The maintenance of intracellular trafficking is essential to neuron survival.
Well-organized intracellular events contribute to synapse effectiveness and efficient
communication between cells. Changes in microtubule trackers, vesicles, mitochondria
or autophagosomes can lead to neurodegeneration. Protein aggregates containing
amyloid-beta peptides and hyperphosphorylated tau are hallmarks of Alzheimer’s
disease and they impair intracellular trafficking. Moreover, dysfunction of intracellular
transport might increase the formation of protein aggregates. In this chapter it is
discussed the association between intracellular trafficking and Alzheimer’s disease
with emphasis in protein aggregation, cholesterol transport, molecular motors, rab
proteins, autophagy, endoplasmic reticulum, mitochondria and calcium homeostasis.
Keywords: Actin, APOE, Anterograde Trafficking, Dynein, Dinactin, Endoplasmic
Reticulum, Kinesin, Microtubules, Mitochondria, Miro, Rab Proteins,
Retrograde Trafficking.
