SCN2A

The SCN2A gene encodes a protein (the 2 subunits of voltage-gated type II sodium channels) that helps neuronal firing throughout the brain (R).

If this gene is more active, it results in more firing between important brain regions involved in higher cognitive function.  This results in better informational processing (R).

The brain regions involved are key regions supporting a broad range of cognitive processes including attention, working memory, conflict detection, and behavioral control (R).

Mutations in SCN2A is implicated in disorders such as autism and schizophrenia (R).

Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient.

The SCN2A gene encodes the 2 subunits of voltage-gated type II sodium channels, which contribute to the generation and propagation of action potentials throughout the brain (R).

The 2 subunit encoded by SCN2A (Na_v1.2) specifically mediates the conformational change of sodium channels based on voltage differences across cell membranes (R). Studies in mice (R) and humans (R) have linked mutations in SCN2A with abnormal electrical activity in the form of epileptic seizures (R). Furthermore, antiepileptic drugs that inhibit Na_v1.2 activity (e.g., topiramate) are associated with a diminished intellectual function.

Mutations in SCN2A is implicated in disorders such as autism and schizophrenia, where impaired cognitive performance is often observed (R).

This gene increases the capacity for information processing between the dorsolateral prefrontal cortex and dorsal anterior cingulate cortex, which support higher cognitive functions (R).

This gene may contribute to the development of cortical and hippocampal circuits (R). The dorsolateral prefrontal cortex and dorsal anterior cingulate cortex are key nodes supporting a broad range of cognitive processes including attention, working memory, conflict detection, and behavioral control (R).

The voltage-gated type II sodium channels process sensory inputs, including visual processing and/or disorders characterized by visual deficits (R). This is thought to be mediated by the communication between the dorsolateral prefrontal cortex and  the middle occipital gyrus (R).

     From NCBI Gene: Benign familial neonatal-infantile seizuresEarly infantile epileptic encephalopathy 11From UniProt: Seizures, benign familial infantile 3 (BFIS3): An autosomal dominant disorder in which afebrile seizures occur in clusters during the first year of life, without neurologic sequelae. [MIM:607745] Epileptic encephalopathy, early infantile, 11 (EIEE11): An autosomal dominant seizure disorder characterized by neonatal or infantile onset of refractory seizures with resultant delayed neurologic development and persistent neurologic abnormalities. Patients may progress to West syndrome, which is characterized by tonic spasms with clustering, arrest of psychomotor development, and hypsarrhythmia on EEG. [MIM:613721]

     From NCBI Gene: Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel alpha subunit gene family. It is heterogeneously expressed in the brain, and mutations in this gene have been linked to several seizure disorders. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined. [provided by RefSeq, Jul 2008] From UniProt: Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient.

If you have the SCN2A gene that results in lower intelligence you need to take a GSK3 beta inhibitor. GSK3 inhibitors significantly increase the current of voltage-gated sodium (Na(v)) channels (R), which is lower in certain variations of the gene (R). My top GSK3 beta inhibitors are:

• Lithium (R),
• Zinc (50mg) (potent) (R),
• Celery juice,
• Cinnamon,