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Jichen Zheng

Publications and source records attributed to Jichen Zheng.

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Component-Level Lesioning of Language Models Reveals Clinically Aligned Aphasia Phenotypes

Large language models (LLMs) increasingly exhibit human-like linguistic behaviors and internal representations that they could serve as computational simulators of language cognition. We ask whether LLMs can be systematically manipulated to reproduce language-production impairments characteristic of aphasia following focal brain lesions. Such models could provide scalable proxies for testing rehabilitation hypotheses, and offer a controlled framework for probing the functional organization of language. We introduce a clinically grounded, component-level framework that simulates aphasia by selectively perturbing functional components in LLMs, and apply it to both modular Mixture-of-Experts models and dense Transformers using a unified intervention interface. Our pipeline (i) identifies subtype-linked components for Broca's and Wernicke's aphasia, (ii) interprets these components with linguistic probing tasks, and (iii) induces graded impairments by progressively perturbing the top-k subtype-linked components, evaluating outcomes with Western Aphasia Battery (WAB) subtests summarized by Aphasia Quotient (AQ). Across architectures and lesioning strategies, subtype-targeted perturbations yield more systematic, aphasia-like regressions than size-matched random perturbations, and MoE modularity supports more localized and interpretable phenotype-to-component mappings. These findings suggest that modular LLMs, combined with clinically informed component perturbations, provide a promising platform for simulating aphasic language production and studying how distinct language functions degrade under targeted disruptions.

cs.CL

Bridging Brains and Models: MoE-Based Functional Lesions for Simulating and Rehabilitating Aphasia

The striking alignment between large language models (LLMs) and human brain activity positions them as powerful models of healthy cognition. This parallel raises a fundamental question: if LLMs can model the intact brain, can we lesion them to simulate the linguistic deficits of the injured brain? In this work, we introduce a methodology to model aphasia - a complex language disorder caused by neural injury - by selectively disabling components in a modular Mixture-of-Experts (MoE) language model. We simulate distinct aphasia subtypes, validate their linguistic outputs against real patient speech, and then investigate functional recovery by retraining the model's remaining healthy experts. Our results demonstrate that lesioning functionally-specialized experts for syntax or semantics induces distinct impairments that closely resemble Broca's and Wernicke's aphasia, respectively. Crucially, we show that freezing the damaged experts and retraining the intact ones on conversational data restores significant linguistic function, demonstrating a computational analogue for rehabilitation. These findings establish modular LLMs as a powerful and clinically-relevant potential framework for modeling the mechanisms of language disorders and for computationally exploring novel pathways for therapy.

q-bio.NC