Rab7 effector FYCO1 induces clearance of A53T-alpha-synuclein aggregates

Dinter, Elisabeth; Saridaki, Theodora; Nippold, Markus; Roos, Andreas; Diederichs, Leonie; Fensky, Luisa; Falkenburger, Björn H.

doi:10.1016/j.baga.2017.02.019

Cited by 1 publication

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“…These Rab proteins are relevant to α-Syn-induced defects in trafficking and regulate α-Syn aggregation/toxicity (Gao et al., 2018). For instance, Rab1, Rab7, Rab8, and Rab11 have all been shown to ameliorate α-Syn toxicity in Drosophila (Cooper et al., 2006; Yin et al., 2014; Breda et al., 2015; Dinter et al., 2016). Rab1, a regulator of ER-to-Golgi trafficking, rescues α-Syn-mediated DA neuron loss, compromised autophagy (Cooper et al., 2006; Winslow et al., 2010), and Golgi fragmentation upon α-Syn overexpression in nigral DA neurons (Coune et al., 2011; Rendon et al., 2013).…”

Section: α-Syn In Trafficking: Interaction With Rab Proteinsmentioning

confidence: 99%

α-Synuclein Trafficking in Parkinson’s Disease: Insights From Fly and Mouse Models

Cheng

Lü

et al. 2018

ASN Neuro

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Protein aggregation and accumulation are common pathological hallmarks in neurodegenerative diseases. To efficiently clear and eliminate such aggregation becomes an important cellular strategy for cell survival. Lewy bodies inclusion and aggregation of α-Synuclein (α-Syn) during the pathogenesis of Parkinson’s disease (PD) serve as a good example and are potentially linked to other pathological PD features such as progressive dopaminergic neuron cell death, behavioral defects, and nonmotor symptoms like anosmia, cognitive impairment, and depression. Years of research have revealed a variety of mechanisms underlying α-Syn aggregation, clearance, and spread. Particularly, vesicular routes associated with the trafficking of α-Syn, leading to its aggregation and accumulation, have been shown to play vital roles in PD pathogenesis. How α-Syn proteins propagate among cells in a prion-like manner, either from or to neurons and glia, via means of uptake or secretion, are questions under active investigation and have been of central interest in the field of PD study. This review covers components and pathways of possible vesicular routes involved in α-Syn trafficking. Events including but not limited to exocytosis and endocytosis will be discussed within the context of an overall cellular trafficking theme. Recent advances on α-Syn trafficking mechanisms and their significance in mediating PD pathogenesis will be thoroughly reviewed, ending with a discussion on the advantages and limitations of different animal PD models.

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