Special Issue "Frontiers in Parkinson’s Disease (PD)"
Deadline for manuscript submissions: closed (10 November 2019) | Viewed by 24002
Parkinson’s Disease (PD) is the most common motor deteriorating neurodegenerative disease with a majority of cases being sporadic in nature. Over the past decade, researchers have begun to understand the physiological roles of different proteins that are mutated in monogenic forms of PD. These insights provide information into what types of biological processes may go awry in sporadic PD and aid in our understanding of the pathophysiological changes occuring during degenerative processes. The effort of multiple research groups elucidated the mechanism by which PINK1 and Parkin (two genes mutated in recessive PD) target damaged mitochondria for autophagic removal. Recently, the substrates and phorphosylation sites for leucine-rich repeat kinase 2 (LRRK2) have been identified. LRRK2 is the gene most commonly mutated in autosomal dominant forms of PD.
Newly published large-scale genome wide association studies (GWAS) have identified risk loci and candidate genes that are also involved in PD. It is imperitive that research efforts identify the function of these newly identified canidate genes (if unknown) and how these genes possibly contribute to neurodegeneration. The aim of this Special Issue, “Frontiers in Parkinson’s Disease,” is to encourage the publication of new experimental, translational and clinical findings to advance our understanding of the pathophysiological changes that occur in Parkinson’s Disease.
Assist. Prof. Alicia M. Pickrell
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- Parkinson’s disease
- Dopaminergic neurons
- Substantia nigra