👉 PCSK9 & Alzheimer’s disease — lipids meet neurodegeneration PCSK9 is moving beyond lipidology into the neurodegeneration arena. 👆 Mechanistic rationale is strong: Degradation of neuronal LDLR, LRP1, ApoER2 → disrupted brain cholesterol handling. 👆 Downstream experimental effects: ↑ Amyloid-β accumulation ↑ Tau phosphorylation ↑ Neuroinflammation ↓ Synaptic integrity 👆 Overexpression accelerates amyloid pathology and cognitive decline (preclinical). 👆 Inhibition or genetic deletion mitigates these pathways and preserves cognition in models. Human evidence tells a different story 👆 Some cohorts show higher PCSK9 levels in CSF and brain tissue. 👆 But large genetic and Mendelian randomization analyses: No causal association with Alzheimer’s risk. 📍 PCSK9 inhibitors • Powerful LDL-C reduction. • No cognitive harm signal in trials. • Limited blood–brain barrier penetration → effects likely indirect. 📍 Take-home • Strong biology. • Weak human causality. • PCSK9 sits at the crossroads of lipid metabolism and neurodegeneration — best viewed today as a disease modifier or biomarker, not a driver. 🔗 Open Access 10.3390/life15121851 @society_eas

👉Primary Prevention Aspirin, Lipoprotein(a), and Cardiorenal Outcomes in Chronic Kidney Disease New data from the CRIC study ☝️In CKD patients without clinical CVD, aspirin use was associated with 38% lower MI risk and 28% lower ESRD risk — but only when Lp(a) ≥50 mg/dL. ☝️No significant benefit was seen when Lp(a) <50 mg/dL, and bleeding risk did not increase. @society_eas @Lpa_Doc @rblument1 @MichaelJBlaha @JACCJournals Open access 🔓 sciencedirect.com/science/ar…