Abstract: The physical aging of amorphous solids is crucial for understanding their glass transition, mechanical deformation, and crystallization behavior, with the core focus on constructing aging models to elucidate relaxation mechanisms and predict the evolution of their mechanical and physical properties. This study investigates the structural state evolution of Zr46Cu46Al8 amorphous alloy during heating from room temperature to the supercooled liquid region by testing its shear modulus and dynamic mechanical parmaters. The study assumes that changes in shear modulus are proportional to variations in defect concentration and derives the temperature-dependent evolution of defect concentration. The current work considers that defect concentration evolution towards equilibrium during physical aging follows a first-order kinetic equation, assuming an Arrhenius temperature dependency for the characteristic time. A semi-quantitative calculation of the temperature dependence of defect concentration in amorphous alloys is provided. Results show that, under an isoconfigurational state, the shear modulus of both crystalline and amorphous alloys approximately decreases linearly with temperature. For as-cast amorphous alloys, the temperature dependence of the shear modulus exhibits three distinct regions: a nearly linear decrease in the deep glassy state under isoconfigurational conditions, a moderate temperature range where aging induces a relative increase in the shear modulus, and a rapid decline in the shear modulus above the glass transition temperature. The relaxation of the shear modulus is closely related to the evolution of defect concentration in non-equilibrium amorphous alloys. The defect concentration evolution calculated using a first-order kinetic aging model aligns well with that derived from shear modulus data. Furthermore, based on the temperature dependence of dynamic mechanical parameters, the impact of aging on the evolution of complex modulus was analyzed, revealing that the excess wing behavior in the present system is attributable to changes in the α relaxation spectrum caused by aging, rather than conventional secondary relaxation processes.