Table 1.

Rab proteins involved in neurodegenerative diseases.

	Rab Protein	Rab Alterations Associated with the Disease	References
Alzheimer’s Disease (AD)	Rab6	Increased levels but decrease of active, membrane-associated Rab6 and defective recycling of vesicle	[74,75]
	Rab5	Upregulated and over-activated	[76,77]
	Rab7a	Upregulated	[76,77]
	Rab4	Upregulated	[77]
	Rab27	Upregulated	[77]
	Rab10	Phosphorylated and upregulated	[78,79]
	Rab11	Genetic association of Rab11 with late-onset AD; affects Aβ production	[80]
Parkinson’s Disease (PD)	Rab39b	Loss-of-function mutations	[81,82,83,84]
	Rab8a/b	Defective phosphorylation by pathogenic leucine-rich repeat kinase 2 (LRRK2) leading to centrosomal defects and influencing neurite outgrowth, cell polarization and migration. Abolished phosphorylation in PTEN-induced putative kinase (PINK1)-caused PD	[85,86]
	Rab7a	Decreased activity; defective endosomal trafficking and degradation in LRRK2-caused PD	[87,88]
	Rab29 (Rab7L1)	Upregulated and present in a risk locus for sporadic PD; over activates LRRK2 PD-mutants by increasing their recruitment to the Golgi	[89,90,91]
Amyotrophic Lateral Sclerosis (ALS)	Rab1	Dysfunctional in sporadic ALS; its effector C9orf72 is mutated in ALS, resulting in a decreased autophagy. Rab1-dependent endoplasmic reticulum (ER)-Golgi transport inhibited in superoxide dismutase 1 (SOD1), TAR DNA binding protein (TDP-43), and Fused in Sarcoma (FUS)-associated ALS.	[92,93]
Charchot–Marie–Tooth 2B (CMT2B)	Rab7a	Missense mutations characterized by excessive activation that cause a reduced autophagic flux, premature neurotrophine receptor degradation, impaired axonal trafficking of the receptor, and inhibition of neurite outgrowth	[94,95,96,97,98]
Huntington’s Disease (HD)	Rab11	Decreased activity and defects in endosomal recycling	[99,100,101,102]