Introduction: The Wnt/β-Catenin pathway is associated with embryogenesis, cell proliferation, and tissue modulation, and its impairment is linked to some pathologies such as cancer. Recent studies have suggested that this signaling pathway is implicated in the genesis and progression of neurodegenerative diseases like Alzheimer’s disease (AD) in a multi-mechanistic way, for example affecting synaptic plasticity processes through the regulation of amyloidβ (Aβ) levels, a peptide closely related to AD development. In this context, the development and implementation of computational models of these molecular pathway and its interaction with synaptic plasticity process are valuable tools that could aid in understanding the underlying mechanisms of these complex processes. Methods: In this study, we propose to model the impact of regulation Aβ levels by activating or deactivating the Wnt/β-Catenin pathway over a previously reported synaptic plasticity computational model developed by Dainauskas et al. (2023) [8]. For the Wnt/β-Catenin pathway model, we implemented differential equations in Python to analyze five key elements of the pathway in the context of AD: Wnt, GSK3-β, β-Catenin, BACE1 gene, and Amyloid-β. The proposed methodology includes the implementation of Python code with NEURON libraries. For the evaluation of the effect, membrane potential, NMDA receptor conductance and synapse weight will be measured in different conditions of WNT/Aß levels, based in concentrations reported in vitro studies. Results: We evaluated different levels of Wnt, the dynamics of the Wnt pathway model were adapted to in vitro experimental results. Also the connection with the synaptic plasticity model shows the influence of Wnt levels on the modulation of synaptic weight through the regulation of NMDA receptor conductance levels. When we analyse each element in the pathway in our model we validate that these elements had a consistent behaviour according to experimental data. This model recreates an in silico approximation of the Wnt pathway and its relationship with synaptic plasticity process.