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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 protein Protein modulation EV source Analytical technique Observations Reference
P-S396-tau, P-T181-tau and Aβ1-42 Upregulation in AD NDE Immunoassay Predictor of AD development prior to clinical onset [54]
SNAP-25 Downregulation in AD NDE Immunoassay Negative correlation between the levels of SNAP-25 and cognitive status [55]
Gelsolin Downregulation in DLB compared to AD Plasma-derived EVs Proteomics Potential biomarker able to differentiate DLB and AD [56]
Growth-associated protein 43 and synapsin 1 Downregulation in AD but not in dementia patients NDE Immunoassay Possible early differential diagnosis marker to differentiate AD and dementia [57]
β/γ-secretase and sAPPβ Upregulation in AD NDE Immunoassay Astrocyte-derived exosomes of AD patients show up to 20-fold upregulation than neuron-derived exosomes [58]
pS396 tau and Aβ Upregulation in AD Cortical grey matter EVs Immunoassay [59]
ANXA5, VGF, GPM6A and ACTZ Presence Cortical grey matter EVs Quantitative proteomics and machine learning EVs signature panel of proteins in AD [59]
Total and phosphorylated tau Upregulation in AD CSF from AD Braak stage 3 Immunoassay Considered patients with mild AD [60]
  1. NDE plasma circulating neuronal-derived exosomes, DLB dementia with Lewy bodies, CSF cerebrospinal fluid