Trace Amines in Neuropsychiatric Disorders

Sherwani, S.I.; Khan, Haseeb A.

doi:10.1016/b978-0-12-803603-7.00018-5

Cited by 5 publications

(3 citation statements)

References 106 publications

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“…Tyramine binding to G-protein-coupled receptors in the synaptic cleft reduces the activity of serotonergic and dopaminergic receptors [107], and imbalance in tyramine levels has been reported to be associated with Parkinson's disease, depression, schizophrenia, migraine, and elevated blood pressure [108][109][110][111]. Our results suggest that it is one of the reasons for the progression of pathology in AD.…”

Section: Discussionmentioning

confidence: 53%

Amelioration of Alzheimer’s Disease by Gut-Pancreas-Liver-Brain Interaction in an App Knock-In Mouse Model

Minamisawa

Sato

Ishiguro³

et al. 2021

Life

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In this study, we observed disease progression, changes in the gut microbiota, and interactions among the brain, liver, pancreas, and intestine in a mouse model of Alzheimer’s disease (AD), in addition to attempting to inhibit disease progression through the dietary supplementation of L-arginine and limonoids. Wild-type mice (WC) and AD mice were fed a normal diet (AC), a diet supplemented with L-arginine and limonoids (ALA), or a diet containing only limonoids (AL) for 12–64 weeks. The normal diet-fed WC and AC mice showed a decrease in the diversity of the gut microbiota, with an increase in the Firmicutes/Bacteroidetes ratio, and bacterial translocation. Considerable bacterial translocation to the pancreas and intense inflammation of the pancreas, liver, brain, and intestinal tissues were observed in the AC mice from alterations in the gut microbiota. The ALA diet or AL diet-fed mice showed increased diversity of the bacterial flora and suppressed oxidative stress and inflammatory responses in hepatocytes and pancreatic cells, bacterial translocation, and neurodegeneration of the brain. These findings suggest that L-arginine and limonoids help in maintaining the homeostasis of the gut microbiota, pancreas, liver, brain, and gut in AD mice.

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Section: Discussionmentioning

confidence: 53%

Amelioration of Alzheimer’s Disease by Gut-Pancreas-Liver-Brain Interaction in an App Knock-In Mouse Model

Minamisawa

Sato

Ishiguro³

et al. 2021

Life

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“…TAAR1 has been found to heterodimerize with the dopamine receptor 2, which is thought to silence glycogen synthase kinase 3 beta (GSK3β) implicated in various mental disorders [3]. Imbalances in levels of tyramine have been reported to be associated with Parkinson's disease, depression, schizophrenia, migraines and increased blood pressure [1,[4][5][6]. In mammalian cells, tyramine has been found to be toxic [7], to cause oxidative damage [4] and to have effects on mitochondrial respiratory function [8].…”

Section: Introductionmentioning

confidence: 99%

Tyramine and Amyloid Beta 42: A Toxic Synergy

Dhakal

Macreadie

2020

Biomedicines

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Implicated in various diseases including Parkinson’s disease, Huntington’s disease, migraines, schizophrenia and increased blood pressure, tyramine plays a crucial role as a neurotransmitter in the synaptic cleft by reducing serotonergic and dopaminergic signaling through a trace amine-associated receptor (TAAR1). There appear to be no studies investigating a connection of tyramine to Alzheimer’s disease. This study aimed to examine whether tyramine could be involved in AD pathology by using Saccharomyces cerevisiae expressing Aβ42. S. cerevisiae cells producing native Aβ42 were treated with different concentrations of tyramine, and the production of reactive oxygen species (ROS) was evaluated using flow cytometric cell analysis. There was dose-dependent ROS generation in wild-type yeast cells with tyramine. In yeast producing Aβ42, ROS levels generated were significantly higher than in controls, suggesting a synergistic toxicity of Aβ42 and tyramine. The addition of exogenous reduced glutathione (GSH) was found to rescue the cells with increased ROS, indicating depletion of intracellular GSH due to tyramine and Aβ42. Additionally, tyramine inhibited the respiratory growth of yeast cells producing GFP-Aβ42, while there was no growth inhibition when cells were producing GFP. Tyramine was also demonstrated to cause increased mitochondrial DNA damage, resulting in the formation of petite mutants that lack respiratory function. These findings indicate that there can be a detrimental synergy between Aβ42 and tyramine, which could be considered in Alzheimer’s disease. This work also demonstrates the utility of yeast as a model for studying toxic agents such as Aβ42, tyramine, and agents that might exacerbate AD pathology.

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“…2 Endogenous arylethylamines including dopamine and serotonin underlie the neurochemistry of emotion, memory, and addiction. [3][4][5] Drugs with incorporated arylethylamine connectivity have been developed to treat heart disease 6 and cancer 7 (Scheme 1A) among numerous other indications. The arene and ethylene portions bear several potential sites of substitution that can act as synthetic handles to tune the molecule's metabolic and pharmacokinetic profile.…”

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confidence: 99%

A general alkene aminoarylation enabled by N-centered radical reactivity of sulfinamides

Noten

Wolesensky

et al. 2022

Preprint

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We disclose an intermolecular 1,2-aminoarylation of alkenes using aryl sulfinamide reagents as bifunctional amine and arene donors. This reaction features excellent regio- and diastereoselectivity on a variety of activated and unactivated substrates. Using a weakly oxidizing photoredox catalyst, a sulfinamidyl radical is generated under mild conditions and adds to an alkene to form a new C–N bond. A desulfinylative Smiles-Truce rearrangement follows to form a new C–C bond. In this manner, biologically active arylethylamines and valuable building blocks can be rapidly assembled from abundant alkene feedstocks. Additionally, we demonstrate that chiral information from the sulfinamide can be transferred via rearrangement to a new carbon stereocenter in the product, thus advancing development of traceless asymmetric alkene difunctionalization methodologies.

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Trace Amines in Neuropsychiatric Disorders

Cited by 5 publications

References 106 publications

Amelioration of Alzheimer’s Disease by Gut-Pancreas-Liver-Brain Interaction in an App Knock-In Mouse Model

Amelioration of Alzheimer’s Disease by Gut-Pancreas-Liver-Brain Interaction in an App Knock-In Mouse Model

Tyramine and Amyloid Beta 42: A Toxic Synergy

A general alkene aminoarylation enabled by N-centered radical reactivity of sulfinamides

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