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Broad immune cell populations and soluble toxic species is a composite therapeutic target profile primarily associated with Therapeutic Plasma Exchange (TPE) and albumin replacement therapy in the treatment of Alzheimer's disease (Boada et al., 2020). This approach targets the systemic environment rather than a single molecular receptor, aiming to clear circulating soluble toxic species—specifically amyloid-beta oligomers—that are in equilibrium between the brain and the blood (Grifols, 2020). By removing these toxins from the plasma, the therapy facilitates a peripheral sink effect, encouraging the clearance of neurotoxic proteins from the central nervous system. Simultaneously, the procedure targets broad immune cell populations by filtering out inflammatory cytokines and replacing them with fresh albumin, which possesses antioxidant and immunomodulatory properties that help reset the systemic immune response (NIH, 2022). This dual-action strategy is designed to slow cognitive decline by addressing both the proteinopathy and the chronic neuroinflammation characteristic of neurodegenerative disorders.
The mechanism of action involves the peripheral sink hypothesis, where the removal of soluble toxic species (such as amyloid-beta) from the plasma via exchange with albumin promotes the efflux of these species from the brain into the periphery (Boada et al., 2020). Additionally, the therapy modulates broad immune cell populations by removing pro-inflammatory mediators and providing fresh albumin, which has inherent antioxidant and immunomodulatory properties that help stabilize systemic inflammation (Grifols, 2020).
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