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