Neurological disorders such as Alzheimer’s and Parkinson’s disease are increasingly linked to disrupted cerebrospinal fluid (CSF) dynamics, abnormal CSF volume regulation, and impaired glymphatic clearance of neurotoxic proteins from the central nervous system. This work presents a multiphysics computational framework that quantitatively couples CSF hydrodynamics, CSF volume dynamics, and glymphatic transport to protein aggregation processes in neurodegeneration. The model integrates cardiac-driven intracranial pressure oscillations with CSF flow and solute transport within physiologically realistic geometries derived from empirical observations of the spinal cord. Simulations predict peak cross-sectional pressure gradients ranging from approximately -27 Pa to +27 Pa and spatially heterogeneous velocity fields with maxima on the order of 10^-3 m/s. CSF flow and volume regulation are governed by the incompressible Navier–Stokes equations combined with continuity-based volume balance, driven by pulsatile inlet conditions extracted from cardiac waveforms and coupled to lumped compliance elements representing intracranial and spinal elastance. Transport of neurotoxic species, including amyloid-beta and tau, is modeled using transient diffusion equations incorporating clearance and exchange terms to account for glymphatic outflow and parenchymal uptake. The fully coupled system is implemented in COMSOL Multiphysics, enabling integrated simulations of CSF hydrodynamics and solute transport. Under baseline physiological conditions, inlet molar fluxes lie in the 10e-11– 10e-10 mol/s range and exhibit progressive attenuation toward the outlet. To investigate non-pharmacological modulation of CSF transport, boundary-condition perturbations were introduced to mimic the effects of physical exercise and slow yogic breathing on intracranial pressure waveforms and CSF stroke volume. In the baseline case, the inlet molar flow decreases by approximately 47% over 4 s, whereas under enhanced pulsatility it decreases by about 52%. Slow yogic breathing increases net CSF volume by approximately 20% and outlet molar flux by 25%, while exercise-like conditions produce roughly 50% higher peak pressure amplitudes and 40% higher peak solute transport rates.