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Fig. 1 | Molecular Medicine

Fig. 1

From: Genotype-driven therapeutic developments in Parkinson’s disease

Fig. 1

Converging pathways in Parkinson’s disease pathophysiology and relevant genes associated. The main disease mechanisms and current drug targets for mPD and GBA-PD are summarized. The links between key pathophysiological aspects are highlighted with double arrows indicating that translational therapies targeting related pathways may also be of use for a plethora of mPD, GBA-PD and IPD cases. Panel A depicts the aggregation of monomeric to oligomeric α-synuclein aggregates resulting in the formation of Lewy's bodies. Panel B.I and B.II symbolize endosomal disturbances, resulting in impaired neurotransmitter release (in particular VPS35) or impaired degradation of complex molecule structures by autophagy. Panel C illustrates mitochondrial damage, e.g., caused by oxidative stress (highlighted with thunderbolts), which can result in impaired mitochondrial dynamics (fusion and fission processes) among other downstream effects. ATP13A2: ATPase Cation Transporting 13A2. DNAJC13: DnaJ Heat Shock Protein Family (Hsp40) Member C13. DNAJC6: DnaJ Heat Shock Protein Family (Hsp40) Member C6. FBXO7: F-Box only protein 7. GBA: Glucosylceramidase Beta. GBA-PD: GBA-associated Parkinson’s disease. LRRK2: Leucine Rich Repeat Kinase 2. mPD: monogenic Parkinson’s disease. PARK7: oncogene DJ-1. PINK1: PTEN-induced kinase 1. PLA2G6: Phospholipase A2 Group VI. POLG: Mitochondrial Polymerase Gamma. PRKN: Parkin. SNCA: α-synuclein. SYNJ1: Synaptojanin 1. VPS13C: Vacuolar Protein Sorting 13 Homolog C. VPS35: VPS35 Retromer Complex Component

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