The Effects of Taurine Exposure on the Brain and Neurological Disorders

Roysommuti, Sanya; Wyss, J. Michael

doi:10.1016/b978-0-12-411462-3.00022-9

Cited by 7 publications

(8 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to its role in proteinogenesis and cell metabolism, glycine is involved in regulating NMDA receptor signaling as an important coagonist at glutamatergic synapses. − Choline plays a central role in brain development because it is an essential brain precursor of the acetylcholine neurotransmitter. − Consistent with this finding, deficits in choline levels in the brain during gestation are known to cause alterations in cognitive functions. , In addition to choline, the VIP score also indicates a variation in other choline class compounds, such as GPCho and PCho . Finally, taurine appears to act as a major inhibitory neurotransmitter/modulator in the embryonic and early postnatal brain, having much higher concentrations than GABA in most brain areas . Interestingly, these three molecules increase at the same time-points (E13.5 and P7), indicating an overall change in neurotransmission in these phases (see Supporting Information Figure S4).…”

Section: Discussionmentioning

confidence: 87%

Prenatal and Early Postnatal Cerebral d-Aspartate Depletion Influences l-Amino Acid Pathways, Bioenergetic processes, and Developmental Brain Metabolism

et al. 2020

View full text Add to dashboard Cite

D-Amino acids were believed to occur only in bacteria and invertebrates. Today, it is well known that D-amino acids are also present in mammalian tissues in a considerable amount. In particular, high levels of free D-serine (D-Ser) and Daspartate (D-Asp) are found in the brain. While the functions of D-Ser are well known, many questions remain unanswered regarding the role of D-Asp in the central nervous system. D-Asp is very abundant at the embryonic stage, while it strongly decreases after birth because of the expression of D-aspartate oxidase (Ddo) enzyme, which catalyzes the oxidation of this D-amino acid into oxaloacetate, ammonium, and hydrogen peroxide. Pharmacologically, D-Asp acts as an endogenous agonist of N-methyl D-aspartate and mGlu5 receptors, which are known to control fundamental brain processes, including brain development, synaptic plasticity, and cognition. In this work, we studied a recently generated knockin mouse model (R26 Ddo/Ddo ), which was designed to express DDO beginning at the zygotic stage. This strategy enables D-Asp to be almost eliminated in both prenatal and postnatal lives. To understand which biochemical pathways are affected by depletion of D-Asp, in this study, we carried out a metabolomic and lipidomic study of Ddo knockin brains at different stages of embryonic and postnatal development, combining nuclear magnetic resonance (NMR) and high-resolution mass spectrometry (HRMS) techniques.Our study shows that D-Asp deficiency in the brain influences amino acid pathways such as threonine, glycine, alanine, valine, and glutamate. Interestingly, D-Asp is also correlated with metabolites involved in brain development and functions such as choline, creatine, phosphocholine (PCho), glycerophosphocholine (GPCho), sphingolipids, and glycerophospholipids, as well as metabolites involved in brain energy metabolism, such as GPCho, glucose, and lactate.

show abstract

Section: Discussionmentioning

confidence: 87%

Prenatal and Early Postnatal Cerebral d-Aspartate Depletion Influences l-Amino Acid Pathways, Bioenergetic processes, and Developmental Brain Metabolism

et al. 2020

View full text Add to dashboard Cite

show abstract

“…However, once treated with taurine, an enhanced expression of nerve growth factor (NGF) and the consequent activation of neurotrophic tyrosine kinase receptor type A (TrkA) were observed, together with lower cytochrome‐c release and apoptotic rate (Wu et al, 2020). In comparison to rats, studies have pointed out that humans exhibit lower levels of cerebral taurine (Roysommuti & Wyss, 2015). Since these taurine alterations in the animal models might not be completely translational, similar imaging protocols may be conducted in patients with obesity and type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

Functional imaging and neurochemistry identify in vivo neuroprotection mechanisms counteracting excitotoxicity and neurovascular changes in the hippocampus and visual cortex of obese and type 2 diabetic animal models

Caramelo

Alfredo

Martins

et al. 2023

Journal of Neurochemistry

View full text Add to dashboard Cite

Functional MRI (fMRI) with 1H‐MRS was combined on the hippocampus and visual cortex of animal models of obesity (high‐fat diet, HFD) and type 2 diabetes (T2D) to identify the involved mechanisms and temporal evolution of neurometabolic changes in these disorders that could serve as potentially reliable clinical biomarkers. HFD rats presented elevated levels of N‐acetylaspartylglutamate (NAAG) (p = 0.0365 vs. standard diet, SD) and glutathione (GSH) (p = 0.0494 vs. SD) in the hippocampus. NAAG and GSH levels in this structure proved to be correlated (r = 0.4652, p = 0.0336). This mechanism was not observed in diabetic rats. Combining MRS and fMRI‐evaluated blood‐oxygen‐level‐dependent (BOLD) response, elevated taurine (p = 0.0326 vs. HFD) and GABA type A receptor (GABAAR) (p = 0.0211 vs. SD and p = 0.0153 vs. HFD) were observed in the visual cortex of only diabetic rats, counteracting the elevated BOLD response and suggesting an adaptative mechanism against hyperexcitability observed in the primary visual cortex (V1) (p = 0.0226 vs. SD). BOLD amplitude was correlated with the glutamate levels (r = 0.4491; p = 0.0316). Therefore, here we found evidence for several biological dichotomies regarding excitotoxicity and neuroprotection in different brain regions, identifying putative markers of their different susceptibility and response to the metabolic and vascular insults of obesity and diabetes.

show abstract

“…Taurine is one of the most abundant amino acids in the human brain, although, its concentration declines with age, with decreasing values that range from 4–20 μmol/g during development to 1–9 μmol/g at adulthood ( Wójcik et al, 2010 ; Roysommuti and Wyss, 2015 ). A study in adult male Wistar rats identified heterogeneous concentrations of taurine among different brain regions, showing higher levels in the pyriform cortex, caudate-putamen, cerebellum, and supraoptic nucleus, and lower concentrations in the midbrain reticular formation ( Palkovits et al, 1986 ).…”

Section: Taurine and Brainmentioning

confidence: 99%

“…Synthesis of taurine in the brain follows a similar enzymatic pathway compared with other tissues, such as muscle, adipose tissue and liver, however, the rate of production differs from one to another ( Roysommuti and Wyss, 2015 ). This explains the slight differences in taurine concentrations between the brain and other tissues, reporting 9 μmol/g in the adult brain compared to 6 μmol/g in heart, 5 μmol/g in skeletal muscle, 2 μmol/g in the liver, and up to 40 μmol/g in retina ( Wójcik et al, 2010 ).…”

Section: Taurine and Brainmentioning

confidence: 99%

“…The third pathway consists in the degradation of coenzyme-A yielding cysteamine, which is later transformed to hypotaurine by 2-aminoethanethiol dioxygenase ( Banerjee et al, 2008 ). All three pathways form hypotaurine, which can be either transformed into taurine and released as such, or be released as hypotaurine and undergo its conversion to taurine in another cell, such as neurons ( Roysommuti and Wyss, 2015 ; Figure 1 ).…”

Section: Taurine and Brainmentioning

confidence: 99%

See 1 more Smart Citation

Taurine and Astrocytes: A Homeostatic and Neuroprotective Relationship

Ramírez-Guerrero

Guardo-Maya

Medina-Rincón

et al. 2022

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Taurine is considered the most abundant free amino acid in the brain. Even though there are endogenous mechanisms for taurine production in neural cells, an exogenous supply of taurine is required to meet physiological needs. Taurine is required for optimal postnatal brain development; however, its brain concentration decreases with age. Synthesis of taurine in the central nervous system (CNS) occurs predominantly in astrocytes. A metabolic coupling between astrocytes and neurons has been reported, in which astrocytes provide neurons with hypotaurine as a substrate for taurine production. Taurine has antioxidative, osmoregulatory, and anti-inflammatory functions, among other cytoprotective properties. Astrocytes release taurine as a gliotransmitter, promoting both extracellular and intracellular effects in neurons. The extracellular effects include binding to neuronal GABAA and glycine receptors, with subsequent cellular hyperpolarization, and attenuation of N-methyl-D-aspartic acid (NMDA)-mediated glutamate excitotoxicity. Taurine intracellular effects are directed toward calcium homeostatic pathway, reducing calcium overload and thus preventing excitotoxicity, mitochondrial stress, and apoptosis. However, several physiological aspects of taurine remain unclear, such as the existence or not of a specific taurine receptor. Therefore, further research is needed not only in astrocytes and neurons, but also in other glial cells in order to fully comprehend taurine metabolism and function in the brain. Nonetheless, astrocyte’s role in taurine-induced neuroprotective functions should be considered as a promising therapeutic target of several neuroinflammatory, neurodegenerative and psychiatric diseases in the near future. This review provides an overview of the significant relationship between taurine and astrocytes, as well as its homeostatic and neuroprotective role in the nervous system.

show abstract

The Effects of Taurine Exposure on the Brain and Neurological Disorders

Cited by 7 publications

References 51 publications

Prenatal and Early Postnatal Cerebral d-Aspartate Depletion Influences l-Amino Acid Pathways, Bioenergetic processes, and Developmental Brain Metabolism

Prenatal and Early Postnatal Cerebral d-Aspartate Depletion Influences l-Amino Acid Pathways, Bioenergetic processes, and Developmental Brain Metabolism

Functional imaging and neurochemistry identify in vivo neuroprotection mechanisms counteracting excitotoxicity and neurovascular changes in the hippocampus and visual cortex of obese and type 2 diabetic animal models

Taurine and Astrocytes: A Homeostatic and Neuroprotective Relationship

Contact Info

Product

Resources

About