Table 1.

Summary of the putative causes of Golgi fragmentation in neurodegenerative diseases (see text for details).

Neurodegenerative Disease	Cause of Fragmentation	Main Model Used	References
PD	Alterations in the levels of Rab1: 2 and 8 and the SNARE protein syntaxin 5	Differentiated PC12 cells treated with 6-hydroxydopamine or methamphetamine	[59]
	Prefibrillar aggregates of α-synuclein	COS-7 cells overexpressing α-synuclein	[75]
	Defects in Rab1 dependent ER-Golgi transport	Substancia nigra from rats injected with vectors for α-synuclein and Rab1	[149]
	Enhanced phosphorylation of Rab7L1 by mutant LRKK2 (TGN fragmentation)	HEK293 cells expressing Rab7L1 and LRRK2 mutant	[78]
AD	Accumulation of Aβ which causes activation of cdk5 and phosphorylation of GRASP65	Transgenic mice/CHO cells expressing APP and PS1 mutants	[60]
	Accumulation of phospho-tau	Neurons from neocortex and hippocamous of AD patients	[113]
	Tau secretion	Primary cortical neurons	[112]
ALS	Endosomal abnormalities due to altered dynein-dependent transport	SOD1-ALS mouse	[120]
	Mutations in optineurin	Motor neuron-like NSC-34 cells	[131]
	Interruption of ARF1/TBCE cross-talk that coordinate COPI formation and microtubule polymerization	Motor neurons from progressive motor neuropathy mice	[20]
	Rab1-dependent ER-Golgi transport	Neuro2a cells transfected with TDP-43, FUS or SOD1	[130]
	Stathmin 1/2-triggered microtubule destabilization	Transgenic SOD1mutants mouse motor neurons	[136]
SMA	Low levels of α-COP	SMA patient fibroblasts	[144]