Parkinson＇s disease （PD） is an age-related neurodegenerative disorder characterized by typical motor signs and symptoms that are due to dopamine （DA） depletion in the basal ganglia. The treatment of PD is symptom...Parkinson＇s disease （PD） is an age-related neurodegenerative disorder characterized by typical motor signs and symptoms that are due to dopamine （DA） depletion in the basal ganglia. The treatment of PD is symptomatic, and aims at replacing the lost DA input using either L-DOPA or DA agonists. The causes of PD are unknown in approximately 90% of the cases, whereas about 10% of the cases are familial and imputable to mutations in a handful of genes （the gene mutations with the strongest association with PD are shown in Table 1; for a detailed review see （Poulopoulos et al., 2012））. The genetic forms of PD have spurred an intense research on molecular pathways of neurodegeneration that converge on proteostatic deficits, mitochondrial dysfunction and oxidative stress.展开更多
基金supported by grants to M.A.C.from the Michael J Fox Foundation for Parkinson’s Researchthe Swedish Parkinson Foundation+4 种基金The Swedish Research Council(project no.K201261X-13480-13-5)European Community’s Seventh Framework Programme FP7/2008 under grant agreement no.215618(project acronym,Neuromodel)the Basal Ganglia Disorders Linnaeus Consortium(BAGADILICO)Greta and Johan Kocks Foundationhlen Foundation
文摘Parkinson＇s disease （PD） is an age-related neurodegenerative disorder characterized by typical motor signs and symptoms that are due to dopamine （DA） depletion in the basal ganglia. The treatment of PD is symptomatic, and aims at replacing the lost DA input using either L-DOPA or DA agonists. The causes of PD are unknown in approximately 90% of the cases, whereas about 10% of the cases are familial and imputable to mutations in a handful of genes （the gene mutations with the strongest association with PD are shown in Table 1; for a detailed review see （Poulopoulos et al., 2012））. The genetic forms of PD have spurred an intense research on molecular pathways of neurodegeneration that converge on proteostatic deficits, mitochondrial dysfunction and oxidative stress.
