Authors: G. G. Neznamov and E. S. Teleshova (Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 108, No. 3, pp. 33–42, March, 2008.)
As the population gets older, there is increasing interest in the question of treatment for cognitive disorders, especially what is considered “mild” cognitive disorders. “Mild” cognitive disorders are those involving impairments of memory and other higher brain function beyond the age norm, but not leading to social issues or being classified as dementia. This state is not actually well-defined (medically) and exist as a concept for people who are between normality and mild dementia.
The rate of cognitive disease in elderly and aged people is between 11% and 17%. Once you are over 65, the the rate is 5% for every year.
An alarming statistic is that during the four years they looked at, once mild cognitive had been detected, there was a 55-70% chance that it was transformed into dementia.
It is really important to detect cognitive disorders at an early stage because the medical treatments available work better on those patients.
The use of agents with nootropic properties is seen as one of the major approaches to treat the diseases due to organic brain damage, including those involving cognitive deficit. Nootropic agents work because of their positive influence of higher integrative brain functions, plastic processes in the central nervous system, energy metabolism, and the resistance of the brain to a variety of unfavorable factors
Since the discovery of piracetam and the coining of the term nootropics, researchers have tried to create substances with different chemical structures and mechanisms of action that do more than just have influence on intellectual and memory functions. They are looking for substances that are not just nootropics, but nootropics + “desirable effect.” Some of the effects they have formulated are nootropics with stimulatory, anti-anxiety, antidepressant and other effects.
This study was performed as a randomized comparative clinical trial assessing the therapeutic efficacy (does it work?) and safety (is it safe?) of Noopept. In the the study they will compare it to the prototypical and “grandfather” nootropic, piracetam.
The study was a randomized comparative clinical trial of Noopept and piracetam performed on two groups totaling 53 patients. One group contained 37 patience who were over 50 years old, with central nervous system diseases. The other group contained 16 patients, aged 18-60 years old, with post-tramuatic CNS damage.
To be included in the study, patients had to have a diagnosed cognitive insufficiency, a score not more than 27 points on the MMSE, and no other neurological diseases. They also excluded people with severe dementia, delusions, hallucinations, alcoholics, etc.
The study lasted 56 days, with patients either receiving piracetam 3 times a day or noopept 2 times a day. Out of the 37 patients with CNS disorders, 21 received Noopept (16 received piracetam). Out of the 16 with post-concussional syndrome 10 received not (6 received piracetam).
Investigation was done using 7 different methods before and during the trial. The first method provides objective data on the symptoms and actions of substances. The second is the Mini Mental State Examination (MMSE) which evaluates cognitive functions in attention, memory, speech and other areas and a score “not greater than 27” was required of all participants in the study. The 3rd method of testing assesses the severity of the individual parts of cognitive impairment. The 4th test measures cognitive functions like memory, counting and object grouping. The 5th test provides data on therapeutic abilities of an agent, as well as tolerance, safety, and side effects. The 6th method is lab analysis of the blood and urine. And finally they ECG traces.
The results are then input into software that uses a model weighing the different inputs for significance and then determines an objective assessment. The sets of data are compared using statistical analysis software that takes into account measuring groups of different sizes.
A total of 41 patients completed their 56-day treatment and most of them experienced decreases in neurosis-like symptoms and cognitive disorders. In the patients with organic emotionally labile (asthenic) disorder of vascular origin, the effects of Noopept were apparent from the first week of treatment, with reductions in irritability and improvements in going to sleep. From the second week of treatment there were reductions in fatigue, listlessness, weakness, tiring, apathy, and daytime drowsiness. From the third week on there were reductions in anxiety, depressed mood, and hyperesthesia. These changes were seen in addition to autonomic-system normalizing that took place, and is consistent with previous data showing that Noopept has anxiolytic and psychostimulatory effects.
For patients with post-concussional syndrome, they also had a positive effect on their irritability, anxiety, and affective lability, as well as with fatigue, weakness, apathy and listlessness. The results in these patients were seen slightly later than in the group with emotionally labile (asthenic) disorder, at 3-4 weeks. Noopept also did not negatively effect their ability to go to sleep, or to the depth and duration of sleep.
At 7-14 days, Noopept produced positive changes in the so