FIGURE 5.

Proposed clearance mechanisms for amyloid beta (Aβ) oligomers and the influence on the use of Aβ oligomers as biomarker. Hypothetic scenario: Aβ monomer production at synapses is dependent on synaptic activity. At a certain time point, aggregation of Aβ monomers leads to the formation of toxic Aβ oligomers which can be cleared by different mechanisms. Aβ oligomers can be degraded by microglia (clearance mechanism #1), diffuse into cerebrospinal fluid (CSF), or be deposited into plaques (clearance mechanism #2) as soon as there are plaques. Formation of plaques in patients with amyloid pathology allows oligomers to be deposited there (clearance mechanism #2), which may well become the preferred fate of Aβ oligomers. Figure created with BioRender.com. APOE ε4, apolipoprotein E ε4 allele.