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Genetic and environmental determinants of adolescent alcohol use
Published in Ilana B. Crome, Richard Williams, Roger Bloor, Xenofon Sgouros, Substance Misuse and Young People, 2019
Toni-Kim Clarke, Richard C. Crist
Targeted studies of single variants or candidate genes have been somewhat more successful than GWAS in identifying genotypic associations with adolescent alcohol use. Altered regulation of monoamine neurotransmitters, such as serotonin and dopamine, is a common factor in many psychiatric diseases, including alcoholism (Yoshimoto et al., 1992). Polymorphisms in the genes regulating neurotransmitter release and downstream signalling may affect susceptibility to alcohol use disorders. The serotonin transporter, 5-HTT, is responsible for the uptake of serotonin from the synaptic cleft. A polymorphic repeat region known as 5-HTTLPR occurs in the 5-HTT promoter and is primarily classified into long and short alleles. Nilsson et al. (2006) found that the genotype at 5-HTTLPR was associated with alcohol consumption during adolescence, while other research identified an association between the polymorphism and early alcohol use (Kaufman et al., 2007). Both studies found that teenagers carrying one long and one short allele were at the highest risk. In a subsequent study in the Netherlands, the short allele of 5-HTTLPR was associated with the rate of increase in alcohol consumption over time by adolescents (van der Zwaluw et al., 2010b).
What the Mental Health Literature Says About Body Dysmorphic Disorder
Published in Mark B. Constantian, Childhood Abuse, Body Shame, and Addictive Plastic Surgery, 2018
Alleles typically have short and long variants. “Serotonin transporter” is a genetically—determined protein that removes serotonin from the spaces between nerve cells in the brain, and so becomes the primary target of serotonin reuptake inhibitor antidepressants (SRI’s). The more serotonin remains, the longer its effect lasts. In one study, a higher percentage of people with body dysmorphic disorder have the short allele of serotonin transporter.41,82 This is interesting, because the short allele for serotonin transporter has also been associated with alcoholism, depression, PTSD, obsessive-compulsive disorder, and social phobia, neuroticism, “impaired agreeableness,”114 alcoholism,115,116 anxiety and depression,117 and affective disorders.118 GABA (gamma-aminobutyric acid), a substance available as the drug gabapentin, is an endogenous inhibitory neurotransmitter used to treat chronic neuropathic pain, epilepsy, anxiety, and other disorders. In one preliminary study, the short allele of the GABA gene is also higher in BDD patients.28,82
Anxiolytics: Predicting Response/Maximizing Efficacy
Published in Mark S. Gold, R. Bruce Lydiard, John S. Carman, Advances in Psychopharmacology: Predicting and Improving Treatment Response, 2018
Serotonergic neurons are activated by nociception and contain serotonin transporter which removes active neurotransmitter. Serotonin transporter is blocked by certain tricyclic drugs, and chronic blockade is associated with increased sensitivity of post synaptic serotonin receptors. Potentiation of serotonergic transmission by monoamine oxidase inhibitors also causes post synaptic receptor supersensitivity. Serotonin neurotransmission is potentiated by enhanced biosynthesis secondary to increased extra cellular concentrations of L-tryptophan.
Narcissism and central serotonergic neurotransmission in depression
Published in The World Journal of Biological Psychiatry, 2023
Paraskevi Mavrogiorgou, Florian Seltsam, David Kiefner, Vera Flasbeck, Georg Juckel
A valid indicator of central serotonergic neurotransmission in the loudness dependence (which is the same as the term ‘intensity dependence’ is referring to in some parts of the literature) of the auditory evoked potentials (LDAEP), whereby a strong LDAEP is associated with reduced serotonergic transmission and vice versa (Juckel 2015). A central serotonergic dysfunction is postulated especially for depressive-affective disorders. Meta-analyses showed a reduced density of serotonin transporters in depression (Jakobsen et al. 2017). The connection between LDAEP and depression has also been shown in several studies (Juckel et al. 2007; Simmons et al. 2011; Lee et al. 2015). However, it should also be mentioned that, possibly due to methodological differences, there are also contradictory and thus also inconsistent findings regarding the connection between LDAEP and central serotonergic neurotransmission (Graßnickel et al. 2015; Park 2015).
New insights on the phytochemical intervention for the treatment of neuropsychiatric disorders using the leaves of Michelia champaca: an in vivo and in silico approach
Published in Pharmaceutical Biology, 2022
Pushpa V. H., Jayanthi M. K., Rashmi H. R., Veeresh Kumar N. Shivamurthy, Shashank M. Patil, Prithvi S. Shirahatti, Ramith Ramu
The regulation of serotonin levels is aided by human serotonin transporters. Serotonin regulates the functioning of the central nervous system as well as other bodily functions such as digestion, cardiovascular function and reproduction. Serotonin is released into the synaptic cleft and diffused by serotonin receptors. Re-uptake of serotonin, on the other hand, causes depression. Antidepressant medicines such as prozac, imipramine and paroxetine have been shown to impede serotonin reuptake, resulting in depression-free state (Coleman et al. 2016). As a result, blocking the human serotonin transporter may pave the way for the development of antidepressant drugs. Doripenem occupies the centre of the binding pocket created by all the transmembrane helices during the molecular docking simulation. Despite the fact that imipramine binds to the pocket's core site, its interactions and binding affinity appear to be inferior to doripenem. The blockage of serotonin reuptake would result in a depression-free state. During drug-likeness and toxicity analysis, imipramine was predicted with probable reproductive health aberrations. However, doripenem was found to be predicted with no risk with all the toxicity parameters used. Even the drug-score of doripenem was found to be more than imipramine. Therefore, doripenem could be employed as a strong inhibitor of human serotonin transporter because of the degree of interaction, lower binding affinity, higher drug-likeness and zero risk of probable toxicity, compared to imipramine.
Nitric oxide pathway as a plausible therapeutic target in autism spectrum disorders
Published in Expert Opinion on Therapeutic Targets, 2022
Rishab Mehta, Anurag Kuhad, Ranjana Bhandari
Factors like prenatal maternal diabetes and prenatal stress usually caused by hormonal imbalance are also considered as associated risk factors as predicted by various meta-analysis studies [54]. It has been reported by these studies that the imbalance between hypothalamus-pituitary-adrenal (HPA) axis leads to immune system dysregulation in the brain causing the enhanced release of pro-inflammatory cytokines, natural killer cells, and leukocytes, and so on, reducing the ability of the brain to fight infection while increasing the risk of hypoxia and neuroinflammation thus being associated with autism [35]. The serotonin transporter (SERT) gene produce SERT protein that is responsible for the transports of extracellular serotonin back to neuron. Genetic aberation in this gene can lead to altered serotonin uptake [84]. This gene is found to be relevant ASD as single nucleotide variation on the SERT gene, Gly56Ala, is linked to increased risk of ASD [85,86]. Furthermore, the S-allele of the SERT gene has been found to be associated with ASD in some studies [87,88,89]. Prenatal stress also influences the processes of GABAergic progenitor, most notably in striatum, and most prominently in male descendants [90]. Major defects have been found in the expression of, GAD67, that is, the enzyme producing GABA that is discovered to be decreased in the postmortem brain of people with ASD [91,92]. Therefore, the impact of prenatal stress on the GABAergic system is also of concern for ASD.