Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.10.30.685574

Non-decision time-informed collapsing threshold diffusion model: A joint modeling framework with identifiable time-dependent parameters

Abstract

Over the past sixty years, evidence accumulation models have emerged as a dominant framework for explaining the neural and behavioral aspects of the process underlying decision making. These models have also been widely used as a measurement instrument to assess individual differences in latent cognitive constructs underlying decision making. A central assumption of most of these models is that decision makers accumulate noisy evidence until a fixed decision threshold is reached. However, both behavioral and neuroscientific findings, along with theoretical considerations related to optimality, have suggested that the decision threshold varies over time. Although time-dependent threshold models often provide a better account of empirical data, a major challenge associated with these models is the unreliable estimation of their parameters. This limitation has led researchers to emphasize model-fitting comparisons rather than interpreting parameter values or accounting for individual differences in the dynamics of the decision threshold. In this work, we address the reliability issue of parameter estimation in time-dependent threshold diffusion models by proposing a joint modeling approach that links non-decision time to external observations. Parameter recovery simulations demonstrate that informing the diffusion model with trial-level noisy measurements of non-decision time substantially improves the reliability of parameter estimation for time-dependent threshold diffusion models. Additionally, we reanalyzed the experimental data from two perceptual decision-making tasks to illustrate the feasibility of the proposed modeling approach. Non-decision time measurements were extracted from electroencephalography (EEG) recordings using the hidden multivariate pattern method. The cognitive modeling results revealed that, in addition to the reliable parameter estimation, constraining non-decision time improves the absolute fit to behavioral data.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Hadian Rasanan, A. H., Schumacher, L., D Nunez, M., Weindel, G., Rieskamp, J.. 2025-10-31. Non-decision time-informed collapsing threshold diffusion model: A joint modeling framework with identifiable time-dependent parameters. https://doi.org/10.1101/2025.10.30.685574

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↗