Vital for brain health
Patented Citicoline (Cognizin®) - natural substance found in our body
Helps to regulate memory & cognitive functions
Aid neural communication; maintain healthy level of acetylcholine (neural transmitter)
- Cognizin® Citicoline clinically proven to improve brain health
- Improve memory and thinking speed
- Ensure absorption
- Fortified with multivitamins & minerals to provide nutrients to the body and support general wellbeing
Each chewable contains: Citicoline(Cognizin) – 60mg Multivitamins and Minerals blend (Vitamin A, Vitamin B1, Vitamin B2, Vitamin B3, Vitamin B5, Vitamin B6, Vitamin D3, Vitamin E, Biotin, Folic Acid, Calcium, Iodine, Iron, Magnesium, Phosphorus, and Zinc) – 48mg
Cognizin® Citicoline (CDP-Choline) – A natural occurring nutrient produced in the body. Cognizin® Citicoline is known as the natural “brain nutrient”.
Added with Multivitamins & Minerals blend (Vitamin A, Vitamin B1, Vitamin B2, Vitamin B3, Vitamin B5, Vitamin B6, Vitamin D3, Vitamin E, Biotin, Folic Acid, Calcium, Iodine, Iron, Magnesium, Phosphorus, and Zinc) to support healthy body and brain functions.
Cognizin® Citicoline is patented and produced by Kyowa Hakko, Japan
Memomax helps to improve memory, focus, mood and energy.
Citicoline is a complex organic molecule that functions as an intermediate in the biosynthesis of cell membrane phospholipids. Citicoline is also known as CDP-choline or cytidine diphosphate choline (cytidine 5’–diphosphocholine). CDP-choline belongs to the group of biomolecules in living systems known as nucleotides that play important roles in cellular metabolism.
The pharmacologic action of citicoline appears to involve mechanisms that extend beyond phospholipid metabolism. Citicoline metabolites – choline, methionine, betaine, and cytidine-derived nucleotides – enter a number of metabolic pathways.
Biochemical markers of cholinergic nerve transmission are known to be deficient in conditions characterized by degeneration of cholinergic neurons, such as Alzheimer`s disease. Citicoline modestly improves cognitive function in Alzheimer`s disease by serving as an acetylcholine precursor. The brain uses choline preferentially for acetylcholine synthesis, which can limit the amount of choline available for phosphatidylcholine production.
Citicoline has been investigated as a therapy for stroke patients. Three mechanisms are postulated: (1) repair of the neuronal membrane via increased synthesis of phosphatidylcholine; (2) repair of damaged cholinergic neurons via potentiation of acetylcholine production; and (3) reduction of free fatty acid build-up at the site of stroke-induced nerve damage.
Citicoline protects cholinergic neurons from autocannibalism, a process in which membrane phospholipids are catabolized to provide choline for synthesis of acetylcholine. This occurs when choline supplies are depleted, necessitating sacrifice of membrane phospholipids to maintain neurotransmission. As an exogenous source of choline for acetylcholine production, citicoline thus spares membrane phospholipids (in particular, phosphatidylcholine) and prevents neuronal cell death.
Citicoline is a water-soluble compound with greater than 90% bioavailability. PK studies in healthy adults have shown oral doses of citicoline to be rapidly absorbed, with less than 1% excreted in the feces. Plasma levels peak in a biphasic manner, at 1 hr after ingestion followed by a second larger peak at 24 hrs post-dosing.
Citicoline is metabolized in the gut wall and liver. The byproducts of exogenous citicoline formed by hydrolysis in the intestinal wall are choline and cytidine. Following absorption, choline and cytidine are dispersed throughout the body, enter systemic circulation for utilization in various biosynthetic pathways and cross the blood-brain barrier for re-synthesis into citicoline in the brain.
Pharmacokinetic studies using 14C citicoline show citicoline elimination occurs mainly via respiratory CO2 and urinary excretion, in two phases, mirroring the biphasic plasma peaks. The initial peak in plasma concentration is followed by a sharp decline, which then slows over the next 4 to 10 hrs. In the second phase, an initially rapid decline after the 24-hr plasma peak is similarly followed by a slower elimination rate. The elimination t½ is 56 hrs for CO2 and 71 hrs for urinary excretion.