A class of endogenous steroid molecules, often synthesized locally within the nervous system or peripherally, that exhibit direct or indirect actions to preserve neuronal structure and function against acute injury or chronic degradation. These compounds operate independently of classical gonadal steroid receptor pathways for some of their protective functions. They are vital components of intrinsic neural defense mechanisms.
Origin
This term specifically identifies steroids—lipids derived from cholesterol—that demonstrate protective qualities (“neuroprotective”) within the neural milieu. Examples include allopregnanolone and certain metabolites of progesterone and DHEA.
Mechanism
Their action frequently involves rapid, non-genomic signaling by interacting directly with ligand-gated ion channels, such as the GABA-A receptor, altering neuronal excitability. Additionally, they can influence mitochondrial respiration and reduce lipid peroxidation, thereby decreasing oxidative damage following insults like traumatic brain injury or stroke. This direct membrane interaction bypasses slower genomic pathways.
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