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Dani S Bassett

Publications and source records attributed to Dani S Bassett.

2 recordsLinked to original sources

Task Context Shapes Component Roles in Language Models

Large language models reuse the same attention heads across tasks, but identifying these shared heads does not explain what they do differently in each task. A natural source of inspiration is task-dependent interactions among shared brain regions, which motivate a network view of language-model computation. Here, we compare fixed model components across tasks using identical graph facts, statements specifying which directed connections are present. We measure how interventions affect attention heads and the activation state in later layers (influence), as well as the answer (importance). Task changes redistribute the influence in five open-weight models spanning four families and 1.5-14 billion parameters. In Gemma-2-9B and Qwen3-14B, an activation edit changes an early internal activation vector and switches which fact the model reads while the written instruction stays fixed. The same heads then respond to different graph facts and influence later components differently. For each prompt, we construct two linear response maps, one before the edit and one after it. Each map predicts a later head's response from a measured change in an earlier head. For a separate factual intervention, the map for the corresponding condition reduces mean squared prediction error by 53.6% in Gemma and 5.0% in Qwen compared with the average of the two maps. These findings show that task context changes both which graph facts the shared components respond to and how their outputs affect later computation. A network account may help explain how models use shared parameters to perform different computations. Measurements of task-dependent influence could also guide interventions intended to alter one behavior while preserving others.

cs.CL↗

Activity-dependent epidemic spreading on multiscale brain networks predicts Alzheimer's disease progression

Neurodegenerative diseases can be viewed as spreading processes on brain networks, in which pathological proteins propagate between anatomically connected brain regions. Mathematical models have been used to study this process, but they generally ignore the influence of neuronal activity, even though experimental studies show that neuronal firing promotes protein transmission. Here, we couple a general node-activity process to susceptible--infected--susceptible dynamics. In this framework, an epidemic threshold determines whether small pathological seeds can grow, while a dominant network mode determines where growth begins. We derive approximations showing how neuronal activity shifts this threshold and redirects spreading by mixing structural network modes. For networks with multiscale structure, we decompose these changes into contributions from regional mean activity and within-region activity variation, allowing us to account for activity heterogeneity that is not resolved by brain imaging. Stochastic simulations validate the theoretical results across synthetic networks. We next use longitudinal human positron emission tomography to test whether neuronal activity predicts where and how broadly pathology spreads. Regional glucose metabolism serves as a proxy for neuronal activity, while tau accumulation measures disease progression. Adding neuronal activity to the network model captures spatial patterns of disease progression that are not explained by structural connectivity and established disease markers alone. Across individuals, predicted epidemic thresholds are also associated with how broadly pathology spreads through the brain. Together, these results connect epidemic theory to neurodegeneration, implicate neuronal activity as a driver of Alzheimer's disease progression, and motivate activity-modulating therapies to slow or prevent pathological spread.

q-bio.NC↗