Parkinson’s disease (PD), a typical Parkinson syndrome, is seen as a progressive multisystem neurodegenerative disease with α-synuclein–containing Lewy bodies and neurites, affecting 1–2 per 1000 of the global population. The prevailing view of PD etiology is that it is the result of cell-autonomous and non-autonomous processes, starting in the olfactory nerve and the autonomous nervous system of the gut, spreading retrogradely through synaptically coupled networks in a topographically predictable sequence to postsynaptic brainstem neurons, affecting the nuclear grays of the basal midbrain and forebrain and finally the neocortex. Cell-autonomous processes (e.g., mitochondrial damage and a defective autophagy by lysosomal and ubiquitin proteasome systems) result in pathologic accumulation of intracellular α-synuclein oligomers and aggregates. Non–cell-autonomous processes comprise the spread of synucleinic pathology in dying neurons to neighboring dopaminergic, cholinergic, serotinergic, and adrenergic neurons and/or to astrocytes, microglia, and lymphocytes across brain regions, plus decreased brain-derived neurotrophic factors and/or microglial-induced inflammatory responses.