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In the brain, extracellular blisters (EVs) play a vital role in the neuron-glial cell interface and ensure the brain's in-line with the peripheral.
currently, some studies have linked pathogenic dysfunction in EVs to the risk of developing lipoprotein E gene mutations (APOE) and Alzheimer's disease (AD).
To better understand the role of APOE 4 in preclinical AD, researchers recently stratited the absence (APOE 4-) or presence (APOE4) of APOE by layering levels of pathogenic, neurotrophic, and inflammatory proteins in the plasma of patients with external EVs (pEVs) and cognitive impairment, dementia-free (CIND).
the study, levels of 15 neurodegenerative, neurotrophic and neuroinstitive proteins were quantified in pEVs and compared with plasma levels in cognitively normal CIND participants.
results showed lower levels of neurotrophic and inflammatory markers in pEVs of APOE 4 plus.
in CIND individuals with APOE 4 plus, the pEVs measured the five serotonin-2/α-synuclein ratio to predict the five years before AD became ill.
therefore, the results show that the endometrial pathways of APOE 4 plus have changed, and the pEVs phenoxysamine-2/α-synuclein ratio can be used as an early biomarker of AD susceptibleness.
