Author: Denуs Pavlovich Sukhachov
Scientific institution: Asgard Technology
Abstract
The article proposes the architecture of an innovative reverse neurointerface — a neurotransmission device capable of writing semantic information directly into the cerebral cortex.
The principle of operation is based on the reverse action to electroencephalography (EEG) — instead of reading brain waves, the device generates controlled patterns of electromagnetic or electrical stimulation corresponding to linguistic units (letter, word, idea).
To optimize the brain’s neuroplastic response, pharmacological and neurotrophic agents that activate the mechanisms of synaptogenesis and long-term potentiation (LTP) are considered.
The basic functional architecture of the device is presented and its neurophysiological feasibility is justified.
1. Introduction
Neuroplasticity is a key property of the nervous system to change its morphology and functional activity in response to external stimuli, learning, or trauma.
Modern brain-computer interfaces (BCIs) mainly function in the direction of reading brain activity. However, an effective system for transmitting information to the brain without traditional sensory interpretation, which could activate specific cognitive images or language structures, has not yet been implemented.
2. Device architecture
2.1. Basic components:
– Semantic encoder: Converts words/ideas into electrophysiological patterns.
– Stimulation generator: Creates signals of the desired frequency, amplitude, and phase.
– Matrix delivery system: Transmits the stimulus to specific areas of the brain.
– Feedback system: Analyzes the brain’s response and adapts the stimulus.
– Control processor/AI: Machine learning for individual pattern customization.
2.2. Principle of operation:
Words or concepts are encoded as unique neural signals based on previously collected data (EEG/fMRI). These signals are then generated by hardware and delivered to the brain to reproduce the corresponding neural response.
3. Pharmacological support for neuroplasticity
3.1. Pharmacological agents:
– Nootropics: piracetam, noopept, aniracetam.
– Antidepressants: escitalopram, agomelatine.
– Ketamine (in low doses): stimulation of mTOR and rapid antidepressant effect.
3.2. Natural supplements:
– Omega-3 fatty acids (DHA).
– Curcumin.
– Magnesium L-threonate.
3.3. Experimental approaches:
– Microdosed psychedelics: LSD, psilocybin.
– Optogenetics, DREADD (in animals).
4. Biosafety and ethical aspects
Any brain stimulation must undergo clinical testing. Prolonged or uncontrolled activation of neuroplasticity can lead to epileptic discharges, pathological activity patterns, or the formation of “phantom” sensory sensations.
5. Conclusion
The presented device model creates a conceptual basis for the formation of a new class of interfaces that do not read but transmit information to the brain using electrophysiologically optimized stimulation in combination with pharmacological support.
6. References
1. Giurgea, C. (1972). Pharmacology of integrative activity of the brain.
2. Duman, R. S., & Monteggia, L. M. (2006). A neurotrophic model for stress-related mood disorders. Biological Psychiatry.
3. Abdallah, C. G., et al. (2015). Ketamine and rapid-acting antidepressants.
4. Gómez-Pinilla, F. (2008). Brain foods: the effects of nutrients on brain function.
5. Ly, C., et al. (2018). Psychedelics promote neural plasticity. Cell Reports.
6. Slutsky, I., et al. (2010). Brain magnesium enhancement. Neuron.
7. Carhart-Harris, R. L., et al. (2016). Neural correlates of the LSD experience. PNAS.
7. List of recommended drugs for stimulating neuroplasticity
Pharmacological support should provide a favorable environment for the formation of new synaptic connections. Examples of substances that can potentially be used are given below:
Drug Mechanism of action Category
Piracetam Modulation of glutamatergic transmission Nootropic
Aniracetam Improvement of AMPA receptors Nootropic
Noopept Effect on NGF and BDNF Peptide nootropic
Ketamine (low doses) NMDA antagonist; stimulates mTOR Antidepressant, experimental
Escitalopram Serotonin reuptake inhibitor Antidepressant
Omega-3 (DHA) Synaptic membrane enhancement Dietary supplement
Curcumin Antioxidant, stimulates BDNF Nutraceutical
Magnesium L-threonate Increases synaptic density Dietary supplement
Psilocybin (microdosing) 5-HT2A agonist; structural plasticity Psychedelic
8. Technical specifications of the device
Below are the basic technical parameters of the experimental neurotransmission device:
Component Characteristics
Central controller ARM Cortex-M / FPGA with low-latency DSP core
Signal generator Multi-channel DAC, range 0.5–1000 Hz, 0.1 mA–2 mA
Stimulation method tDCS, tACS, TMS, or tFUS (optional)
Monitoring system EEG with 32/64-channel electrodes (g.tec, OpenBCI)
Electrode matrix Flexible microelectrodes, up to 256 channels
User interface Speech interpretation + semantic encoder
Power supply 3000 mAh battery, up to 6 hours of autonomous operation
