Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein.

By B. Giasson, J. Duda, Shawn M. Quinn, Bin Zhang, John Q. Trojanowski, V. Lee. Neuron, 2002

602 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Exogenous α-synuclein fibrils seed the formation of Lewy body-like intracellular inclusions in cultured cells (2009, background): “The -Syn within LBs isolated from human PD brains has been demonstrated to be insoluble (10, 19).”
Genetic Animal Models of Parkinson’s Disease (2010, unknown): “Similar to parkin knockout mice, PINK1 knockout mice did not exhibit any major abnormality (Table 2) (Gautier et al., 2008; Gispert et al., 2009; Kitada et al., 2007).”
Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, unknown): “Increased level and accumulation of mutated a-syn in transgenic mice caused paralyzes and death (Giasson et al., 2002).”
Α-synuclein misfolding and Parkinson's disease. (2012, background): “gregation promoters includes tau [345], histones [345], tubulin [329, 346], and agrin [181].”