Activation-Guided Neuron Intervention to Induce Alzheimer's-Related Computational Language Phenotypes in a Large Language Model

• URL: http://arxiv.org/abs/2608.03067v2
• Date: Wed, 05 Aug 2026 18:56:48 GMT
• Title: Activation-Guided Neuron Intervention to Induce Alzheimer's-Related Computational Language Phenotypes in a Large Language Model
• Abstract summary: Changes in spontaneous speech provide an early signal of cognitive dysfunction in Alzheimer's disease.<n>We introduce an activation-guided intervention framework using Qwen3-8B.<n>Amplifying AD-associated neurons produced graded impairments in story recall, verbal fluency, working memory, procedural discourse, scene construction, and coreference resolution.
• Score: 11.44806025415537
• License: http://creativecommons.org/licenses/by-nc-sa/4.0/
• Abstract: Changes in spontaneous speech provide an early signal of cognitive dysfunction in Alzheimer's disease (AD) that large language models (LLMs) can detect. However, detection alone cannot establish whether the underlying model representations contribute functionally to behavior. We introduce an activation-guided intervention framework using Qwen3-8B. The framework identifies feed-forward neurons with higher activation rates for AD than control transcripts and modulates their output contributions during generation by scaling the corresponding down-projection weights. This yielded nine edited variants differing in intervention direction, magnitude, and scope. The original and edited models completed the same 12-turn neuropsychological battery, assessed through blinded human ratings and computational linguistic measures. Amplifying AD-associated neurons produced graded impairments in story recall, verbal fluency, working memory, procedural discourse, scene construction, and coreference resolution. Attenuation largely preserved performance and selectively improved several outcomes. Amplification also reduced lexical surprisal, idea density, syntactic complexity, and discourse quantity, broadly paralleling changes reported in human AD speech. These findings show that neurons identified solely from clinical language differences can influence behavior across multiple cognitive domains, providing proof of concept for an AD-related computational phenotype and a controlled framework for experimentally examining links between language and broader cognitive dysfunction.

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