Table 1.

EV cargo molecules in major neurodegenerative disorders

Neurodegenerative Disorder	Main EV-related Findings	References
AD	Exosomes from microglia spread toxic A3 and phosphorylated tau between cells Exosomal proteins, such as Alix and flotillin-1, accumulate around amyloid plaques in AD patients	[6, 20, 58, 61]
ALS	EVs have been shown to spread SOD1 and TDP-43 within the brain and spine Some studies indicate that these EVs are often exosomes originating from astrocytes Spinal motor neurons derived from induced pluripotent stem cells from C9orf72-ALS patients released dipeptide repeat proteins in EVs	[77–79]
HD	EVs carry expanded CAG-repeat RNA and polyQ protein	[80]
MS	EVs released by microglia and endothelial cells have been implicated in breaking down the blood-brain barrier These EVs have been found to contain pro-inflammatory signals, including IL-13, interferon-y, tumor necrosis factor (TNF), caspase 1 and the P2X7 receptor	[32, 81–83]
PD	L1CAM+ EV populations are increased in PD patients, and a correlation to disease severity has been shown Exosomes have been shown to spread a-Syn to the extracellular environment	[84, 85]
Prion Disease	Neuronal exosomes aid in the spread of scrapie-form prions These exosomes have increased levels of miRNAs associated with neurological disorders, including miRs-29b, 128a, 146a	[86, 87]
TBI	Increased levels of tau are found in blood-derived exosomes from CTE- risk cohort (former contact sports athletes) Exosomes mediate deposition of periventricular and perivascular tau and TDP43	[88, 89]