Can Language Models Get "Aphasia" From Neuronal Ablation?

Overview & Synopsis

Progressive neuronal loss is the hallmark of neurodegenerative disease, yet how loss of neurons shapes the pattern of cognitive decline remains poorly understood. Here we systematically ablate neurons (computational units) in language models spanning recurrent long short-term memory (LSTM) and Transformer architectures and apply limited fine-tuning as a simple proxy for compensatory plasticity. With whole-unit ablation, LSTMs degrade gradually with syntactic and semantic faculties declining in parallel across mild-to-moderate damage. By contrast, Transformers exhibit late threshold-like collapse under feedforward multi-layer perceptron (MLP) ablation and smoother sigmoid-like decline under attention-head ablation. Qualitatively, MLP-ablated models continue to make within-category semantic substitutions (semantic paraphasias) alongside rising non-responses, paralleling Wernicke-type aphasia, while attention-head ablation produces a trend toward loss of semantic specificity similar to the semantic variant of primary progressive aphasia (svPPA). These findings indicate that feedforward and attentional pathways have functionally distinct failure modes, suggesting that architecture-dependent failure profiles may offer new computational perspectives on aphasic syndromes and neurodegenerative diseases as an in silico model. Notably, early accuracy retention under Transformer attention-head ablation qualitatively parallels pre-symptomatic reserve before the 40--60% neuronal loss reported by Gomez-Isla et al. (1996) when clinical symptoms emerge in Alzheimer's disease, whereas the steadier LSTM decline parallels the symptomatic progression described by DeKosky and Scheff (1990) and Terry et al. (1991).