Skip to main content
. Author manuscript; available in PMC: 2018 Oct 1.
Published in final edited form as: Trends Neurosci. 2017 Oct;40(10):592–602. doi: 10.1016/j.tins.2017.08.003

Figure 2. Endosomal traffic jams can mediate Alzheimer’s pathophysiology.

Figure 2

As outlined in the flow diagram (upper panel) and illustrated in the figure (lower panel) two disease-relevant pathophysiological consequences occur in the setting of traffic jams:

A reduction of glutamate receptor recycling. Traffic jams in the early endosome reduces the transport of glutamate receptors to the postsynaptic surface of neurons, via recycling endosomes, impairing synaptic health.

An Increase in pathogenic exosomes. Traffic jams in the early endosome either increases the number of intraluminal vesicles (ILVs) in the multivesicular body thereby increasing the number of released exosomes; or, increases the content of exosomes with, for example, βCTF, Aβ or tau. Either increasing exosomal number or increasing exosomal content can accelerate anatomical spread of disease.