Brandon B. Holmes

This paper develops an AI-driven drug discovery framework for NALCN channelopathy, identifying aprepitant as a lead therapeutic candidate through HTS, structural modeling, and experimental validation.

The paper expands the kineTAC toolbox by creating 81 new cytokine receptor-targeting chimeras for cell-type-specific extracellular protein degradation.

This study shows that β-amyloid induces microglial GPC4 and APOE, which increases neuronal tau pathology and toxicity.

The paper uses CRISPRi to screen ASD risk genes in microglia, identifying ADNP's role in synaptic pruning and endocytosis.

The paper identifies specific glycosaminoglycan (GAG) structural requirements for the uptake of Tau, Aβ, and α-synuclein aggregates by cells.