Alzheimer’s disease (AD) is marked by the accumulation of amyloid plaques, which are strongly influenced by ionic environments. High-salt diets have been linked to elevated phosphorylated tau and AD-like pathology, yet the molecular mechanisms by which salt ions and modulators (Li⁺) interact with amyloids remain poorly understood. Li⁺ has been shown to mitigate tau pathology and slow disease progression, while Mg²⁺, essential for neural function, may exert neuroprotective effects, though its role under salt-rich conditions is unclear. We propose an engineering-oriented, molecular-level investigation combining computational chemistry, and AI-driven modeling to: Quantify the effects of salt and modulator ions on amyloid plaque initiation. Identify mutant structures capable of inhibiting plaque formation. The project aims to rational design of chaperone-like peptide inhibitors, providing a framework for engineering novel AD therapeutics.