How Much do You Know the Effects of Citicoline？

Exogenous citicoline can be hydrolyzed into cytidine and choline. The decomposed choline and cytidine can be phosphorylated again, and catalyzed by cytidine triphosphate-phosphocholine cytidine transferase, cytidine triphosphate and choline monophosphate are synthesized into citicoline. Citicoline and diacylglycerol synthesize phosphatidylcholine, which forms the double-layer lipid structure of the cell membrane.

The choline decomposed by citicoline is acetylated to produce the neurotransmitter acetylcholine. Another product, trimethylammonium hydantoin from the decomposition of choline, generates S-adenosyl-L-methionine through the methionine pathway, and finally further synthesizes glutathione with antioxidant effect.

In vitro experiments have confirmed that insufficient choline degrades phosphatidylcholine and sphingomyelin in nerve cell membranes, thereby causing cell apoptosis. Due to the continuous supply of choline in the catabolism of exogenous citicoline, it can prevent nerve cell membrane damage and cholinergic nerve death.

Citicoline is classified as a neuroprotective agent, but the direct treatment of acute ischemic stroke itself has not yet been confirmed. Internationally, the application of citicoline combination therapy has been proposed. It will explore the use of different therapeutic drugs to prevent the cascade of strokes, that is, the pathophysiological and biochemical reactions triggered by cerebral ischemia. For example, combined therapy after focal cerebral ischemia. 

The application of low-dose citicoline and diazeppine or basic fibroblast growth factor can significantly reduce the infarct volume, but a small-dose drug alone is ineffective.

It also includes the combined use of thrombolysis and neuroprotective agents. It is hoped that more neuroprotective treatments that are effective for acute ischemic stroke will soon appear, and that this treatment can be combined with thrombolysis to enhance the therapeutic effect.