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The Centriolar Damage Accumulation Theory of Aging (CDATA) proposes that the structural and functional decline of centrioles and associated structures acts as a candidate integrator and driver of cellular aging, contributing to stem cell exhaustion and tissue dysfunction. To test this hypothesis computationally and explore its systemic consequences, we developed Cell DT, a high-performance, multi-track simulator built in Rust using an Entity Component System (ECS) architecture. Cell DT models seven parallel, interacting aging tracks: (A) ciliary dysfunction from appendage damage, (B) mitotic spindle infidelity, (C) telomere erosion, (D) epigenetic drift, (E) mitochondrial ROS-driven centriolar damage, (F) integrated division rate regulation, and (G) myeloid shift and inflammaging feedback. We further incorporate a thermodynamic layer based on Arrhenius kinetics, a multi-tissue model with systemic signaling (SASP, IGF-1), and clonal hematopoiesis dynamics. Simulations from a baseline human model (5 stem cell niches) recapitulate key aging phenomena: progressive accumulation of centriolar damage (0.006 to 0.577 over 70 years), decline in ciliary (0.991 to 0.215) and spindle (0.999 to 0.713) functions, increasing Systemic Degradation Index (SDI: 0.206 to 0.914), and death at ~80 years. Model outputs were compared to empirical benchmarks, showing consistency in trends for myeloid bias and epigenetic acceleration, while identifying areas for refinement. Multi-tissue simulations (25 niches across five tissues) predict synchronized systemic collapse near age 75, driven by stem cell pool depletion (~7% remaining). We successfully model clonal hematopoiesis (CHIP), with complete clonal takeover by age 79, and a progressive myeloid shift (bias ≈ 0.45 at age 70). Sensitivity analysis identified the midlife damage multiplier as the most critical parameter governing lifespan. Intervention modules (e.g., senolytics, centrosome transplant) demonstrate the platform's utility for in silico therapeutic screening, with quantified effects (e.g., calorie restriction extended lifespan by ~15%). Cell DT provides a rigorous, extensible, and open-source framework for simulating the CDATA and exploring its implications for geroscience, offering a "digital twin" approach to understanding the integrated mechanics of aging.