata ↓

Abstract

ObjectiveTo examine how binocularly asymmetric glaucomatous visual field damage affects processing of binocular disparity across the visual field. DesignCase-control study. Participants and ControlsA sample of 18 patients with primary open-angle glaucoma, 16 age-matched controls, and 13 young controls. MethodsParticipants underwent standard clinical assessments of binocular visual acuity, binocular contrast sensitivity, stereoacuity, and perimetry. We employed a previously validated psychophysical procedure to measure how sensitivity to binocular disparity varied across spatial frequencies and visual field sectors, i.e. with full-field stimuli spanning the central 21{degrees} of the visual field, and with stimuli restricted to annular regions spanning 0{degrees}-3{degrees}, 3{degrees}-9{degrees} or 9{degrees}-21{degrees}. Main Outcome MeasuresWe verified the presence of binocularly asymmetric glaucomatous visual field damage by comparing--between the two eyes-- the mean deviation values obtained from the Humphrey Field Analyzer (HFA) 24-2 test. To assess the spatial-frequency tuning of disparity sensitivity across the visual field of patients and controls, we fit disparity sensitivity data to log-parabola models and compared fitted model parameters. Lastly, we employed disparity sensitivity measurements from restricted visual field conditions to model different possible scenarios regarding how disparity information is combined across visual field sectors. We adjudicated between the potential mechanisms by comparing model predictions to the observed patterns of disparity sensitivity with full-field stimuli. ResultsThe interocular difference in HFA 24-2 mean deviation was greater in glaucoma patients compared to both young and age-matched controls (ps=.01). Across participant groups foveal regions preferentially processed disparities at finer spatial scales, whereas periphery regions were tuned for coarser scales (p<.001). Disparity sensitivity also decreased from the fovea to the periphery (p<.001) and across participant groups (ps<.01). Finally, similar to controls, glaucoma patients exhibited near-optimal disparity integration, specifically at low spatial frequencies (p<.001). ConclusionsContrary to the conventional view that glaucoma spares central vision, we find that glaucomatous damage causes a widespread loss of disparity sensitivity across both foveal and peripheral regions. Despite these losses, cortical integration mechanisms appear to be well preserved, suggesting that glaucoma patients make the best possible use of their remaining binocular function.

Explore related subjects

neurosciencePreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Maiello, G., Kwon, M.. 2022-11-30. Despite impaired binocular function, binocular disparity integration across the visual field is spared in normal aging and glaucoma. https://doi.org/10.1101/2022.11.28.518250

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

KEEP EXPLORING

Related preprints

bioRxiv2026

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↗
bioRxiv2026

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↗
bioRxiv2026

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↗