NEUROPLASTICITY ENHANCERS | NOOTROPICS GUIDE

Neuroplasticity, is also known as neural or brain plasticity, is the ability of neural networks in the brain to change through growth and reorganization. Changes may range from individual neuron pathways making new connections, to systematic adjustments. Nootropics are well known supplements that enhance the cognitive performance by increasing the mental function such as memory, attention, creativity or motivation. The influence of nootropics on the brain has been widely studied as they affect the brain performance through a number of mechanisms or pathways such as dopaminergic and cholinergic system.

There are two different types of nootropics; synthetic and natural/herbal nootropics. Synthetic compounds are lab created such as piracetam while the natural nootropics include products such as Ginkgo biloba. Natural nootropics are proven in boosting the brain function while keeping the brain healthier by acting in different ways such as a vasodilator against the small arteries and veins in the brain. There is significant increase in the blood circulation to the brain and at the same time provide the important nutrient and increase energy and oxygen flow to the brain. Despite the brain being 3% weight of the total body weight, the brain receives around 15% of the body’s total blood supply and oxygen. The energy generated from the glucose is crucial for maintenance, electrical, and neurotransmitter purposes.

The administration of nootropics will protect the brain from toxins and minimising the effects of brain aging. Effects of natural nootropics in improving the brain function are also contributed through the stimulation of the new neuron cell. As incentive from the new neuronal cell, the activity of the brain is increased, enhancing the thinking and memory abilities, thus increasing neuroplasticity. Natural nootropics have been disclosed to stimulate the release of dopamine, uptake of choline, cholinergic transmission, function of α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor, turnover of phosphatidylinositol, and activity of phosphatase A2.

A neuron has a known structural and functional plasticity or termed as synaptic plasticity, responsible for synaptic remodelling or known as cellular learning. There are few suggested mechanisms mediating the effects of nootropics in cognitive performance such as;  glutamatergic signaling,cholinergic system, amyloid precursor protein. Glutamatergic transmission is an example of synaptic plasticity. There are two different types of glutamate receptors: ionotropic (AMPA, kainite and NMDA receptors) and metabotropic receptors, distributed on the pre- and postsynaptic sites of the neuron. The release of glutamate will activate N-methyl-D-aspartate (NMDA) and AMPA receptors. AMPA receptor is responsible for synaptic transmission, while NMDA receptor is responsible for classic learning and memory. The brain will respond by opening the Na⁺/K⁺ ion channel and depolarising the cell membrane.

Pyrrolidine derivatives are commercially available, including piracetam, oxiracetam, aniracetam, and paramiracetam. The synthesis of nootropic from pyrrolidinone derivatives has common features including enhancing the learning process, diminishing the impaired cognition, and protecting against brain damage. Piracetam is widely used in treating senile dementia and Alzheimer’s disease while also enhancing memory and learning. Treatment of piracetam causes activation of AMPA receptor thus stimulating the influx of Ca²⁺ in the brain and increasing the density of AMPA receptors in the synaptic membrane of the cortex. Piracetam also causes the release of glutamate stimulated by potassium in the hippocampal nerves.

Introduction of aniracetam is usually related to the involvement of AMPA receptor, cholinergic system, and metabotropic receptor, as part of cognition function. Aniracetam, including pyrrolidinone derivative compounds, is established to diminish the cognitive impairment. Nicotine is found to improve learning and memory properties and enhance the memory impairment due to lesion of the septohippocampal pathways or aging. Downregulated expression of nicotinic receptor is observed in Alzheimer’s disease patients. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026746/