Unveiling citicoline's mechanisms and clinical relevance in the treatment of neuroinflammatory disorders

Theodor Bilharz Research Institute

Bibliographic Information

Authors: Cavalu S.; Saber S.; Ramadan A.; Elmorsy E.A.; Hamad R.S.; Abdel-Reheim M.A.; Youssef M.E.

Journal: FASEB Journal

Publisher: John Wiley and Sons Inc

Publication Date: 2 September 2024

Volume / Issue: Volume 38 / Issue 17

Article No.: e70030

ISSN: 8926638

DOI: 10.1096/fj.202400823R

Scopus: View on Scopus

PubMed: 39221499

Document Type: Review

Access: All Open Access; Hybrid Gold Open Access

Authors and Affiliations

Cavalu S., Faculty of Medicine and Pharmacy, University of Oradea, Oradea, Romania; Saber S., Department of Pharmacology, Faculty of Pharmacy, Delta University for Science and Technology, Gamasa, Egypt; Ramadan A., Department of Biochemistry, Faculty of Pharmacy, Delta University for Science and Technology, Gamasa, Egypt; Elmorsy E.A., Department of Pharmacology and Therapeutics, College of Medicine, Qassim University, Buraidah, Saudi Arabia; Hamad R.S., Biological Sciences Department, College of Science, King Faisal University, Al Ahsa, Saudi Arabia, Central Laboratory, Theodor Bilharz Research Institute, Giza, Egypt; Abdel-Reheim M.A., Department of Pharmaceutical Sciences, College of Pharmacy, Shaqra University, Shaqra, Saudi Arabia, Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni Suef, Egypt; Youssef M.E., Department of Pharmacology, Faculty of Pharmacy, Delta University for Science and Technology, Gamasa, Egypt

Abstract

Citicoline, a compound produced naturally in small amounts in the human body, assumes a pivotal role in phosphatidylcholine synthesis, a dynamic constituent of membranes of neurons. Across diverse models of brain injury and neurodegeneration, citicoline has demonstrated its potential through neuroprotective and anti-inflammatory effects. This review aims to elucidate citicoline's anti-inflammatory mechanism and its clinical implications in conditions such as ischemic stroke, head trauma, glaucoma, and age-associated memory impairment. Citicoline's anti-inflammatory prowess is rooted in its ability to stabilize cellular membranes, thereby curbing the excessive release of glutamate—a pro-inflammatory neurotransmitter. Moreover, it actively diminishes free radicals and inflammatory cytokines productions, which could otherwise harm neurons and incite neuroinflammation. It also exhibits the potential to modulate microglia activity, the brain's resident immune cells, and hinder the activation of NF-κB, a transcription factor governing inflammatory genes. Clinical trials have subjected citicoline to rigorous scrutiny in patients grappling with acute ischemic stroke, head trauma, glaucoma, and age-related memory impairment. While findings from these trials are mixed, numerous studies suggest that citicoline could confer improvements in neurological function, disability reduction, expedited recovery, and cognitive decline prevention within these cohorts. Additionally, citicoline boasts a favorable safety profile and high tolerability. In summary, citicoline stands as a promising agent, wielding both neuroprotective and anti-inflammatory potential across a spectrum of neurological conditions. However, further research is imperative to delineate the optimal dosage, treatment duration, and underlying mechanisms. Moreover, identifying specific patient subgroups most likely to reap the benefits of citicoline as a new therapy remains a critical avenue for exploration. © 2024 Federation of American Societies for Experimental Biology.

Keywords

cell signaling; citicoline; CNS disorders; neuroinflammation; new therapies; Animals; Anti-Inflammatory Agents; Clinical Relevance; Cytidine Diphosphate Choline; Humans; Neuroinflammatory Diseases; Neuroprotective Agents; Nootropic Agents; glutamic acid; phosphatidylcholine; transcription factor; antiinflammatory agent; neuroprotective agent; nootropic agent; antiinflammatory activity; brain injury; cell membrane; central nervous system disease; clinical significance; cognitive defect; drug therapy; glaucoma; head injury; human; immunocompetent cell; major clinical study; memory disorder; microglia; nerve degeneration; nervous system inflammation; neuroprotection; nonhuman; prevention; review; side effect; signal transduction; therapy; treatment duration; animal; metabolism

Citation Information

Scopus Citations: 25

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