Pharmacological treatment of cerebrovascular disorders was introduced at the beginning of the 20th Century. Since then, a multitude of studies have focused on the development of a consensus for a well defined taxonomy of these disorders and on the identification of specific patterns of cognitive deficits associated with them, but with no clear consensus.
Nevertheless, citicoline has proved to be a valid treatment in patients with a cerebrovascular pathogenesis for memory disorders. A metanalysis performed on the entire database available from the clinical studies performed with this compound confirms the experimental evidence from the animal studies which have repeatedly described the multiple biological actions of citicoline in restoring both the cell lipid structures and some neurotransmitter functions.
As a drug, citicoline has been proposed for use in traumatic brain injures, stroke, vascular dementia, Parkinson's disease, and brain aging where it has the function of stabilizer of cell membranes and reduces the presence of free radicals. In particular, there is some evidence of a stimulating role of citicoline for the release of dopamine neurotransmitters in the brain.
Citicoline, by activating the central cholinergic system, also increases plasma adrenocorticotropic hormone (ACTH) levels and potentiates serum thyrotrophin (TSH) levels. The stimulation of central nicotinic and muscarinic receptors also increases growth hormone (GH) and luteinizing hormone (LH) serum levels. This activity on the cholinergic system is of high therapeutic usefulness in those clinical conditions where alterations of acetylcholine metabolism are considered one of the primary causes of disease, eg, Alzheimers Disease (AD).
The biological activity attributed to citicoline has suggested a possible role of citicoline on improving memory (McDaniel 2003). Some clinical studies have given evidence to this hypothesis; and there is a proposal for studying citicoline in mild cognitive impairment (MCI) with the aim of confirming both its efficacy in these patients and a possible role as a retardant agent for the cognitive deterioration of the eventual subsequent dementia.