<p>The pathogenesis of HE is complicated, the mainstream theories include Ammonia Toxicity Theory and False Neurotransmitter Theory. Apart from endeavoring to metabolize ammonia (see details in our Design page) , we also put insights into reducing false neurotransmitters in our preliminary designs.</p>
<p>The pathogenesis of HE is complicated, the mainstream theories include Ammonia Toxicity Theory and False Neurotransmitter Theory. Apart from endeavoring to metabolize ammonia (see details in the Design section of our Description Page) , we also put insights into reducing false neurotransmitters in our preliminary designs.</p>
<p>A false neurotransmitter is a chemical substance that closely resembles and mimics the function of a neurotransmitter in the nervous system. Examples include 5-MeO-αMT, which mimics serotonin, and α-methyldopa.These chemicals can be accumulated by a neuron or secretory cell, are then packaged in secretory / synaptic vesicles, and then released with other neurotransmitters when an action potential provides the necessary stimulus for release[8]. Patients who develop liver failure can not digest those aromatic amino acids properly, and this can lead to false neuro-transmitters accumulation, causing neuro system symptoms.</p>
<h4>TPH1: metabolize Trp</h4>
<p>Tryptophan, through different metabolic pathways, can be converted into kynurenine, serotonin, and indole[9]. Tryptophan hydroxylase 1 (TPH1), enabling the conversion of tryptophan (Trp) into serotonin (5-HT) and reducing excess aromatic amino acids. Since serotonin synthesized in the gut cannot cross the blood-brain barrier or affect central nervous system function, there is no concern about adverse effects on the central nervous system. Therefore, we designed a plasmid to express TPH1 as our metabolic module(Figure 7a).</p>
