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.
Reward models (RMs) play a central role in aligning large language models (LLMs) with human preferences. However, RMs are often sensitive to spurious features such as response length. Existing inference-time approaches for mitigating these biases typically focus exclusively on response length, resulting in performance trade-offs. In this paper, we propose causally motivated intervention for mitigating multiple types of biases in RMs at inference time. Our method first identifies neurons whose activations are strongly correlated with predefined bias attributes, and applies neuron-level intervention that suppresses these signals. We evaluate our method on RM benchmarks and observe reductions in sensitivity to spurious features across diverse bias types, without inducing performance trade-offs. Moreover, when used for preference annotation, small RMs (2B and 7B) with our method, which edits less than 2% of all the neurons in RMs, enable LLMs to improve alignment, achieving performance comparable to that of a state-of-the-art 70B RM on AlpacaEval and MT-Bench. Further analysis reveals that bias signals are primarily encoded by neurons in early layers, shedding light on the internal mechanisms of bias exploitation in RMs.