Triphenyl phosphate (TPhP) is a widely used organophosphate flame retardant with disproportionate exposure burdens in infants and toddlers, yet its potential to programme later-life neurodegenerative susceptibility remains unclear. We exposed zebrafish embryos to TPhP (20-1000 μg/L, 2-120 hpf) and conducted life-course assessments after depuration at larval (7 dpf), juvenile (30 dpf), and adult (3 mpf) stages. Developmental TPhP exposure reduced whole-brain monoaminergic terminal signals in Tg (vmat2: GFP) larvae, increased acridine orange/propidium iodide (AO/PI)-defined neural cell death, impaired cerebrovascular growth, and produced a hypoactive locomotor profile. Co-exposure with apomorphine partially mitigated larval hypolocomotion at 20 μg/L. Persistent behavioral disturbances emerged with maturation, including hypolocomotion, abnormal light-dark preference, and adult deficits in spatial learning/memory and social interaction. Adult brains showed Parkinson's disease (PD)-relevant injury signatures, including reduced tyrosine hydroxylase immunoreactivity, dopamine depletion, and pronounced α-synuclein accumulation. Transcriptomic profiling implicated sustained remodelling of protein-folding programs, mitochondrial redox homeostasis, and ferroptosis-related pathways, which was functionally supported by reduced mitochondrial complex I activity, elevated oxidative DNA and lipid damage (8-OHdG, 4-HNE), and impaired antioxidant defenses (slc7a11, park7, GPX4). Molecular docking suggested structurally plausible interactions of TPhP with tyrosine hydroxylase (TH)and D2-type dopamine receptors (DRD2a/b). Collectively, transient developmental TPhP exposure extends beyond early neurotoxicity and is associated with persistent dopaminergic vulnerability and PD-like phenotypes across the life course.