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While IMCLs themselves can be benign energy stores, the specific accumulation of toxic lipid intermediates like DAGs and ceramides is central to pathology ( Concurrently, the liver avidly takes up the excess systemic FFAs, which serve as a substrate for the hepatic overproduction of triglyceride-rich VLDL ( Beyond this shared origin in lipid overflow, novel mechanisms underscore the direct crosstalk

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Besides, the DOPAL-induced oxidative stress enhancement, enzymatic inhibition, mitochondrial impairment and disturbances of cellular proliferation and death signaling pathways, cooperatively contribute to the DA-relevant toxicity in PD pathogenesis [9]

Follow-up : Follow-up: Recovery doesnt end with the last treatment