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Table 2 Extensive review analysis of CNS-derived EVs findings in the context of AD

From: Alzheimer’s disease progression characterized by alterations in the molecular profiles and biogenesis of brain extracellular vesicles

Exosome-associated proteinProtein modulationEV sourceAnalytical techniqueObservationsReference
P-S396-tau, P-T181-tau and Aβ1-42Upregulation in ADNDEImmunoassayPredictor of AD development prior to clinical onset[54]
SNAP-25Downregulation in ADNDEImmunoassayNegative correlation between the levels of SNAP-25 and cognitive status[55]
GelsolinDownregulation in DLB compared to ADPlasma-derived EVsProteomicsPotential biomarker able to differentiate DLB and AD[56]
Growth-associated protein 43 and synapsin 1Downregulation in AD but not in dementia patientsNDEImmunoassayPossible early differential diagnosis marker to differentiate AD and dementia[57]
β/γ-secretase and sAPPβUpregulation in ADNDEImmunoassayAstrocyte-derived exosomes of AD patients show up to 20-fold upregulation than neuron-derived exosomes[58]
pS396 tau and AβUpregulation in ADCortical grey matter EVsImmunoassay[59]
ANXA5, VGF, GPM6A and ACTZPresenceCortical grey matter EVsQuantitative proteomics and machine learningEVs signature panel of proteins in AD[59]
Total and phosphorylated tauUpregulation in ADCSF from AD Braak stage 3ImmunoassayConsidered patients with mild AD[60]
  1. NDE plasma circulating neuronal-derived exosomes, DLB dementia with Lewy bodies, CSF cerebrospinal fluid