The role of PARKIN in parkinson’s disease

Parkinson’s disease (PD) is the most common movement disorder and the second most common neurodegenerative disorder. Patients often present with heterogeneous symptoms, reflecting the underlying complex nature of pathogenesis (1). Prevalent motor-related symptoms include bradykinesia, rigidity, resting tremor, and postural instability due in large part to the loss of pigmented, dopaminergic neurons in the substantia nigra pars compacta (SNpc). However, additional brain regions that influence cognitive decline and other psychiatric conditions are affected both prior and subsequent to neurodegeneration in the midbrain, an important factor when considering pathogenic mechanisms in PD (2). In sporadic disease, lesions first occur in the dorsal motor nucleus of the glossopharyngeal and vagal nerves and anterior olfactory nucleus. Gradually, nuclear grays and cortical areas become affected as the disease process in the brain stem follows an ascending course. Lesions then appear in the anteromedial temporal mesocortex and neocortex, with end-stage dysfunction in first-order sensory association/premotor areas and primary sensory and motor fields (3).