1. Maintaining energy homeostasis: Preventing "energy depletion" type nerve damage
Neurons are extremely sensitive to energy. In scenarios such as ischemia, hypoxia, and neurodegenerative diseases (such as Alzheimer's disease), nerve cells will rapidly deplete ATP, leading to the failure of ion pumps (such as the inability of Na⁺/K⁺ pumps to maintain membrane potential), synaptic function collapse, and ultimately cell necrosis or apoptosis.
Creatine monohydrate, after entering nerve cells, is converted into phosphocreatine (PCr), which is an "instant high-energy reserve": When energy supply is interrupted (such as during a cerebral ischemia attack), PCr can quickly transfer phosphate groups to ADP to generate ATP, delaying the sudden drop in ATP levels and buying nerve cells "self-rescue time" (such as maintaining ion balance and repairing membrane damage).
2. Inhibit oxidative stress: Reduce free radical-mediated cell damage.
Creatine monohydrate combats oxidative stress through a dual pathway:
Protecting mitochondrial function: Stabilizing mitochondrial membrane potential (preventing the massive release of ROS due to membrane potential collapse), enhancing the activity of mitochondrial antioxidant enzymes (such as superoxide dismutase SOD), reducing ROS generation at the "source";
Directly scavenging ROS: Creatine molecules themselves have a certain antioxidant capacity, which can directly neutralize some ROS (such as hydroxyl radicals), reducing the direct damage of oxidation to nerve cells.
3. Antagonizing excitotoxicity: Blocking the death of "overactivated" neurons
The protective effects of creatine monohydrate are manifested in:
Maintaining energy supply to support the function of the glutamate transporter: This transporter is responsible for pumping excess glutamate from the synaptic cleft back into the cell (preventing its accumulation), and its operation depends on ATP energy supply; when energy is sufficient, the transporter can effectively clear excess glutamate, reducing receptor overactivation; Mitigating calcium overload damage: Stable energy can maintain the activity of the Ca²⁺ pump on the cell membrane, promoting Ca²⁺ efflux, while protecting mitochondria (calcium overload can damage mitochondrial structure), indirectly reducing the cascade damage caused by calcium overload.

