Piracetam....A Nootropic "smart drug" and its effects on brain chemistry
Piracetam is a nootropic type drug that suggests great benefits for the treatment of Alzheimer's disease, Attention Deficit Disorder, and even looks promising for the prevention of cognitive deficiencies associated with dementia (1). Piracetam is known international name for 2 - oxo - pyrrolidine acetamide, which is very similar in structure to the amino acid Pyroglutamate ( 2 - oxo - pyrrolidine carboxylic acid ) (3). In fact ,Piracetam is recognized as being a derivative of pyrrolidine C6 H10 N2 O2, a first class nootropic drug and neuroprotective agent intended to prevent damage to the brain from trauma, convulsions, and hapoxia. But certainly one of the most exciting claims of Piracetam is that this drug appears to be virtually non toxic (1).
Piracetam is also known as a "smart drug", and it is currently in high demand by seekers of supplemental cognitive enhancers since it is reported to be an intelligence booster and a stimulant to the central nervous system with no addictive properties. Testimonials of this wonder drug can be found throughout different pharmaceutical mail order websites overseas. Yet, don't rush to buy Piracetam as a health supplement or as the miracle drug you were hoping for because it is not sold in the US. Piracetam has yet received approval by the FDA. Moreover, if purchased through the Internet, anyone runs the chance of having the FDA confiscate their shipment since Piracetam is considered an illegal drug in the United States (2). Interestingly enough, research evidence subsists confirming the use of Piracetam for the treatment of ADHD among other neurological diseases. For instance, a German abstract of an article written by Woelk H explains that Piracetam plays a key role in the process of synaptic transmission by enhancing both of neuronal stimulation and the activation of synaptosomal phospholipase A2 (an enzyme) by almost 50 percent (5). This is great news for many people that suffer from Attention Deficit Disorder, Down syndrome, and myoclonus epilepsy since the enzymatic stimulation of phospholipase A2 by Piracetam appears to be negotiated by a chemical neurotransmitter.
Neurotransmitters are any group of substances that may be released on excitation from an axon terminal of a pre- synaptic neuron of the Central Nervous System or the Peripheral Nervous System in order to carry commands between cells in the brain.
Among these substances that have neurotransmitter properties are acetylcholine, noradrenaline, adrenaline, dopamine, glutamic acid, endorphins, enkephalins, and seratonin. ADD is known to be a brain condition affected by the short supply of the neurotransmitter substance dopamine, Norepinephrine, seratonin, or the improper operation of these within the brain (1). Furthermore, data collected from research done at Children's National Medical Center, Department of Neurology Research , Washington, DC explains that clinical drug trials of Piracetam and 5 - hydroxyl - L- Tryptophan (drugs available by clinical-research protocols only) seems to control the seizures and improve the quality of life of the patients suffering from progressive myoclonus epilepsy (6).
Investigations on Piracetam reported by a German article written by Fiegel G relating to the effects of the nootropic drug Nootropil ( Piracetam) on the adolescent brain further reaffirms that a continuous period of therapeutic application of Piracetam (up to 14 months) resulted in a convincing and evident improvement in the scholastic performance of the 48 volunteer adolescent students that participated in the study. The students were selected to participate in the study by virtue of their characterized poor school performance. Piracetam results were described by its cerebral metabolic effects, as a leading energy in the activation of cerebral functions as well as to brain protection. The report concluded that Piracetam performed with highly selective activity on the cerebral cortex, which is known to be responsible for the higher mental functioning abilities of the brain. Definite signs of improvement in consciousness, vigilance, and enhanced memory were reported (6).
Additional clinical trials on this so called "smart drug" ( Piracetam ) have also reported significant improvement as an aid for dyslexic students. A 21day trial using a double -blind cross over technique done in Berlin reported excellent results when the 14 male dyslexic children that participated in the study were examined again as adults. Reports revealed that a notable increase in their verbal learning was measured to be 15.0% higher over the 8.6% increase noted of students that were given the placebo (6).
All these studies suggest that Piracetam is not a new wonder drug that just began circulating since it is evident that this drug has been tested first on the rats, cats, dogs, and finally clinically tried on humans. Moreover, Piracetam is currently being prescribed by
doctors in the UK, Canada, and can even be purchased over the counter in Mexico. Even reports of equitable application of such drug by the Department of Neurology, Aristotelian University School of Medicine, AHEPA Hospital, Thessalokini in Greece were reported due to the dramatic effects of Piracetam on a 70 year old hypertensive female. The woman, in question, was selected for the application of the drug due to the extent of her subarachnoid hemorrhage trauma she had suffered that soon was followed by a delayed vasospasm in the basal cerebral arteries. Such trauma culminated in serious multiple ischaemic lesions in the right middle cerebral arterial region of this 70 year old woman's brain. However, with the administration of high doses of Piracetam ( 24-36g/day), the eradication of myoclonus was observed on this patient.
These fantastic results were published in the Journal of Internal Medicine, Jul-Aug; 27 of 1999. Nevertheless, the article indicated that this was the first report indicating the evident benefits of Piracetam monotherapy on post-ischaemic palatal myoclonus, even though, previous clinical trials had reported similar results in patients of skeletal myoclonus (6).
Consequently, what is holding up the FDA approval of Piracetam and the use of such drug, which evidently has reported such remarkable results in many different medical situations is a question that will remain unanswered until the FDA decides to issue its findings relating to Piracetam and other nootropic drugs. The Department of Pediatrics, at George Washington University in DC, revealed in 1995 the mechanism of actions of the antiepileptic and antimyoclonic effects of other drugs such as the anticonvulsant dizocilpine and remacemide, which target glutamate receptors or associated ion channels. Yet for some drugs like Piracetam, many effects were reported, but no mechanisms of action were established back in 1995 ;even though, there is evidence that supports claims of virtually no toxicity exhibited by Piracetam (6).
What is so fascinating is the fact that in 1989 the effects of Piracetam (PIR) and of its structural analogs, ucb L059 and ucb L060, and the optical isomer of ucb L059, were Investigated on cholinergic function in a guinea pig ileum in vitro. Researchers Wulfert E, Hanin I, and Verloes R, reported the facilitation of calcium-dependent cholinergic function by ucb L059, which is a second generation nootropic agent just as Piracetam is a second generation nootropic. The results of their study revealed that ucb L059 is a close structural analog of Piracetam, and it seems to facilitate cholinergic function, in vitro, through a stereospecific mechanism (6).
An additional study was performed by the Department of Pharmacology, Suzhou Medical College, and led by Qian ZN, Gu ZL, Jin LQ, Xie ML, and Chen BQ, in China (1992) in order to evaluate the antioxidant effects of Piracetam on Na (+) ,K (+) , ATPase, and monoamine oxidase in a rat brain. The results revealed that Piracetam had the potential action of scavenging free radicals. It was claimed that Piracetam (ig 600 mg.kg -1 for 30 days) caused a significant 20% decrease in the activity of Na(+),Ka(+) , ATPase, and monoamine oxidase (MAO), in vitro. This was great news for the scientific community, yet, no studies had been performed on humans until the Key Institute for Brain-Mind research, University Hospital of Psychiatry, Zurich, Switzerland which decided to do so by measuring the effects of a single-dose of Piracetam on humans. They used 12 healthy young volunteers for the measuring on global complexity measures of human spontaneous multi-channel EEG, and 1 1/2 hours after oral ingestion of Piracetam (four treatment dosage levels were used, 2.4, 4.8, and 9.6 g ), brain electric activity was measured. Results revealed that a single dose of Piracetam (dose dependently) affected the spontaneous electroencephalogram (EEG) in these normal volunteers by showing significant decreases from placebo to 2.4g of Piracetam. The decreased EEG complexity can be interpreted as a definite improvement of brain functional processes (6).
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