Study type: Human research · Status: Verified against declared source

Modulation of Amyloid-β and Tau in Alzheimer's Disease Plasma Neuronal-Derived Extracellular Vesicles by Cerebrolysin® and Donepezil.

Journal of Alzheimer's disease : JAD · 2022

Study scale: In this study, two sets of participants’ samples were included and processed for neuronal EV cargo.

Product or molecular entity relationships

Cerebrolysin: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.

Plain-language verified summary

Question

Characterization of the behavior of these plasma NDEV biomarkers throughout the entire AD continuum could be relevant for the design and monitoring of therapeutic interventions in clinical trials with MCI and AD patients.

Methods

Blood samples for determinations of NDEV proteins were obtained at baseline for AD and control cases; as well as at baseline and week 28 (study endpoint) for RCT AD patients.

Scale or participants

In this study, two sets of participants’ samples were included and processed for neuronal EV cargo.

Key findings

NDEV levels of Aβ42, total tau, P-T181-tau, and P-S393-tau were higher and those of neurogranin and REST were lower in mild-to-moderate AD than in controls (p < 0.05 to p < 0.001).

Limitations and uncertainty

In AD patients, plasma NDEV levels of Aβ42 were found to be increased as compared with controls [10–12, 17–20], to correlate with CSF Aβ42 levels and with PET imaging of brain amyloid plaque load [12, 19], but not with measures of cognitive impairment [18], and to represent an efficient blood biomarker [7].

Verified against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.