Abstract:Although mechanism-based interpretability has generated an abundance of insight for discriminative network analysis, generative models are less understood -- particularly outside of image-related applications. We investigate how much of the causal circuitry found within image-related variational autoencoders (VAEs) will generalize to tabular data, as VAEs are increasingly used for imputation, anomaly detection, and synthetic data generation. In addition to extending a four-level causal intervention framework to four tabular and one image benchmark across five different VAE architectures (with 75 individual training runs per architecture and three random seed values for each run), this paper introduces three new techniques: posterior-calibration of Causal Effect Strength (CES), path-specific activation patching, and Feature-Group Disentanglement (FGD). The results from our experiments demonstrate that: (i) Tabular VAEs have circuits with modularity that is approximately 50% lower than their image counterparts. (ii) $β$-VAE experiences nearly complete collapse in CES scores when applied to heterogeneous tabular features (0.043 CES score for tabular data compared to 0.133 CES score for images), which can be directly attributed to reconstruction quality degradation (r = -0.886 correlation coefficient between CES and MSE). (iii) CES successfully captures nine of eleven statistically significant architecture differences using Holm--Šidák corrections. (iv) Interventions with high specificity predict the highest downstream AUC values (r = 0.460, p < .001). This study challenges the common assumption that architectural guidance from image-related studies can be transferred to tabular datasets.
Abstract:Extreme neural network sparsification (90% activation reduction) presents a critical challenge for mechanistic interpretability: understanding whether interpretable features survive aggressive compression. This work investigates feature survival under severe capacity constraints in hybrid Variational Autoencoder--Sparse Autoencoder (VAE-SAE) architectures. We introduce an adaptive sparsity scheduling framework that progressively reduces active neurons from 500 to 50 over 50 training epochs, and provide empirical evidence for fundamental limits of the sparsification-interpretability relationship. Testing across two benchmark datasets -- dSprites and Shapes3D -- with both Top-k and L1 sparsification methods, our key finding reveals a pervasive paradox: while global representation quality (measured by Mutual Information Gap) remains stable, local feature interpretability collapses systematically. Under Top-k sparsification, dead neuron rates reach $34.4\pm0.9\%$ on dSprites and $62.7\pm1.3\%$ on Shapes3D at k=50. L1 regularization -- a fundamentally different "soft constraint" paradigm -- produces equal or worse collapse: $41.7\pm4.4\%$ on dSprites and $90.6\pm0.5\%$ on Shapes3D. Extended training for 100 additional epochs fails to recover dead neurons, and the collapse pattern is robust across all tested threshold definitions. Critically, the collapse scales with dataset complexity: Shapes3D (RGB, 6 factors) shows $1.8\times$ more dead neurons than dSprites (grayscale, 5 factors) under Top-k and $2.2\times$ under L1. These findings establish that interpretability collapse under sparsification is intrinsic to the compression process rather than an artifact of any particular algorithm, training duration, or threshold choice.
Abstract:Mechanistic interpretability of deep learning models has emerged as a crucial research direction for understanding the functioning of neural networks. While significant progress has been made in interpreting discriminative models like transformers, understanding generative models such as Variational Autoencoders (VAEs) remains challenging. This paper introduces a comprehensive causal intervention framework for mechanistic interpretability of VAEs. We develop techniques to identify and analyze "circuit motifs" in VAEs, examining how semantic factors are encoded, processed, and disentangled through the network layers. Our approach uses targeted interventions at different levels: input manipulations, latent space perturbations, activation patching, and causal mediation analysis. We apply our framework to both synthetic datasets with known causal relationships and standard disentanglement benchmarks. Results show that our interventions can successfully isolate functional circuits, map computational graphs to causal graphs of semantic factors, and distinguish between polysemantic and monosemantic units. Furthermore, we introduce metrics for causal effect strength, intervention specificity, and circuit modularity that quantify the interpretability of VAE components. Experimental results demonstrate clear differences between VAE variants, with FactorVAE achieving higher disentanglement scores (0.084) and effect strengths (mean 4.59) compared to standard VAE (0.064, 3.99) and Beta-VAE (0.051, 3.43). Our framework advances the mechanistic understanding of generative models and provides tools for more transparent and controllable VAE architectures.
Abstract:In medical imaging, anomaly detection is a vital element of healthcare diagnostics, especially for neurological conditions which can be life-threatening. Conventional deterministic methods often fall short when it comes to capturing the inherent uncertainty of anomaly detection tasks. This paper introduces a Bayesian Variational Autoencoder (VAE) equipped with multi-head attention mechanisms for detecting anomalies in brain magnetic resonance imaging (MRI). For the purpose of improving anomaly detection performance, we incorporate both epistemic and aleatoric uncertainty estimation through Bayesian inference. The model was tested on the BraTS2020 dataset, and the findings were a 0.83 ROC AUC and a 0.83 PR AUC. The data in our paper suggests that modeling uncertainty is an essential component of anomaly detection, enhancing both performance and interpretability and providing confidence estimates, as well as anomaly predictions, for clinicians to leverage in making medical decisions.