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Centrophenoxine is a cholinergic compound that contains a dimethylaminoethanol (DMAE) component and a paracholrphenoxyacetic (PCPA) component that functions as a superior absorbed transporter of DMAE into the brain. Dimethylaminoethanol is a naturally occurring food component that can be found in fish although it is also a natural metabolite within the human body. On the other hand, PCPA is a synthetic component that is similar to auxins (a group of plant hormones). Centrophenoxine has a superior absorption rate and efficiency across the blood brain barrier compared to DMAE.Centrophenoxine is also referred to as Lucidril (brand name), or Meclofenoxate. DMAE is the natural chemical from which Centrophenoxine is synthesized, and it has been observed to enhance cognition and mood. Its (DMAE) mechanism of action is not very clear. Centrophenoxine was originally developed as treatment for degenerative conditions like dementia. It can be obtained online or as an over counter drug/nootropic agent. Centrophenoxine is lipid soluble.

Centrophenoxine is quite well researched compared to other nootropic agents and it is known to enhance cognition and general brain health. It has a broad range of positive effects in memory, mind, cognition and overall brain health. Since it increases the presence of acetylcholine neurotransmitter within the brain, it is a cholinergic nootropic. This property of Centrophenoxine is vital since it profoundly affects intellect and prevents memory loss as a result of aging. Centrophenoxine reverses aging signs like the accumulation of waste product in the brain (an example is the build-up of Potassium that lowers efficiency of brain cells and causes death). It achieves this by reducing lipofuscin and increasing uptake of glucose and oxygen into the brain (these two enhance the overall functioning of the brain cells). Centrophenoxine can be taken alone or stacked with other nootropic agents since it also promotes and maintains neuron health. It is a popular nootropic agent because of its anti-aging and cognitive enhancing properties. Centrophenoxine is one of the earliest mental enhancers and clinical studies into its therapeutic significance have been carried out for the last 50 years.


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Centrophenoxine has an extensive history that extends over five decades of research since it was first discovered at the French Scientific Research Centre in 1959. This means Centrophenoxine is five years older than Piracetam -the first racetam to be discovered in 1964. Being one of the original nootropic agents, it has been widely researched and hence its benefits are supported by over 50 years of scientific research. As a result, it is very popular and trusted. Its administration is always often as a stack with racetam agents.

Centrophenoxine has a rich history of success among the nootropic and medical fraternities. It has been broadly studied for its therapeutic properties against Alzheimer's and a variety of other related cognitive disorders. Much of the published benefits of Centrophenoxine are mainly focused on its positive effects on memory performance and boosting basic brain power. It has also been observed to generate mental stimulation that leads to increased perceived focus and energy.


A study conducted in 1986 sought to test the effects of Centrophenoxine on cognition and memory in male albino rats. The rats were first trained on the basic shuttle-box training test that incorporated a staircase maze and some other basic cognitive tests. After the training, the rats were administered with dosages of Centrophenoxine daily for seven days. After the 7-day therapy session, the rats were observed to have enhanced learning and retention. When some rats were administered with a dosage twice the initial one, they exhibited a significantly higher improvement in learning and retention. These improvements persisted even ten days after the Centrophenoxine treatment had been terminated. The tolerance for Centrophenoxine is also very high as observed in a number of scientific studies and clinical trials regardless of its powerful effects. In 2008, a study that engaged 24 male patients (Chinese), a comparison was done between a dose of 200mg Centrophenoxine and a dose of 200mg tablet formulation. The two formulations gave similar results and tolerance in both cases was high with no reports of any side effects.

In a study performed by Dr. Raymond Bartus, the stacking of Piracetam was evaluated. The study indicated that Piracetam had higher levels of efficacy in improving memory and learning when it was stacked with acetyl-L-Carnitine and a cholinergic agent like meclofenoxate (Centrophenoxine). Clinical trials in humans have shown that Centrophenoxine restores intellectual well-being. Other studies have also established that Centrophenoxine effectively lowers deposits of lipofuscin within nerve cells in the brain and, therefore, enhances mental capacity in senile dementia patients and healthy adults. Various studies have also shown that it reverses decreases in RNA that are brought about by aging. RNA boosts the turnover of proteins and helps in anti-aging.

In a study conducted in India, Centrophenoxine was evaluated for its effects on acetylcholinesterase activity within the hippocampus of aged rats. The study results indicated that Centrophenoxine boosted the activities of acetylcholinesterase in the brain stems of aged rats. Based on the outcome of this study, the researchers concluded that the increased activities of acetylcholinesterase could be linked to the reversal of neuro-degradation caused by the aging effects.

In a human modeled study, a double-blind, randomized, and comparative clinical trial indicated that Centrophenoxine was able to enhance the cognitive performance in individuals who had senile dementia. Centrophenoxine was observed to significantly lower the deterioration index in the patients who were featured in the trial. The trial lasted for three months with a total of 63 study subjects being administered with either Centrophenoxine or antagonistic-stress. In a trial conducted in patients with medium level dementia, Centrophenoxine was observed to have potential treatment properties. The study carried out in 1989 was a double-blind and lasted for three months with 50 aged individuals who were residing in an old age home being evaluated. In the results of the study, 48% of the patients noted enhancements in cognition after administration of Centrophenoxine when compared to 28% in the placebo group.

Quantitative biochemical studies have been used to evaluate the effects of the build-up of lipofuscin inside secondary lysosomes on metabolic activities of cells in normal diploid human glia cells when under stationary culture system. The glia cells accumulated the lipofuscin-based on the time they were in stationary cultivation in vitro. This build-up of lipofuscin can be lessened by prolonged treatment using Centrophenoxine. Parallel to the drop in lipofuscin levels, Centrophenoxine-treatedglia cells were observed to have improved rates of RNA synthesis, glucose uptake, and protein synthesis. During in vitro, Centrophenoxine treated normal diploid human glia cells are thought to have had the utilization of glucose shift from glycolysis into the pentose phosphate pathway. According to the data, Centrophenoxine stimulated fall in lipofuscin build-up has benefits to cell metabolic functions and leads to delayed cellular aging in human glia cells in vitro.

A cat-based study was used to evaluate the role of adrenergic mechanisms in brain acetylcholine release stimulated by Centrophenoxine. The impacts of propranolol (beta-adrenoceptor antagonist) and phentolamine (alpha-adrenoreceptor antagonist) on the Centrophenoxine stimulated an increase in acetylcholine release were examined in un-anaesthetized cats. The cats had perfusion of the anterior horn of the lateral cerebral ventricle performed before the commencement of the study. Propranolol on its own did not affect the amount of spontaneously released acetylcholine, and it reversed the effect of Centrophenoxine. On the other hand, Phentolamine on its own lowered the amount of spontaneously released acetylcholine, and it did not cause any alterations on the Centrophenoxine effect. The impacts of Centrophenoxine on the levels of acetylcholine release are linked to its action on pre-synaptic adrenoreceptors located at the terminals of the structures that underlies the anterior horn in the lateral cerebral ventricle.

A comparative neurophysiological study was conducted on Centrophenoxine and Piracetam. The effects of these two nootropic compounds on transcallosal evoked potential (TEP) as well as effects of EEG spectra of the animal brain cortex and hippocampus were evaluated. The two compounds were found to bring about similar effects on the amplitude of the primary TEP components and lead to increase in TEP. The two nootropic drugs caused various effects on secondary positive TEP component i.e. Centrophenoxine stimulates an alteration in non-basic rhythm of EGG in rats. Concerning the study results, the researchers considered potential neurophysiological mechanisms of the nootropic effect and came up with comparative analysis on the actions of the two nootropic drugs.

A study was conducted in which the effects of Centrophenoxine on the counting behavior in rats were evaluated. Centrophenoxine was administered through intraperitoneal injections after training on a 20 fixed-consecutive-number schedule of reinforcement. The key measure was the total progressive lever presses by the rats. The total progressive lever presses after treatments were noted to be lower compared to the baseline measures. Despite the drop in the number of consecutive presses, measures of variability showed that this could not be explained regarding potential short-term physiological effects that influence performance. When effects of Centrophenoxine were evaluated in 76 healthy elderly individuals with significant intellectual impairment, it was established that Centrophenoxine enhances storage of new information within long term memory and at the same time it boosts alertness and vigilance after some weeks of treatment.

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