Citicoline Affects Appetite and Cortico-Limbic Responses ...

Cytidine-5&#;-diphosphocholine (citicoline) has a variety of cognitive enhancing, neuroprotective, and neuroregenerative properties. In cocaine-addicted individuals, citicoline has been shown to increase brain dopamine levels and reduce cravings. The effects of this compound on appetite, food cravings, and brain responses to food are unknown. We compared the effects of treatment with citicoline (500 mg/day versus mg/day) for six weeks on changes in appetite ratings, weight, and cortico-limbic responses to images of high calorie foods using functional magnetic resonance imaging (fMRI). After six weeks, there was no significant change in weight status, although significant declines in appetite ratings were observed for the mg/day group. The higher dose group also showed significant increases in functional brain responses to food stimuli within the amygdala, insula, and lateral orbitofrontal cortex. Increased activation in these regions correlated with declines in appetite ratings. These preliminary findings suggest a potential usefulness of citicoline in modulating appetite, but further research is warranted.

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The stimulation paradigm has been described in detail in several previous reports ( Killgore, et al., ; Killgore & Yurgelun-Todd, a , b , ). In brief, participants were scanned while viewing a series of colorful visual images that included both high-calorie foods (e.g., cheeseburgers, hot dogs, french-fries, ice cream, cake, cookies) and control images of non-food objects with similar visual complexity, texture, and color (e.g., rocks, shrubs, bricks, trees, flowers). The stimulation paradigm was 150 seconds in duration, and comprised 5 alternating 30-second periods (i.e., control, high-calorie, control, high-calorie, control). Each alternating block consisted of ten photographs ( msec stimulus presentation and a 500 msec inter-stimulus interval). Stimuli were controlled by a Macintosh computer running Psyscope ( Macwhinney, Cohen, & Provost, ) and were back-projected onto a screen placed at the rear of the scanner. Participants viewed the stimuli via a mirror mounted on the head coil. The same stimuli were presented at baseline and again following six weeks of treatment.

Participants completed two interview/functional imaging scanning sessions separated by six weeks. At the first visit, participants completed a medical and psychiatric interview and several questionnaires about food and lifestyle preferences, and were asked to rate their typical appetite on a 10-point Likert scale from 1 (never hungry) to 10 (always hungry). Following the interview and questionnaires, participants underwent an fMRI scan to examine responses to images of high calorie foods. Participants were scanned at approximately the same time of day to minimize circadian influences. No attempts were made to restrict food intake prior to the scans and participants were allowed to follow their normal diets. In an open label design, participants were randomly assigned to one of two conditions, a Low Dose or a High Dose administration of citicoline (Cognizin&#;, Kyowa Hakko Kogyo Co., Ltd, Japan). Eight participants (4 male, 4 female) were assigned to consume the Low Dose (i.e., one 500 mg capsule/day) of citicoline over the intervening six week period, while the other eight participants were assigned to consume the High Dose (i.e., four 500 mg capsules/day) during the same time period. Participants were contacted by twice per week to improve compliance and to allow for reporting of any adverse effects. Participants returned to the neuroimaging center to repeat the questionnaires and fMRI scanning procedure after six weeks of treatment. Changes in appetite ratings and weight were calculated for each participant by subtracting scores at Visit 1 from those at Visit 2.

Sixteen healthy adults (8 men; 8 women; 12 right-handed by self-report) ranging from 40 to 57 years (M = 47.3, SD = 5.4) were recruited from the community of Belmont, MA. At intake, the Body Mass Index (BMI) of participants ranged from 20.1 to 38.6 (M = 25.3, SD = 5.2). Volunteers were screened for a wide range of potential medical, psychiatric, and health concerns and only those participants that were deemed to be in good medical and psychiatric health were included. Participants had normal or corrected-normal vision (with contact lenses). The present study was conducted under the guidelines of the McLean Hospital Institutional Review Board. All participants provided written informed consent and were given a small financial compensation for their participation.

Changes in regional brain activation from Visit 1 to Visit 2 were used to predict corresponding changes in appetite ratings. As evident in , changes in ROI activation when viewing high-calorie food images were associated with changes in appetite between the two visits. Specifically, participants that showed the greatest increase in the task-related activation of the right amygdala (T = 3.76, 146 voxels, x = 28, y = &#;2, z = &#;24), bilateral insula (T = 5.09, 865 voxels, x = 36, y = 12, z = 4; T = 4.36, 22 voxels, x = &#;28, y = 22, z = &#;20; T = 3.75, 624 voxels, x = &#;42, y = 10, z = &#;6), and left lateral orbitofrontal cortex (T = 6.63, 532 voxels, x = &#;36, y = 22, z = &#;16; T = 4.22, 549, voxels, x = 26, y = 24, z = &#;14) tended to show the greatest declines in appetite ratings between the two visits. The correlations were similar for the Low Dose (i.e., right amygdala r = &#;.63, p = .085; right insula r = &#;.89, p = .003; left OFC r = &#;.91, p = .002) and High Dose (i.e., right amygdala r = &#;.91, p = .002; right insula r = &#;.70, p = .051; left OFC r = &#;.88, p = .004) groups. Exploratory analysis of the correlations at the whole brain level revealed no regions showing positive correlations between changes in brain activation and changes in appetite ratings, but did show a number of negatively correlated clusters where increased brain activation between the two testing sessions was associated with decreased appetite ratings. These regions included inferior orbitofrontal cortex, thalamus, and insula, among others (see ).

The effects of High vs. Low Dose citicoline on changes in brain activation were compared for the three ROIs. As evident in , the High Dose group showed significantly greater between-visit increases in activation within the left amygdala (T = 2.25, 40 voxels, MNI coordinates: x = &#;20, y = 0, z = &#;22), bilateral insula (T = 3.59, 92 voxels, MNI coordinates: x = &#;28, y = 32, z = 6; T = 3.49, 25 voxels; MNI coordinates: x = 34, y = 22, z = 10; T = 1.99, 10 voxels, MNI coordinates: x = &#;36, y = &#;10, z = 6), and right lateral orbitofrontal cortex (T = 2.76, 41 voxels, MNI coordinates: x = 34, y = 30, z = &#;22) relative to the Low Dose group. In contrast, there were no ROIs where Low Dose citicoline produced greater change than High Dose citicoline. In contrast to the ROIs, exploratory whole brain comparisons revealed that only one region, located within the right cerebellum (T = 4.35, 10 voxels, MNI coordinates: x = 30, y = &#;56, z = &#;24), showed significantly greater change in activation in the High Dose group relative to the Low Dose group. In contrast, there were no regions that showed greater pre-post changes in activation in the Low Dose group relative to the High Dose group for the exploratory whole brain analysis.

Self-rated appetite declined significantly between Visit 1 (M = 6.8, SD = 1.5) and Visit 2 (M = 6.1, SD = 1.5) for the sample as a whole, t(15) = -2.83, p = .02. The mean change scores for both groups declined between visits, but the magnitude of decline only reached significance for the High Dose group (M = &#;0.88, SD = 0.83), t(7) = &#;2.97, p = .02, while the decline for the Low Dose group did not (M = &#;0.38, SD = 0.92), t(7) = &#;1.16, p = .29. Between group comparison of these changes did not reach statistical significance, however, t(14) = 1.14, p = .27. Similarly, there was no significant change in weight from Visit 1 to Visit 2 for the low (M = &#;6.4 lbs, SD = 11.0, t(6) = &#;1.55, p = .17) or high (M = &#;0.57 lbs, SD = 3.8, t(6) = &#;0.40, p = .71) dose groups and the magnitude of weight change did not differ between the two groups, t(13) = 1.55, p = .15.

Discussion

These preliminary findings suggest that citicoline administration was associated with a modest but significant decline in appetite ratings for the group as a whole. High-Dose citicoline (i.e., mg/day) for six weeks was associated with a significant decline in appetite ratings from baseline, whereas no significant effect was observed for the Low Dose (i.e., 500 mg/day), and no changes were evident in weight status. Because the appetite effect was only significant in the High Dose group, it raises the possibility of a dose-dependent effect of citicoline on appetite suppression. Such findings are consistent with animal studies linking citicoline to increases in dopamine (Agut, et al., ; Rejdak, et al., ) and human evidence suggesting that citicoline may be effective at reducing aspects of craving in cocaine-dependent individuals (Renshaw, et al., ). However, given the preliminary nature of these findings and the lack of significant between-group differences in appetite suppression or weight change, further research that includes larger samples and a placebo control group will be necessary to determine the magnitude and reliability of the effects of citicoline on appetite.

Previous studies using fMRI have shown that visual perception of images of appetizing foods are generally associated with increased activation in a broad network of cortical and limbic regions, including the orbitofrontal cortex, medial prefrontal cortex, amygdala, hippocampus, ventral striatum, insula, and cingulate gyrus (Killgore, et al., ; Killgore & Yurgelun-Todd, b; Siep, et al., ; Stoeckel, et al., ), but activation of these regions is highly dependent upon a number of factors including weight (Killgore & Yurgelun-Todd, a; Stice, Spoor, Bohon, Veldhuizen, & Small, ; Stoeckel, et al., ), mood (Killgore & Yurgelun-Todd, , ), eating disorder diagnostic status (Santel, Baving, Krauel, Munte, & Rotte, ; Schienle, et al., ), and immediate hunger or nutritional state of the individual (Cornier, Von Kaenel, Bessesen, & Tregellas, ; Fuhrer, Zysset, & Stumvoll, ; Siep, et al., ). For the present study, we focused our analyses on three regions that are often associated with cerebral responses to food. These included the lateral orbitofrontal cortex, insular cortex, and amygdala.

In the present study, we found that citicoline administration was associated with dose-dependent changes in functional brain responses to high calorie foods between the two visits. Compared to the Low Dose of citicoline, the High Dose was associated with increased activation within the right lateral orbitofrontal cortex ROI during visual perception of high calorie foods. Medial aspects of the orbitofrontal cortex have been associated with reward processing (Kringelbach & Rolls, ) and this region tends to be activated in during perception of appetizing food stimuli (Rolls & McCabe, ; Schienle, et al., ). In contrast, activation in the lateral orbitofrontal regions has been associated with punishment experiences (Kringelbach & Rolls, ), satiety, and the desire to stop eating (Hinton, et al., ; Killgore & Yurgelun-Todd, ; Small, et al., ). When sated, images of normally appetizing foods produce increased activation of the lateral orbitofrontal cortex (Santel, et al., ). When considered in light of these previous studies, the present findings suggest that the High Dose treatment may have led to appetite changes by increasing the responsiveness of this region to images of calorie-rich and high-fat foods, though this speculation will require further study. High doses of citicoline were also associated with greater activation increases in bilateral insula and the left amygdala in response to the high-calorie food images. Activation of these regions has been associated with anticipation of aversive experiences and visual perception of unpleasant images in previous research (Nitschke, Sarinopoulos, Mackiewicz, Schaefer, & Davidson, ), and the insula has frequently been implicated in the experience and perception of disgust (Stark, et al., ; Wright, et al., ) and interoceptive awareness of visceral/somatic states (Craig, ). The present findings suggest that treatment with the High Dose of citicoline produced significantly greater increases in left amygdala activation than the Low Dose treatment. Previous research has suggested that visual perception of foods, regardless of calorie content, appears to be associated with amygdala activation (Killgore, et al., ). Elevated activation within the amygdala is often associated with negative affective experiences, such as conditioned fear (LaBar, Gatenby, Gore, LeDoux, & Phelps, ) or perception of unpleasant or negatively valenced emotional stimuli (Stark, et al., ). Again, while speculative and in need of further study, these findings tentatively suggest that citicoline may affect appetite by increasing responsiveness of these regions.

Finally, it was hypothesized that change in activation of the three cerebral regions of interest between Visit 1 to Visit 2 would correlate with appetite changes over this same period. This hypothesis was supported, as increased activation within each of the three regions was significantly predictive of reduced appetite by the end of the study. In other words, appetite ratings declined most extensively for those individuals that showed the greatest increases in activation within the amygdala, insular cortex, and lateral orbitofrontal cortex in response to high calorie food images over the six-week period. Findings for the insula and orbitofrontal cortex were further confirmed in the exploratory whole brain analysis. Because activation in these paralimbic regions is often associated with negative affect (Markowitsch, Vandekerckhovel, Lanfermann, & Russ, ), aversive perceptions (Stark, et al., ; Wright, et al., ), and behavioral inhibition (Ridderinkhof, van den Wildenberg, Segalowitz, & Carter, ), increased activation in these regions might indicate that the food images were being perceived as less rewarding and potentially more aversive than at baseline and therefore led to reduced desire to consume food.

Although our hypothesis was based on limited evidence that citicoline may affect the dopamine system (Agut, et al., ; Gimenez, et al., ; Radad, et al., ; Rejdak, et al., ), it is possible that the changes observed here in the High Dose group may have resulted from properties of citicoline other than its effects on the dopamine system. Citicoline has a number of mechanisms of action, including functioning as a precursor of phospholipid and acetylcholine synthesis (Conant & Schauss, ; D'Orlando & Sandage, ), enhancement of the release of other neurotransmitters such as norepinephrine (Lopez, et al., ), counteracting the buildup of beta-amyloid protein and cellular apoptosis in the hippocampus (Alvarez, Sampedro, Lozano, & Cacabelos, ), and repair of neuronal membranes via increased synthesis of phospholipid components including cardiolipin (Rao, et al., ) and sphingomyelin (Adibhatla & Hatcher, ). Growing evidence suggests that citicoline may have neuroprotective effects following stroke or other brain injuries and may enhance cognitive performance in patients suffering from degenerative dementias such as Alzheimer&#;s and Parkinson&#;s Diseases (Conant & Schauss, ). Thus, the mechanisms of action and potential neural systems affected by citicoline are numerous and remain to be fully elucidated. Further research will be necessary to determine the specific appetite systems affected by citicoline and whether this compound shows clinical efficacy at changing appetite or weight status.

We present these findings as preliminary, fully mindful of the limitations inherent in a non-placebo controlled design with a relatively small sample size. Furthermore, because this was an open label trial and participants were aware of the treatment and dosage they received, it is possible that their expectations may have affected their responses to the questionnaires or the stimuli. Future studies would benefit from the use of double blind crossover designs and these findings will need to be replicated with larger samples. It should also be reiterated that despite the decline in appetite ratings, no change in actual weight was noted. However, it is possible that the change in appetite was gradual and that a six week trial may not have been adequate to be expressed in changes in weight. Trials extending for longer durations may clarify this issue. An additional factor to be considered is the potential influence that body mass may play in the effects of citicoline on brain responses, as previous research suggests that body mass is related to brain responses to food images (Killgore & Yurgelun-Todd, a). BMI was not controlled or manipulated in the present study due to the small sample size and limited degrees of freedom, but future investigations should consider the role of this variable in food perception. To avoid the effects of hunger on brain activation, no attempts were made to restrict food intake prior to the scans, but this may have also had some effect on brain responses. Future studies will need to examine the interaction of citicoline and hunger on brain responses to food stimuli. Finally, it is not possible to rule out exposure and habituation effects in the present study, as participants viewed the same stimuli on both occasions. However, this is unlikely in light of the six-week intervening period between the scans and our finding that most participants, particularly those in the High Dose group actually showed increased activation rather than a reduction, arguing against habituation to the food stimuli. In light of the numerous neuroprotective and health promoting effects, high tolerability, and low side-effect profile of citicoline, these tentative findings are intriguing and warrant further research into the efficacy of this substance as a potential supplement for modulating appetite.

Citicoline, also known as cytidine-5&#;-diphosphocholine or CDP-choline, is a fat molecule that is an important part of the cell membrane.

Researchers have studied citicoline in the setting of neurological (brain and nerve) diseases, such as dementia. It is commonly used to enhance cognitive function.

This article discusses citicoline's potential benefits and safety.

Citicoline Supplement Facts

• Active Ingredient(s): Citicoline
• Alternate Name(s): Cytidine-5&#;-diphosphocholine (CDP-choline)

• Legal Status: Over-the-counter (OTC) dietary supplement (United States); prescription drug (Japan and Europe)

• Suggested Dose: The therapeutic dose of citicoline ranges from 500 to 2,000 milligrams (mg) per day.
  Citicoline can be given intravenously (IV, within a vein), intramuscularly (within a muscle), and orally (by mouth).
• Safety Considerations: Caution should be taken if you are pregnant or breastfeeding because the safety of citicoline is unknown in these populations.

What Is Citicoline?

Citicoline has been studied to treat the following conditions:

• Brain stroke
• Dementia prevention and treatment
• Traumatic brain injury
• Nerve pain and injury (animal models)

Citicoline has improved cognition in people with neurological conditions. And it has also improved memory and cognitive function in healthy people.

Citicoline works to protect the brain by:

• Increasing dopamine,

  norepinephrine

  , and serotonin levels
• Serving as a precursor to

  acetylcholine

  , a type of chemical messenger that helps brain and body functions
• Lowering levels of

  glutamate

  , a brain chemical that causes damage to the brain under low oxygen conditions
• Blocking

  phospholipase

  A2, a type of enzyme that then reduces inflammation
  

Older adult solving a crossword puzzle.

Uses

Supplement use should be individualized and vetted by a healthcare professional, such as a registered dietitian (RD) or registered dietitian nutritionist (RDN), pharmacist, or healthcare provider. No supplement is intended to treat, cure, or prevent disease.

Age-Related Cognitive Decline

Citicoline supplementation improved memory in older adults with age-associated memory impairment compared to a placebo (no treatment) group. However, the study is not generalizable to young adults or people with cognitive diseases like dementia and Alzheimer&#;s disease (AD).

A review of a collection of studies showed a positive effect of citicoline on cognitive function in people with mild vascular cognitive impairment, vascular dementia, or AD. Because citicoline was used with the standard treatment (acetylcholinesterase inhibitor) for AD, the effect of citicoline alone on AD is unclear.

Cognitive Enhancement

In a study, a citicoline-caffeine-based drink improved attention, mental alertness, and memory. Since citicoline was combined with caffeine, it is unclear what the effect of citicoline alone is on attention and memory.

Based on a study in young, healthy males, citicoline improved motor function and attention after four weeks of supplementation. However, study results might not apply to populations other than young, healthy males.

Eye Surgery Recovery

Using citicoline eye drops three times a day for one month after eye surgery aided the recovery of corneal sensitivity after LASIK (laser-assisted in situ keratomileusis).

Stroke Treatment

A systematic review of studies found citicoline alone benefited acute ischemic stroke (blood clots in the brain). However, citicoline offers limited benefits on top of standard stroke treatment with rtPA or recombinant tissue plasminogen activator (clot-busting drug).

Furthermore, one study in people with a first ischemic stroke showed that after the stroke, people who received citicoline over two years had reduced cognitive impairment.

Neuroprotection

Citicoline has been studied for the following neuroprotective (protecting the nerves and brain) effects:

While citicoline may benefit various cognitive conditions, further research is needed to confirm these results.

Food Sources

Besides supplementation, another way to increase citicoline levels is by consuming cytidine- and choline-rich foods. Citicoline is composed of cytidine and choline. Cytidine is found in meat, especially organ meats.

Foods rich in choline include the following:

• Beef liver, pan-fried, 3 ounces (356 mg per serving)
• Egg, hard-boiled, 1 large egg (147 mg per serving)
• Beef top round, separable lean only, braised, 3 ounces (117 mg per serving)
• Chicken breast, roasted, 3 ounces (72 mg per serving)
• Beef, ground, 93% lean meat, broiled, 3 ounces (72 mg per serving)
• Fish, cod, Atlantic, cooked, dry heat, 3 ounces (71 mg per serving)
• Beans, kidney, canned, one-half cup (45 mg per serving)
• Quinoa, cooked, 1 cup (43 mg per serving)
• Brussels sprouts, boiled, one-half cup (32 mg per serving)
• Broccoli, chopped, boiled, drained, one-half cup (31 mg per serving)
  

Dosage

The usual therapeutic dose for humans used in clinical trials is 500 to 2,000 mg daily.

Listed below are the citicoline dosing for various conditions used in clinical trials.

For more Is Citicoline A Stimulantinformation, please contact us. We will provide professional answers.

• Add-on therapy in PD: Usual treatment with levodopa/carbidopa for five weeks plus citicoline 1,000 mg intravenously daily from weeks three to five.

• Add-on therapy in MDD: Citicoline 100 mg by mouth every 12 hours plus Celexa 20 mg per day (for the first week) and 40 mg daily by mouth for the following five weeks.
   
• Add-on therapy in schizophrenia: 1,000 milligrams (mg) by mouth per day for three days, 2,000 mg per day (in two divided doses) on day four for four days, and 2,500 mg per day (in two divided doses) starting week two; used with up to 6 mg of risperidone daily in the study.

• Age-related cognitive decline: Two 250 mg capsules of citicoline (500 mg/day) by mouth with breakfast for 12 weeks.

• Cocaine dependence in bipolar I disorder: 500 mg by mouth per day for one week, then 1,000 mg per day at week two, mg per day at week four, and 2,000 mg per day at week six, for 12 weeks total.

• Cognitive enhancement: Beverage consisting of 250 mg of citicoline and caffeine (amount unclear).
  For motor function and attention in adolescent males, 250 or 500 mg capsule by mouth per day for 28 days.

• Glaucoma: Citicoline oral solution of 50 mg per milliliter (mL) (mg/mL) used for a daily dose of 10 mL or 500 mg of citicoline by mouth in the morning.

• Head injury: For moderate to severe head injury, 2 g by mouth for 60 days; for severe head injury, 3 g intravenously (IV) for 21 days.

• Stroke treatment: 250 to 2,000 mg from 10 days to six weeks. In the clinical trials, citicoline was given intravenously, orally, or both intravenously and orally;
  for cognitive impairment in people poststroke, 1 gram (g) daily by mouth for two years.

• Methamphetamine dependence: 1 gram (g) of CDP-choline capsule by mouth twice daily for eight weeks.

• Neuroprotection: In neonates (newborns) with HIE, 10 milligrams (mg) per kilogram (kg) per 12 hours (h) intravenously for four weeks plus other supportive measures.
  
  
• Nonproliferative diabetic retinopathy: One drop of citicoline and vitamin B12 eye drops containing citicoline 2%, hyaluronic acid 0.2%, and cyanocobalamin (vitamin B12) 0.05% into one eye three times daily for 36 months.
  
  

Safety

Citicoline is naturally present in the human body and is a nontoxic substance. Citicoline taken by mouth at amounts of up to 1 g per day has been shown to be safe and well-tolerated.

Overall, citicoline is well-tolerated and has no adverse systemic cholinergic side effects (e.g., increased saliva and tear production, urination and defecation, and decreased heart rate).

Avoid citicoline if you're allergic to it or its components (parts). Seek immediate medical attention if you have a severe allergic reaction (itching, hives, shortness of breath).

Side Effects

Although no serious side effects were noted in some studies, mild side effects include the following:

• Increased appetite
• Weight gain
• Increased flatulence (passing gas)
• Headache
• Increased burping

Common side effects include the following:

• Nausea
• Vomiting
• Dizziness
• Stomach upset
• Fatigue
  

Interactions

While there are few studies on drug interactions with citicoline, citicoline theoretically can increase the effect of levodopa by increasing dopamine levels.

Moreover, citicoline with levodopa allowed for a lower dose of levodopa in studies.

Precautions

Many clinical trials exclude people who are pregnant or breastfeeding. Therefore, the safety of citicoline in people who are pregnant or breastfeeding is unknown. 

Although citicoline is well-tolerated, it is essential not to take more than instructed. 

Please consult with your healthcare provider before starting citicoline. 

Dietary supplements are not regulated like prescription medications in the United States. Therefore, some may be safer than others. When choosing a supplement, consider factors such as third-party testing, potential drug interactions, and other safety concerns. Talk to a healthcare provider or a registered dietitian nutritionist (RD or RDN) about supplement quality and safety.

Similar Supplements

Other supplements that have cognitive-enhancing properties include the following:

• Antioxidant polyphenols: Polyphenols, such as resveratrol, improved cognitive function in people with mild cognitive impairment and Alzheimer&#;s disease in clinical study.

• B vitamins: B vitamins have decreased cognitive decline, and a higher dietary folate intake has been shown to lower dementia risk.

• Medium-chain triglycerides (MCT): Consuming MCT jelly by mouth three times daily for a daily MCT dose of 17.3 g for 30 days improved cognition in people aged between 57 and 87 years with mild to moderate Alzheimer&#;s disease.

• Omega-3 fatty acids: An analysis of a collection of studies revealed that omega-3 supplementation affects cognitive function in adults of advanced age in a positive way.

• Selenium: Supplementation with selenium has been shown to improve cognitive function in people with mild cognitive impairment and Alzheimer&#;s disease.
  
  
• Vitamin D: A clinical trial conducted in China found that daily vitamin D supplementation of 800 international units (IU) by mouth daily for 12 months improved cognitive function by reducing oxidative stress in participants aged 65 and older with mild cognitive impairment.
  
  

Similar to citicoline, the supplements above are believed to improve cognitive function. However, whereas citicoline is naturally found in the human body as CDP-choline, the above supplements are not produced by the human body.

Summary

Not only does citicoline protect the brain, but it also has an excellent safety profile. 

Several clinical studies indicate citicoline's therapeutic potential in various neurological conditions, including age-related cognitive decline and stroke treatment and recovery.

Frequently Asked Questions

• How does citicoline work to improve cognitive function?

  Citicoline works to improve cognitive function by increasing brain choline and promoting the production of acetylcholine, a neurotransmitter essential for memory. Additionally, citicoline increases levels of dopamine, norepinephrine, and serotonin.

• How is citicoline administered?

  Citicoline is administered via the following routes: oral (by mouth), intravenous (within a vein), or intramuscular (within a muscle).
  

• What is the difference between citicoline and choline?

  Once citicoline is ingested, it is broken down into two molecules: cytidine and choline.

  After these two molecules cross the blood-brain barrier separately and reach the brain cells, they combine to form CDP-choline (citicoline) again.
  

  Citicoline serves as a source for making phosphatidylcholine, one of the parts of cell membranes.

  Choline, one of the breakdown products of citicoline, serves as one of the building blocks for the production of acetylcholine, a neurotransmitter (chemical messenger) involved in memory and muscle movement.

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