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4.4 Therapeutic strategies targeting the ferroptosisbloodbrain barrier disruption axis in Alzheimers disease A growing body of evidence indicates a pathological interplay between ferroptosis and bloodbrain barrier (BBB) dysfunction in Alzheimers disease (AD)
This metabolic symbiosis exhibits biphasic regulation: LNCaP cells upregulate Gln catabolic pathways (e.g., GLS1-dependent glutaminolysis), while CAFs activate extracellular matrix (ECM) remodeling pathways
Racemized amino acids that alter the peptide three-dimensional structure
One medication may work better for you than the other, or you may find that one has fewer side effects
Enhancing immunity during aging by targeting interactions within the tissue environment
Semaglutide mimics the effects of the hormone glucagon-like peptide-1 (GLP-1)
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