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These behavioral benefits are underpinned by its marked ability to induce spinogenesis and promote functional synaptogenesis in hippocampal neurons, highlighting its potential as a robust procognitive and antidementia agent [1]

During antithyroid therapy, TSab tends to decline

This protective effect is independent of GSHs classical antioxidant activity and instead relies on its direct interaction with Cu + , which sequesters excess copper and prevents its aberrant binding to lipoylated proteins within the TCA cycle

Currently, the preclinical development of these strategies appears more challenging to avoid strong side effects, but the expected results are commensurate with patients hopes for treatments