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Description

This property enables ALCAR to influence central nervous system functions, including neurotransmitter synthesis, mitochondrial energy metabolism in neurons, and neuroprotection [2][5]

Their frequency then decreases in adulthood but may increase again as one gets older

At the core of this network, ferroptosis acts as a central initiating and amplifying hub, while inflammation and hypoxia function as reciprocal triggers and amplifiers, ultimately converging to promote fibrosis, the terminal pathological feature of CKD