Transgenic models of α-synucleinopathy

Parkinson’s disease (PD) is a common late-onset, progressive neurodegenerative disease characterized by selective loss of neuronal populations, including dopaminergic (DAergic) neurons of substantia nigra, pars compacta (SNpc), and presence of fibrillar, cytoplasmic inclusions called Lewy bodies (LBs) and Lewy neurites (LNs) (1). While degeneration of dopamine (DA) neurons is responsible for much of the motoric symptoms of PD, neuropathology in PD extends well beyond the DAergic systems (2,3). Significantly, non-DAergic pathology may precede DAergic pathology in PD (2,3).